Prevention of

Cancer
Cancer Genetics

Causes of Cancer

Diagnosis and Treatment of Cancer

Myeloma

Prevention of Cancer

Skin Cancer

Stages of Cancer Development

Prevention of
Cancer

Robert G. McKinnell, Ph.D.

Consulting Editor,
Donna M. Bozzone, Ph.D.
Professor of Biology
Saint Michael’s College
the Biology of Cancer: Prevention of Cancer

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McKinnell, Robert Gilmore.
Prevention of cancer / Robert G. McKinnell ; consulting editor, Donna M. Bozzone.
p. cm. — (Biology of cancer)
Includes bibliographical references and index.
ISBN-13: 978-0-7910-8827-2
ISBN-10: 0-7910-8827-8
1. Cancer--Prevention--Popular works. 2. Cancer--Risk factors--Popular works.
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 Contents
♦

Foreword 6
Acknowledgments 10
Introduction 12

1 You are In Control—Well, Mostly 15

2 Smokers are Not Necessarily Stupid 25

3 Skin Cancer—Do Not Risk It! 47

4 Cervical Cancer—Preventable? 62

5 Childhood Cancer Survivors: A Paradox 76

6 Breast Cancer—Preventable? 88

7 Diet and Exercise Do Make a Difference 103

8 A Final Word on Prevention 115

Glossary 126
Further Resources 134
Index 138
About the Author 144
 Foreword
♦

A pproximately 1,500 people die each day of cancer in the United

States. Worldwide, more than 8 million new cases are diagnosed
each year. In affluent, developed nations such as the United States,
around one out of three people will develop cancer in his or her lifetime.
As deaths from infection and malnutrition become less prevalent in
developing areas of the world, people live longer and cancer incidence
increases to become a leading cause of mortality. Clearly, few people
are left untouched by this disease due either to their own illness or that
of loved ones. This situation leaves us with many questions: What causes
cancer? Can we prevent it? Is there a cure?
Cancer did not originate in the modern world. Evidence of humans
afflicted with cancer dates from ancient times. Examinations of bones
from skeletons that are more than 3,000 years old reveal structures that
appear to be tumors. Records from ancient Egypt, written more than
4,000 years ago, describe breast cancers. Possible cases of bone tumors
have been observed in Egyptian mummies that are more than 5,000 years
old. It is even possible that our species’ ancestors developed cancer. In
1932, Louis Leakey discovered a jawbone, from either Australopithecus
or Homo erectus, that possessed what appeared to be a tumor. Cancer
specialists examined the jawbone and suggested that the tumor was due
to Burkitt’s lymphoma, a type of cancer that affects the immune system.


 Foreword 

It is likely that cancer has been a concern for the human lineage for at
least a million years.
Human beings have been searching for ways to treat and cure cancer
since ancient times, but cancer is becoming an even greater problem to-
day. Because life expectancy increased dramatically in the 20th century
due to public health successes such as improvements in our ability to
prevent and fight infectious disease, more people live long enough to
develop cancer. Children and young adults can develop cancer, but the
chance of developing the disease increases as a person ages. Now that
so many people live longer, cancer incidence has increased dramatically
in the population. As a consequence, the prevalence of cancer came
to the forefront as a public health concern by the middle of the 20th
century. In 1971 President Richard Nixon signed the National Cancer Act
and thus declared “war” on cancer. The National Cancer Act brought
cancer research to the forefront and provided funding and a mandate
to spur research to the National Cancer Institute. During the years since
that action, research laboratories have made significant progress toward
understanding cancer. Surprisingly, the most dramatic insights came
from learning how normal cells function, and by comparing that to what
goes wrong in cancer cells.
Many people think of cancer as a single disease, but it actually
comprises more than 100 different disorders in normal cell and tis-
sue function. Nevertheless, all cancers have one feature in common:
All are diseases of uncontrolled cell division. Under normal circum-
stances, the body regulates the production of new cells very precisely.
In cancer cells, particular defects in deoxyribonucleic acid, or DNA,
lead to breakdowns in the cell communication and growth control that
are normal in healthy cells. Having escaped these controls, cancer
cells can become invasive and spread to other parts of the body. As
 Prevention of Cancer

a consequence, normal tissue and organ functions may be seriously

disrupted. Ultimately, cancer can be fatal.
Even though cancer is a serious disease, modern research has
provided many reasons to feel hopeful about the future of cancer treat-
ment and prevention. First, scientists have learned a great deal about
the specific genes involved in cancer. This information paves the way for
improved early detection, such as identifying individuals with a genetic
predisposition to cancer and monitoring their health to ensure the earli-
est possible detection. Second, knowledge of both the specific genes
involved in cancer and the proteins made by cancer cells has made it
possible to develop very specific and effective treatments for certain
cancers. For example, childhood leukemia, once almost certainly fatal,
now can be treated successfully in the great majority of cases. Similarly,
improved understanding of cancer cell proteins led to the development
of new anticancer drugs such as Herceptin, which is used to treat certain
types of breast tumors. Third, many cancers are preventable. In fact, it is
likely that more than 50 percent of cancers would never occur if people
avoided smoking, overexposure to sun, a high-fat diet, and a sedentary
lifestyle. People have tremendous power to reduce their chances of
developing cancer by making good health and lifestyle decisions. Even
if treatments become perfect, prevention is still preferable to avoid the
anxiety of a diagnosis and the potential pain of treatment.
The books in The Biology of Cancer series reveal information about
the causes of the disease; the DNA changes that result in tumor forma-
tion; ways to prevent, detect, and treat cancer; and detailed accounts
of specific types of cancers that occur in particular tissues or organs.
Books in this series describe what happens to cells as they lose growth
control and how specific cancers affect the body. The Biology of Cancer
series also provides insights into the studies undertaken, the research
 foreword 

experiments done, and the scientists involved in the development of the

present state of knowledge of this disease. In this way, readers get to see
beyond “the facts” and understand more about the process of biomedi-
cal research. Finally, the books in The Biology of Cancer series provide
information to help readers make healthy choices that can reduce the
risk of cancer.
Cancer research is at a very exciting crossroads, affording scientists
the challenge of scientific problem solving as well as the opportunity
to engage in work that is likely to directly benefit people’s health and
well-being. I hope that the books in this series will help readers learn
about cancer. Even more, I hope that these books will capture your inter-
est and awaken your curiosity about cancer so that you ask questions
for which scientists presently have no answers. Perhaps some of your
questions will inspire you to follow your own path of discovery. If so, I
look forward to your joining the community of scientists; after all, there
is still a lot of work to be done.

Donna M. Bozzone, Ph.D.

Professor of Biology
Saint Michael’s College
Colchester, Vermont
 Acknowledgments
♦

M y lifetime spouse, Beverly Kerr McKinnell, continued until days

before her death to be of inestimable help and support during
the labor of producing this book. I thank her first. Portions of the early
manuscript were read by the following to whom I am indebted: Tom
Clayton, Regents Professor of English Language and Literature, Univer-
sity of Minnesota; Nancy M. Finney, author, Saint Joseph, Illinois; and
Debra Louise Carlson, Normandale Community College, Bloomington,
Minnesota. It is a pleasure to acknowledge the continued support of
Elaine M. Challacombe and the technical help of James V. Curley,
both of the Owen H. Wangensteen Historical Library of Biology and
Medicine, University of Minnesota. I credit the joint efforts of Chacko
T. Kuruvilla and Haudy Kazemizadeh Gol, Bio-Medical Library, Univer-
sity of Minnesota, for steady hands in keeping my computer and me on
amicable terms.
Ordinarily the young learn from their elders. Sometimes roles are
reversed. Much of what I learned about word processing I learned from
my daughter Susan Kerr McKinnell of the Academic and Distributed
Computer Services of the University of Minnesota and Public TV’s “Tech
Talk.” I thank her for patience and tolerance of me while I learned new
and exotic endeavors at the computer keyboard.

10
 ACKNOWLEDGMENTS 11

James Chambers, Editor in Chief, Facts on File, made many useful

suggestions that enhanced this book. I thank him for his skilled and
thoughtful efforts.
I would be remiss if I did not express my appreciation to Suzanne
Madison Rohman, who encouraged me with her steadfast confidence in
this work. I am indeed indebted to her.
Finally, several young people helped with their support and affection.
The omission of their last names should not be interpreted as lessening
their contributions. They are Emma, Honor, Arthur, Alex, and Lewis.
 INTRODUCTION
♦

Two thousand souls and twenty thousand ducats

Will not debate the question of this straw:
This is the imposthume of much wealth and peace,
That inward breaks, and shows no cause without
Why the man dies.
Hamlet IV, iv, 26-29

I must confess that I never knew what an “imposthume” was, in Hamlet

or anyplace else, until a truly gifted and insightful English professor,
Gordon W. O’Brien, enlightened me. O’Brien, who has since passed
away, stated: “in the medical commentaries of the Renaissance an im-
posthume was more often a tumor than an abscess, and, in the case of
the internal (inward breaking) imposthume, the tumor was more often
malignant than benign: a fatality resulting from an internal imposthume
was almost always judged to be a fatality resulting from cancer.”
O’Brien informed me that Shakespeare knew about cancer.
Obviously the Bard of Avon could not have been aware of molecular
biology, microscopic anatomy, cancer-causing chemicals, or even
epidemiology—but he got the main point straight. As the readers
of this book grow older, they will probably sooner or later become
acquainted with someone dying of cancer. That person is likely to die
with little outward evidence of the cancer other than perhaps weight

12
 Introduction 13

loss (known as cachexia). Note how accurately cancer was described

by Shakespeare, when he wrote, “and shows no cause without (meaning
“superficially or externally”), Why the man dies.”
But what did Shakespeare mean when he also noted “much wealth
and peace”? Consider the former spouse of a vice president, Margaretta
(Happy) Rockefeller; Betty Ford, the wife of President Gerald Ford; Nancy
Reagan, wife of another president; Shirley Temple Black, child star; and
Julia Child, famous television cook. All were afflicted with breast cancer
and none were poor. The list of famous women afflicted by breast cancer
is long. Famous women aside, consider wealthy Marin County, Califor-
nia, with its many affluent residents and what some have characterized
as the highest rate of breast cancer in the nation. Socioeconomic class
is thought by many students of cancer as an established risk factor, or
something that contributes to one’s chances of developing cancer. Is this
the “much wealth and peace” to which Shakespeare refers? If indeed it
is, I bow to his insight.
I respect the immense knowledge Shakespeare had of life, love,
politics, history, and perhaps here, medicine. I feel that English-speak-
ing people are not truly educated if they are not at least introduced
to Shakespeare in high school or college. To form an acquaintance of
significance, one requires more than an introduction; one could do far
worse than to enjoy Shakespeare throughout life.
So what does that have to do with this book? Let me make a judgment
about education. It is no longer acceptable for an enlightened person to
be entirely ignorant of biology any more than it is to be illiterate. Biology
is no less a part of the education of a complete person than is an English
course. Cancer is one facet of the many sided gem that is modern biol-
ogy. Therefore students of English, history, art, mathematics, and other
disciplines, I plead with you to read and take seriously that which is
14 Prevention of Cancer

written in this book. And it goes without saying that biology students are
similarly admonished to learn. Become enlightened and enjoy; learning
is such pleasure. This book discusses the causes and risks connected to
cancer according to current research and how to avoid or reduce them
in your life. Careful reading of this book will add to your knowledge of
biology and cancer, which is essential for an enlightened person—and
it may place you and your loved ones at a lower cancer risk. It is worth
the effort.

Robert G. McKinnell
 1
You Are In Control
—Well, Mostly

Key Points

♦ Not all cancer is caused by modern civilization. It is a prehistoric

disease that has been found in fossilized remains of animals and
humans.

♦ A form of cancer known as multiple myeloma has been found in

fossil remains found throughout the world, including Hungary, Eng-
land, the Pyrenees, and the United States.

♦ Although humans have always been susceptible to cancer, there are

some forms of the disease that are preventable.

The message of this book is that in the matter of cancer prevention

and risk reduction you are responsible. Not the government, not your
teachers, not your family doctor, not even your parents—you alone are

15
16 Prevention of Cancer

responsible. If you wish to remain in a low-cancer risk group, you must

behave in a way that minimizes your chance of developing this group
of related diseases. As you will learn while reading this book, there are
an enormous number of cancer deaths in the United States (well over
half a million each year) due in some large part to personal behavior
that increases cancer risk. By reading this book, you will learn how to
avoid many forms of cancer and become less likely to pay the ultimate
price for uninformed behavior. However, you should know from the very
beginning that even the most careful behavior will not eliminate all risk
of cancer. Some cancer is due to heredity, some is caused by exposure
to natural radiation, and some is due to chemical causing substances
that are yet to be identified. It is difficult indeed to avoid these potential
hazards. Even so, most cancer can be avoided.

Is Cancer a Disease of Civilization?

Many people point accusing fingers at the many kinds of toxic and
potentially lethal substances our society produces as the source of
numerous ills. They fear the exhausts of powerful diesel-driven trac-
tor trailers on our highways and the enormous jet engines that move
our air fleets. They worry about new chemicals that are introduced
each year—chemicals from the stuff used to make non-sticking fry
pans to the flame retardants used in children’s sleepwear. They are
apprehensive about the nearly ubiquitous use of powerful weed con-
trol chemicals used in agriculture and on the lawns of private homes.
They feel that a less-complex civilization would be free of the plague
of cancer.
Here at the beginning of this book, you need to understand that
cancer is not a disease of civilization. Clearly, not all cancer results from
 You are In Control—Well, Mostly 17

Figure 1.1 Many people fear noxious chemicals that pollute our environment.
Shown here are smokestacks emitting possibly toxic fumes and in foreground
an aqueduct dumping industrial waste into a river. (Linda Bartlett/National Cancer
Institute/U.S. National Institutes of Health)

our modern environment and behavior. Some cancer is a response to

factors that are outside our personal control. Let us consider human
biology at a time long before the problem of industrial and chemical
pollution. Although we cannot go back to that time, we can learn if can-
cer afflicted people in prehistoric (and obviously, pre-industrial) times.
Of course, not much remains of the people who lived thousands of years
ago. But in some cases, human bones have been discovered that convey
a message about cancer.
18 Prevention of Cancer

A Cancer Known from Fossils

Multiple myeloma is a cancer of plasma cells found in bone marrow.

It is a form of cancer that afflicted the ancients as it does people today.
Obviously ancient people did not breathe fumes from cars or from
aircraft overhead. They knew nothing about chemicals used to manu-
facture plastics, they had never heard of herbicides or genetically modi-
fied crops, and they had no nuclear energy plants. You might think they
would have had a tranquil life as far as malignant disease is concerned.
But their remains tell us that this isn’t the case. So how did misfortune
come to visit the ancients in the form of cancer? Quite frankly, we do
not know.
If all or most of the ancients who had multiple myeloma came from
one place, there might be clues to causation. However, fossil humans
who are thought to have had the disease have been found in sites located
in Hungary, England, the Pyrenees mountains in Europe, and the United
States (including sites in Kentucky, Florida, Mississippi, California, New
York, and Missouri). Intensive studies would probably reveal even more
sites. Some of the human remains are believed to date from 3,000 to 5,000
years ago. At this point, a skeptical student might ask: How do you know
that the prehistoric humans had a specific cancer? Cancer is a disease
of cells and no intact cells remain in the fossils. Therefore it will never
be known for certain that the bony lesions observed in the fossils were
indeed caused by multiple myeloma. However, many experts who have
studied the peculiar fossil lesions believe the lesions resulted from this
form of cancer. Multiple myeloma cancer cells ultimately cause holes to
form in bone that have a characteristic “punched out” appearance. In
a progressive disease, one would suspect that some incipient (not fully
formed holes) would be present. These are detected by taking an X ray
of the fossil bones.
 You are In Control—Well, Mostly 19

Obviously, the ancients who had multiple myeloma had symptoms

other than bones with holes, but only the fossils of their bones remain.
Today, multiple myeloma patients often have Bence Jones proteins
in their urine. It is likely that some, if not most, of the individuals who
are now fossil relics had these same Bence Jones proteins in their urine
when they were alive. If they did, as experts believe, one might say that
this is an ancient urinary analysis made without the urine. While the
message here is not about urine from antiquity, it does show how much
there is to learn about ancient cancer. What did those prehistoric people
do to get this terrible disease? There is absolutely no way that they could
have prevented the cancer that ultimately killed them. This is an example
from antiquity of a lethal cancer that occurs for unknown reasons. Some
contemporary cases of multiple myeloma probably occur regardless of
what people try to do to prevent it. In other words, although we know
of modern risk factors (such as exposure to radiation), there seems to
be a level of multiple myeloma that occurs because of one or more
unknown factors, such as heredity or exposure to naturally occurring
radiation. The ancients cannot be held accountable for these unknown
factors—and neither can people today. That is why this chapter is titled
“You are in control—well, mostly.”

A Common Childhood Cancer

Another example of a cancer that cannot be prevented with present

medical knowledge is acute lymphoblastic leukemia (ALL). It is the
most common childhood cancer. No one knows what causes ALL in
children. Radiation has been suggested as a cause because of atomic
bomb studies. No American children have been exposed to the horrors
of atomic bombs. Studies of lower dose radiation are disputed by some.
20 Prevention of Cancer

Chemotherapeutic drugs and toxic chemicals have also been suggested

as contributing to the cause of ALL. A genetic component may contribute
to ALL vulnerability, but the fact remains ALL almost always occurs with
no apparent causation. How could a five-year-old child avoid a disease
whose cause is unknown? Of course the child did not smoke, did not
work with radioactive isotopes, was not taking chemotherapeutic drugs
and did not work with industrial chemicals. How, then, could the child
be responsible for his or her leukemia?
Described here are two cancers that are not related to cancer risk
precautions. The message of the two examples—and there are more
examples that could be provided—is that not all cancer is preventable
with present knowledge.

A Simple Truth: Most Cancer Is Preventable

While acknowledging the truth of the preceding paragraphs, the

message of this book is that most cancer is preventable. Margaret M.
Heckler, long time congresswoman from Massachusetts (1967–1982),
who became secretary of Health and Human Services (1983–1985) and
ambassador to Ireland (1985–1989), stated, “Too few Americans realize
the simple truth that cancer is usually caused by the way we live, and
its risks can be reduced by the choices we make.” She estimated that an
astounding 80 percent of cancer is linked to lifestyle and environmental
factors. Earlier I wrote that more than half a million Americans die each
year from cancer (more precisely, the American Cancer Society predicts
that 559,650 Americans will die in 2007—or, about 1,500 per day). The 80
percent that Heckler cites amounts to something like 450,000 needless
deaths per year! Dr. Lee W. Wattenberg from the University of Minnesota
and a former president of the American Association for Cancer Research,
 You are In Control—Well, Mostly 21

Figure 1.2 Most cancer is preventable. This classic poster supports

that view. (National Cancer Institute/U.S. National Institutes of Health)
22 Prevention of Cancer

Inc. wrote, “The most desirable way of eliminating the impact of cancer
is by prevention.” Risk reduction in tobacco smoking is well known.
Almost all lung cancer would be eliminated with the elimination of
smoking. This has been known for two thirds of a century. Skin cancer
is another well-known cancer that is largely preventable. Other cancers
with known risk-reduction potential will be discussed in this book. It

♦ Can cers of the Past

T he study of diseases from antiquity is known as paleopathology. The

prefix paleo- refers to something ancient. Pathology is the scientific
study of disease. Thus, paleopathology is the study of ancient disease in
general and for this book, ancient cancer. Fossil bone is about all that
remains of most ancient animals and humans. A few bony tumors have
been found in fish fossils that are probably 300 million years old. Dinosaur
remains have been discovered from a variety of sites of the Jurassic period
of the Mesozoic era (during the Age of Reptiles, about 150 to 200 million
years ago) in North America and some of these creatures exhibit evidence
of benign tumor growths in bone known as osteomas and, of greater inter-
est, cancerous osteosarcomas, which also affect bone. Clearly, cancer is
not simply a modern affliction of animals and humans.
While benign and malignant tumors are relatively rare among fossils,
the tumors may not have been all that rare in their time. Even now, a wild
animal with cancer or any other disease is less able to evade attacking
animals and is more likely to be eaten. During geologic times, a devoured
animal left behind either nothing, or only minimal fragments which might
 You are In Control—Well, Mostly 23

is my intent to provide information that will impact cancer in the most

desirable way—by prevention.

London and Cholera: A Model for Cancer?

Cancer is a horrible malady—but readers should be aware that the his-

tory of humans has been plagued with many equally dreaded maladies

become fossils. Thus, the rarity of cancer among fossils may not indicate
the actual prevalence of cancer.
Modern Chinese males and people of the Near East including Egypt, are
vulnerable to a cancer known as nasopharyngeal carcinoma, which affects
the nasal cavity and the portion of the pharynx that is adjacent to the nasal
cavity hence “nasopharyngeal.” Egyptian mummies had a relatively high rate
of nasopharyngeal carcinoma. We know this because of the great number
of mummies that have been studied. Modern studies have shown that the
cancer is related in some causal way to infection by a herpesvirus known
as the Epstein-Barr virus. (The Epstein-Barr herpesvirus is not the herpes
virus that causes genital herpes infections; actually, there are many kinds of
herpesviruses affecting many animals and humans.) It is believed that the
nasopharyngeal carcinoma of ancient Egypt had this same relationship to
the Epstein-Barr virus and thus we can now estimate the antiquity of a virus
through paleopathological studies. Furthermore, we can predict that if ever
a cache of Chinese mummies were to be discovered (remember that modern
Chinese males are particularly vulnerable to the cancer), they too will likely
have cases of nasopharyngeal carcinoma. If this were to happen, it would
illustrate the predictive power of paleopathology.
24 Prevention of Cancer

(refer to Chapter 8). One of these dreaded diseases is cholera. Patients

who had cholera prayed. They did not pray for a cure; rather, they prayed
for death. Only death would relieve them of indescribable pain and
suffering. John Snow (1813–1858) of London, one of the greatest doc-
tors of all time, discovered that contaminated water caused the spread
of cholera. To make one of the most remarkable stories in the history
of medicine short, Snow determined that the key to reducing cholera
deaths was prevention. Water for human consumption must be free from
whatever it was that caused the disease. It was not known then but it
is the bacterium Vibrio cholerae, which causes cholera. Snow found
that drinking water not contaminated with sewage prevented the dread
disease. Prevention worked then and it works now! Few students except
those who study history have heard of John Snow or of cholera; that is
because this noxious disease has all but been eliminated in developed
countries—by prevention. It is a reasonable query to wonder if most
cancer could not also be prevented. Indeed it could be, and that is what
this book will explore.

S u mmary

It is true that many elements of modern, industrial society contribute to

causing cancer. However, historical evidence tells us that some types
of cancer can occur in the absence of these factors. Thus, while we
know that we may take steps to greatly reduce the risk for some types
of cancer and that prevention may be the best tool in the fight against
cancer, it is not possible to completely eliminate the risk of all cancer
from our lives.
 2
Smokers Are Not
Necessarily Stupid

Key Points

♦ There are more than 4,000 chemicals, including 55 known carcino-

gens, or cancer-causing substances, in cigarettes.

♦ Nicotine is the substance in cigarettes that causes them to be addic-

tive. There are several drugs, including nicotine patches and gum,
that may help smokers gradually overcome their addiction.

♦ Group therapy, antitobacco public service announcements, and

doctors’ consultations may also help smokers quit or reduce the
number of new smokers.

♦ According to the U.S. Surgeon General, the average male acquires

13.2 years and the average female gains 14.5 years of life expectancy
by never smoking.

25
26 Prevention of Cancer

There are many signs indicating that the university buildings I work
in are smoke-free. Because the buildings are smoke-free, I often see
cigarette smokers standing 25 feet or more away from the entrances
(as required by university regulation so that the smoke does not drift
back into the buildings). Who are those people? Surprisingly, most of
the smokers are health care workers. Health care workers know that
cigarette smoking results in lung cancer (as well as a host of other health
problems). Indeed, just about everyone knows that tobacco causes can-
cer. So why do some smoke? Don’t they agree that smoking is stupid?

Hooked on the Habit

It’s easy to see why so many people, especially young people, decide
to smoke. For one, it’s trendy and seems like a hip and rebellious thing
to do. In the movies, suave and sophisticated-looking characters are
often shown with a cigarette in hand. Add to this the notion that smok-
ing may help control weight or reduce stress. Very effective advertising
of tobacco products, peer pressure, and a host of other factors also
weigh in. Who hasn’t thought about giving it a try? It’s no wonder that
health workers, who are frequently subjected to stress, decide to pick
up the habit.
I was once a smoker, too. I started back in the 1950s during the
Korean War. Even then it was well known that smoking was not healthy.
However, because cigarettes were so cheap (seven cents tax-free to
servicemen during the Korean War; they were a nickel a pack during
World War II), we used to joke that we could not afford not to smoke.
Our chaplains used a big portion of the welfare and recreation fund to
buy more tobacco to give away at special events—smoking was a habit
that had the blessings of our clergymen! At the time, I believed that if
 Smokers are Not Necessarily Stupid 27

tobacco were truly harmful, the government would not let us have it.
And so, I slipped into the smoking habit. In too short a time I developed
a pack-a-day habit and when I was under stress I smoked even more. I
thought I enjoyed the habit and more than likely I did. Smoking was bad
judgment, but not the result of a flaw in my character or intelligence.
While it was easy to “slip into the habit” of smoking, it was exceed-
ingly difficult to stop. I quit, but I had a pervasive feeling of deprivation
that would not go away—for decades. Ultimately, I won, but it was no
piece of cake. So, if you have not started, don’t.

Low Tar Cigarettes

Low tar, low nicotine cigarettes came out during the time that I was
endeavoring to quit. A number of my fellow quitters were switching to
“safer” low tar, low nicotine smokes during that time—it was thought
that smoking light or ultralight cigarettes, while weaning away from the
tobacco habit, would reduce cancer risk. That is not true; “safer” ciga-
rettes are not safer. Stephen Hecht and his coworkers at the University of
Minnesota found that it makes no difference what kind of cigarettes are
smoked with regard to the intake of nicotine and cancer-causing chemi-
cals. His group studied the excretion into the urine of the metabolic
end products of cigarettes. No difference in the chemicals in the urine of
light cigarette smokers versus that of regular cigarette smokers translates
into zero reduction in lung cancer risk.
While considering urinary metabolites of tobacco carcinogens,
a study by University of Minnesota Cancer Center scientists in 2005
revealed that nonsmokers who inhale secondhand smoke excrete
the same end products of cancer-causing chemicals as do cigarette
smokers. Further, nonsmoking workers in bars and restaurants excrete
28 Prevention of Cancer

Figure 2.1 Cigarettes of any kind (regular, filter, low tar, low nicotine) are
hazardous as indicated by the warning label that, by law, appears on all cigarette
packaging. (Bill Branso/National Cancer Institute/U.S. National Institutes of Health)

four to six times more of the noxious chemicals than do nonsmoking

workers in other smoking-permitted workplaces. The scientists could
even tell what days were workdays versus days not worked by examin-
ing urine samples.
The Minnesota Cancer Center workers reported in 2006 that another
group of nonsmokers were inhaling significant amounts of tobacco
smoke and excreting in their urine the same tobacco metabolites as
smokers. This group of nonsmokers did not complain—in fact, they
could not complain. The group was newborn infants and babies of
parents that smoked. Incredibly, the level of tobacco metabolites was
 Smokers are Not Necessarily Stupid 29

similar to levels found in adult smokers. It is my opinion these babies

were abused by the neglect of thoughtless parental smokers. In time,
some group of scientists will discover the health effects of exposure of
babies to secondhand smoke—by that time, it will be too late to reverse
the ill effects.

How Does Tobacco Kill?

I taught a college course on the biology of cancer for 30 years. From

time to time I was asked how smoking causes cancer. That should be
an easy question to answer with all of the research that has gone into
the study of tobacco. Actually, it is far from simple. Let us begin with
nicotine. Nicotine does not cause cancer so why begin with it? Nicotine
is addictive and therein is a great problem. Nicotine forces the smoker
to smoke more and more and makes it nearly impossible to quit. The
smoker inhales increasingly greater amounts of tobacco smoke, which
contains at least 4,000 chemicals, 55 of which are known carcinogens,
or cancer-causing substances (listed by the International Agency for
Research on Cancer, a part of the World Health Organization located
in Lyon, France). The known carcinogens and their metabolic products
cause cancer, by, among other ways, bonding with DNA directly to inter-
fere with proper cell metabolism or by forming mutations to the genetic
material of DNA, which in turn causes cancer. In a sense, it does not
make much difference which carcinogen causes cancer in you or your
friends, the end result is tobacco-caused cancer.

Smoking is Deadly

In 1951, Sir Richard Doll, knighted by Queen Elizabeth II for his

monumental research on smoking among British doctors, began a
30 Prevention of Cancer

prospective study on the effects of tobacco. This means that Doll’s

investigation of cigarette smokers was designed to follow participants
forward in time, rather than retrospectively. The study, which continues
to this day, has identified some surprising facts about smoking. One is
that lung cancer and its companion chronic obstructive pulmonary
disease (COPD), a disease of the airways, account for only about a
quarter of the “excess mortality” among smokers. Excess mortality relates
to premature deaths that would not have occurred had the participants
not smoked. What caused the other 75 percent? One-quarter of the
excess deaths are attributable to coronary heart disease, damage
to the heart as a result of reduced blood supply. The remaining half
of the excess deaths are due to other cancers (these include cancers
of the lips, mouth, esophagus, larynx, pharynx, stomach, pancreas,
cervix, kidney, stomach, bladder, colorectal cancer, and acute myeloid
leukemia), other respiratory diseases, and other vascular disease. While
it is common to think of lung cancer first when considering the ill effects
of smoking, actually lung cancer accounts for but a fraction of the total
deaths caused by tobacco smoke inhalation.
The annual total of unnecessary early deaths in the United States
due to smoking is calculated to be about 438,000 (1997–2001 data from
the Centers for Disease Control and Prevention [CDC], a government
agency). In comparison, AIDS is thought to have claimed the lives of
17,000 Americans in 1998 (2005 Data from the CDC). Thus, smoking-
related deaths are 25 times more common than deaths due to AIDS.
Smoking related deaths claim about 10 times as many deaths as breast
cancer. (In 2007, 40,460 women are expected to die of breast cancer, ac-
cording to American Cancer Society data). Any unnecessary death, be
it by accident, war, AIDS, or whatever, is dreadful. It is not the purpose of
this discussion of numbers to minimize one lethal condition compared
 Smokers are Not Necessarily Stupid 31

with another. Rather, the numbers given here are to hammer home the
incredible cost in lives lost due to tobacco use.
Although lung cancer deaths account for only a fraction of total
deaths due to smoking, lung cancer however does cause over 30 percent
of deaths due to malignancy among males. To give some perspective,
lung cancer kills more men than prostate, kidney, colon, rectal, all forms
of leukemia and pancreatic cancers put together. Lung cancer is the most
common cause of death by cancer of both men and women. Sir Richard
Doll has stated that about half of all cigarette smokers will be killed by
their habit. Writing elsewhere, I state that there is no procedure in surgery,
radiation, chemotherapy, or any combination thereof, available now or
even rationally hoped for in the future, that could come close to doing
more to reduce cancer deaths than simply quitting smoking. Cancer
research is extraordinarily expensive—smoking cessation not only costs
nothing, but it would also saves an incredible number of lives. It also saves
money lost to time away from jobs, as well as the expense of prescription
drugs, hospital and nursing home care, disability costs, and of course, the
cost of premature end-of-life expenses such as cremation and burial.
A good high school student is wise to be skeptical. The wise student
may be inclined to doubt the importance of cancer deaths, thinking,
“We all die sometime and thus, who cares how we die?” True we all die,
but is the notion of not caring how and when wise?
The CDC has calculated that cigarette smoking by citizens of the
United States results in 5.5 million years of potential life lost annually.
How does that translate into years of life lost to individuals? Sir Richard
Doll did the math. People 25 to 34 years of age who stop smoking at
that age gain 10 years of life expectancy. (Note: If you are 16 years old
now, 10 years is all the time you have enjoyed since the first grade—not
a trivial span of time.) A lifetime smoker 60 years of age gains three
32 Prevention of Cancer

Figure 2.2  AP Images

years by quitting. The Surgeon General of the United States writes that
the average male acquires 13.2 years and the average female gains 14.5
years by never smoking. I quit when I was in my 30s. If I am average, my
gain in life expectancy from quitting smoking has made the difference of
seeing my grandchildren grow. I do not want to check out just yet. Life is
simply too good to give up. Ask any grandpa how much fun it is to take
a grandchild fishing and you will get the same answer, as you likely will
from the grandchild. I hope readers agree with me that an extra 10 or
more years of life is worth quitting or never smoking.
 Smokers are Not Necessarily Stupid 33

Tax on Tobacco—Cheap

Smoking is the principal cause of premature death in the United

States but, if the lethal aspects of smoking are insufficient to attract
attention, consider the fact that for every pack of cigarettes sold per
year, there are costs not covered by taxes. Those costs are smoking-
caused health care expenses and lost productivity which has been
calculated to be an average of $7.18 per pack smoked but as high as
$11.25 per pack in the District of Columbia (data from the U.S. Centers
for Disease Control and Prevention). Direct medical expenses due to
smoking in Illinois in 2004 was an astonishing $4.11 billion. Our coun-
try spent $75 billion in direct medical costs to which must be added
$92 billion in lost productivity for a total of $167 billion in annual
health related loss due to smoking. This leads to an inescapable con-
clusion that tobacco taxes are cheap and that the nonsmoking public
subsidizes (and thus inadvertently encourages) smoking. Is it ethical
not to collect money that would offset expenses directly related to
the effects of smoking? The economic costs, published by the U.S.
Centers for Disease Control and Prevention are real. However, one
aspect of smoking actually saves the taxpayer money. Social Security
benefits are not paid to dead individuals and because smokers have
a reduced life expectancy, they are actually helping the nation pay
for retirement. A nongovernmental source has stated that premature
death saves the government 32 cents per pack sold and this with an
average of 53 cents of tax imposed per pack on cigarettes “profits”
the government by 85 cents per pack sold. Obviously the govern-
ment is not profiting when the high cost of smoking is factored into 
the equation.
34 Prevention of Cancer

Lung Cancer also Targets the Brain

Metastasis refers to the spread of cancer. Cancer is rarely a localized

disease. Instead, it spreads throughout the body. This is what makes
cancer such a difficult disease to treat. A surprising bit of medical lore
relates to the fact that physicians often order a chest X ray when a patient
shows symptoms of a cancer in the brain. Why look at the chest? The an-
swer is that cancer seldom metastasizes randomly; rather the malignant
cancer cells tend to spread to specific tissues or organs. The brain is one
of those organs that lung cancer cells particularly like and consequently,
when symptoms appear that suggest a brain cancer, it is possible that
the patient has lung cancer. Remember lung cancer cells that home for
one’s brain the next time you inhale on a cigarette deeply—is that last
drag (or any drag) on a butt worth it?

Nicotiana Tabacum, King James,

a New Orleans Surgeon, and Sex

Most people are aware of the New World origin of tobacco. Pre-Co-
lumbian Native Americans consumed burning tobacco for religious
purposes. That consumption was noted by explorers who took
tobacco seeds and leaves back to Europe. In 1556, Jean Nicot de Vil-
lemain, the French ambassador to Lisbon, sent tobacco to the court of
Catherine de Médicis, queen of France. The ambassador’s name was
given to this plant, Nicotiana. Only nine years later, Sir Walter Raleigh
was reputed to have introduced tobacco to England during the reign
of Elizabeth I (1558–1603). James I of England (who was also James
VI of Scotland and is the “James” of the biblical King James Version)
followed Elizabeth on the throne and he reigned from 1603 to 1625.
James put the first tobacco tax in place. His tax was a 400-year head
 Smokers are Not Necessarily Stupid 35

Figure 2.3 Colored computed tomography scan of the head of a patient with
brain cancer that metastasized from a carcinoma in a lung. ( DU CANE MEDICAL
IMAGING LTD/Photo Researchers, Inc.)
36 Prevention of Cancer

start on the recognition that taxes (and therefore prices) affect con-
sumption. He hated tobacco and wrote in 1604 that smoking was: “A
custome lothsome to the eye, hateful to the Nose, harmefull to the

♦ Wh at is Metastasis?

M etastasis is what both physicians and patients fear—it absolutely

defines a growth as malignant. The practical significance of metas-
tasis is that prior to that event, simple removal of the growth is all that is
needed for permanent cure. Metastatic cancer is a problem of a far more
dangerous nature. For metastasis to occur, the original cancer (known as
the “primary” cancer) must grow, invade normal nearby tissue, and gain
access to a blood or lymph vessel, circulate in the blood or lymph, exit
the vessel and move into new tissue where the cancer cells grow and form
“secondary” colonies. The whole process is repeated again and again until
there are multiple metastatic cancer growths.
A surgeon can remove a primary cancer from virtually any part of
the body. Removal of all multiple metastatic colonies at diverse locations
throughout the body is ordinarily an impossible task. If untreated, the
multiple cancer growths will lead to the death of the victim. This is why
metastasis is justly feared.
Normal cells ordinarily do not move about in the body. Normal brain
tissue remains in the brain and normal liver cells remain in the liver. Some
noncancerous cells do however move about during embryonic development
and adult life. Sex cells do not have their origin in the ovaries and the
testes. During embryological development, the embryonic sex cells migrate
to the appropriate sex organ. This normal cell behavior mimics to a limited
 Smokers are Not Necessarily Stupid 37

braine, daungerous to the Lungs, and in the blacke stinking fume

thereof, nearest resembling the horrible Stigian smoke of the pit that
is bottomelesse.”

degree metastasis. Some women suffer from endometriosis, a non-malignant

but inappropriate wandering of uterine cells to a distant location in the
abdomen. While the uterine cells that wander are not normal, neither are
they cancer. Such examples may provide cancer researchers with clues to the
cell mechanisms of metastatic behavior. The clues may lead to the eventual
control of metastasis—which is the control of cancer itself.
Chemotherapy, the use of chemicals to fight cancer, is a treatment
that recognizes that cancer is rarely a localized disease. Chemotherapeutic
drugs are given that treat cancer at its many locations in the body. Che-
motherapy thus is treatment of metastasis.
As described in another chapter, malignant melanoma has the poten-
tial to metastasize, just like lung cancer can metastasize to the brain’s
tissues. The establishment of metastatic melanoma colonies can occur
in essentially every tissue and organ in the body. Common sites of early
melanoma metastasis include skin, connective tissue under the skin, and
lymph nodes.
Early diagnosis for any cancer is extraordinarily important. It has been
estimated that most, perhaps three out of four, cancers have already un-
dergone metastasis at the time of initial diagnosis. As indicated above,
metastatic cancer is far more difficult to treat than the simple surgical
removal of a localized lump. A monthly check of moles and other “spots”
may increase awareness of skin cancer and perhaps lead to an early lifesav-
ing diagnosis by a dermatologist.
38 Prevention of Cancer

Much more recently than the time of King James, Alton Ochsner of
Tulane University in New Orleans, became interested in lung cancer.
His interests developed after World War I when veterans of the war
developed lung cancer. Ochsner was far ahead of his medical profes-
sion and scientists when he argued for prevention—his view was do
not smoke but if you do smoke, stop now. Prevention was preached
by Ochsner and it is as critically important now as it was 50 years ago.
Tulane University’s surgeon was truly one of the great doctors of the
20th century. Fast forward to The Health Consequences of Smoking: A
Report of the Surgeon General, which was published in 2004. This report
confirmed the findings of Alton Ochsner and Sir Richard Doll.
The issue to be discussed at this point is how to assist in smoking
cessation. The lifelong nonsmoker already has an enhanced life expec-
tancy. What can we do to assist those who consume tobacco to quit?

♦ smo k ing—more conc ern s th a n c a nc e r

Supplementary to a concern for cancer is the following, which is addressed

to young male readers: This addendum is in italics and is separated from
the main part of the chapter because, while it is extra material deserving of
contemplation, it does not concern cancer and the Surgeon General of the
United States cautions that conclusive evidence is not yet available. However,
there is emerging evidence from careful studies in the United States, England,
Iran, Italy, Egypt, Finland, and other places, that smoking contributes to, or
may cause, erectile dysfunction. If not cancer, perhaps erectile problems may
elicit concern. Enough said?
 Smokers are Not Necessarily Stupid 39

Figure 2.4 A man wearing a nicotine patch designed to control cravings for
nicotine and help with smoking cessation. ( Doug Martin/Photo Researchers, Inc.)

Smoking Cessation:
Preventive Medicine’s Most Difficult Area

Starting smoking is easy—it is extraordinarily difficult to quit. The

success rate is low and recidivism (meaning to “fall back” or relapse)
is high. Obviously, epidemiologists and physicians have a lot to learn
about what helps a smoker quit. I believe that smokers will profit from
direct discussions with their doctor. If you smoke, there are several ways
to help you quit the habit.
40 Prevention of Cancer

Group Programs to Help in Smoking Cessation

Individual counseling yields few quitters. However, group counseling is
often effective. Groups provide mutual support for those who wish to
quit smoking.
In one smoking cessation study, a group of high school students
were offered weekly discussions of smoking problems. The students
were shown videos and had the opportunity to talk with a doctor about
their addiction. They became aware of how much others in their group
wanted to quit. They discussed the smoking habits of their friends and
parents and how to obtain support for quitting. The students were taught
how to manage their desire to smoke and the stresses and social con-
sequences of quitting. They were offered a drug (with parental permis-
sion—the drug, bupropion, discussed on the following page) to assist
in smoking cessation. These approaches were tailored to the needs of
individual students. Was the program a success? Only a little more than
a quarter of the students quit, but that quit rate is actually high. Worthy
of mention is that two-thirds of the students who continued to smoke
reduced their tobacco consumption.

Nicotine to Assist in Smoking Cessation

Nicotine has been likened to cocaine or heroin in its addictive power.
Because the goal is to eliminate nicotine intake, it may seem odd that
nicotine is used to assist in quitting. The rationale is to use nicotine to
combat withdrawal symptoms that occur when a smoker stops. When
smokers quit “cold turkey,” an intense desire or craving for a cigarette oc-
curs, which may be accompanied by irritability and anxiety. As a result,
it is better to taper off and quit.
Carefully controlled doses of nicotine can be helpful in enduring
difficulties of withdrawal. Nicotine chewing gum and transdermal
 Smokers are Not Necessarily Stupid 41

patches that transfer the drug through the skin are well known options
for smokers who want to quit. Hard candy with nicotine (also known
as lozenges or troches) is also available. These sources of nicotine are
available over the counter (no prescription required) at drugstores.
However, consult with your doctor before using of any of these nicotine
products. They are potentially dangerous with powerful side effects of
their own if not properly used. A prescription from a physician is neces-
sary to obtain inhalers or nasal sprays containing nicotine.
Another drug used alone or with nicotine replacement therapy is
bupropion. Bupropion is a popular antidepressant, and is sold under
several trademarked names. The drug has potentially dangerous side
effects for young people and, like all prescription drugs, it must be
used only under the direct care of a doctor. Buspirone and a similar
drug, nortriptyline, reduce the uneasy feelings associated with smoking
withdrawal, but probably have little direct effect in helping smokers quit.
(Buspirone hydrochloride and nortriptyline are also generic nonpropri-
etary names.)
As stated above, the efficacy of drugs in the management of smok-
ing cessation is not outstanding. The majority of treated individuals will
resume smoking.

Public Efforts to Aid in Smoking Cessation

Most young people, as well as many adults, have limited money. It was
stated previously in this chapter that cigarette taxes are indeed cheap.
Many experts believe that a significant increase in both federal and state
taxes on cigarettes will reduce cigarette consumption. Many people
consider cigarette taxes fair despite their unpopularity. The taxes are
unpopular because they increase the cost of cigarettes but fair because
42 Prevention of Cancer

♦ A B oy w ith a Modest Origin

B ec omes a Medica l Hero

T he boy referred to here was born Monday, May 4, 1896, at Kimball,

South Dakota, and was named Edward William Alton Ochsner, although
he was far better known as simply Alton Ochsner. After growing up in
Kimball, Ochsner worked his way through the University of South Dakota
and graduated in 1918 with a near A average. He was inducted into Phi
Beta Kappa, the highest academic honorary society on campus. This was
followed by medical training at Washington University in Saint Louis, Mis-
souri. Before long, he was a 30-year-old surgeon teaching at the University
of Wisconsin in Madison, which was soon followed by an invitation to
become head, at age 31, of the Department of Surgery, Tulane University,
New Orleans, Louisiana. While he was an extraordinarily gifted surgeon
(he was cofounder and long time coeditor of the medical journal Surgery
with University of Minnesota’s Owen Wangensteen), he is remembered here
because of his pioneering efforts devoted to education about the hazards
of smoking. Dr. Ochsner wrote:

When I was a medical student in 1919, we admitted a patient with

lung cancer to Barnes (hospital in Saint Louis). As usual, the patient
died, because the mortality was about 100 percent. Dr. Dock (a
medical school professor) had us witness the autopsy because he
said that the condition was so rare that we’d never see another case
for as long as we lived. I didn’t see another case for 17 years—until
1936. Then there were nine cases in six months. An epidemic. There
had to be a cause. They were all men, all smoked cigarettes heavily, all
began smoking in the First World War. When I researched the history
 Smokers are Not Necessarily Stupid 43

Figure 2.5 Alton Ochsner was a pioneer in establishing the link between
smoking and lung cancer. (National Library of Medicine/U.S. National Institutes of
Health)

of smoking, I found that very few cigarettes had been consumed

prior to World War I. In 1936, I had the temerity to state—not
suggest—that cigarettes caused this new plague.

In 1939, Alton Ochsner repeated his view on the cause of lung can-
cer: “It’s our conviction that the increase in the incidence of pulmonary
carcinoma is due largely to the increase in smoking, particularly cigarette
smoking, which is universally associated with inhalation.”

(continues)
44 Prevention of Cancer

(continued)

Few believed the New Orleans surgeon. Dr. Evarts A. Graham, professor
of surgery at Washington University School of Medicine, a 50-year smoker
himself, simply viewed Ochsner’s notion as “how dumb and how stupid.”
Dr. Graham thought of the relationship between smoking and lung cancer
as coincidental and remarked that the sale of women’s silk stockings paral-
leled the increase in lung cancer also—a coincidence but certainly not
causal. Graham later apologized to Dr. Oschner for his silk stocking remark.
The apology related to the illness of Dr. Graham, the smoker, who shortly
thereafter died of lung cancer.
Ochsner wrote a number of medical articles during the 1930s and 1940s
associating lung cancer with smoking. While there were other pioneers
who related smoking to lung cancer, Dr. Alton Ochsner was particularly
believable because of his stature as an extraordinarily gifted surgeon.
He was particularly powerful in linking lung cancer to smoking because,
as a chest surgeon, he saw the effects of smoking on the lungs close up
and first hand. The initial report on smoking and health of the Surgeon
General of the United States was in 1964, a quarter of a century after Dr.
Ochsner’s clinical studies and 10 years after Ochsner’s 1954 book, Smoking
and Cancer: A Doctor’s Report.
Not a bad career for a boy born in a sod house on the prairie.

of the great medical cost of smoking, which should be borne by smok-

ers; recall that failure to collect appropriate tobacco taxes are a subsidy
to the smoker and to the tobacco industry. Nonsmokers have a right to
ask why they must support an unhealthy habit and a wealthy industry.
 Smokers are Not Necessarily Stupid 45

Many people become billboards for their clothing with the out-
side tags and maker’s logos. Brand loyalty is real for clothing, and as
a former smoker, I know it is also just as real for cigarettes. Smoking
manufacturers are also aware of brand loyalty and tailor their efforts to
generate loyalty among young people. Dr. Dale Kunkel of the University
of Arizona has written that point of sale marketing practices urgently
need legislative control. This refers to how cigarettes are promoted and
advertised at retail stores, which does indeed promote smoking among
young people. Dr. Kunkel noted that in 1969, the U.S. Congress banned
all advertising for tobacco on radio and television. More recently, the
use of cartoon characters such as Joe Camel was banned as well as all
outdoor advertising and sponsorship of events that had significant youth
audiences. Our government is moving but the pace is slow.
Minnesota was among the first states with clean indoor air legisla-
tion. Many states and foreign countries have followed. Canada, Australia,
New Zealand, Norway, Sweden, and Ireland all have laws controlling
smoking. Obviously, these laws deter smoking and help in smoking ces-
sation. Further, noxious secondhand smoke (at least in the smoke-free
areas) is greatly reduced.
Informational posters and television spots regarding wrinkles and
premature aging of the skin probably are effective. Wrinkling of skin
has been repeatedly observed among heavy smokers. A more ominous
feature of skin damage due to tobacco is slower healing after surgery.
Will these bits of information decrease smoking? Probably not by them-
selves but if they become widely known, it may enhance other smoking
cessation programs.
Finally, a word about your friendly doctor. A three minute discus-
sion of the hazards of smoking at your physical examination seems to
be about as effective as drugs, focus groups, television ads, etc. The
46 Prevention of Cancer

etymology (relating to the origin of a word) of doctor is “teacher.” It is

hoped that smokers who read this chapter will get that three-minute
teaching lecture. Listen and heed the advice of someone who knows
the horror of disease.

Summary

Smoking causes not only lung cancer but also cardiovascular diseases
and other forms of cancer. There is no difference in health risk between
smoking light cigarettes or regular cigarettes. Because nicotine is ad-
dictive, quitting smoking is very difficult, but there are treatments,
including drugs and therapy, available to help. Society can take steps
and implement laws and programs to discourage people from starting or
continuing smoking and to help those who wish to kick the habit.
 3
Skin Cancer—Do Not Risk It!

Key Points

♦ Much skin cancer is prevented by reducing exposure to ultraviolet

radiation from the sun, tanning beds, and other forms of ultraviolet
(UV) light. Avoiding the midday sun and applying sunscreen are
other ways to reduce your exposure to UV light.

♦ There are three forms of skin cancer: basal cell carcinoma, squa-
mous cell carcinoma, and malignant melanoma. Basal cell carci-
noma accounts for 3 out of every 4 cases of skin cancer. Malignant
melanoma is the most lethal of the three.

♦ Check your body at least once a month for irregular spots. When
caught early, skin cancer is completely curable.

I was privileged to be selected for officer training at the University of

Notre Dame during World War II. For a boy like me, who grew up in
the Missouri Ozarks, Notre Dame was a big deal! The campus, even

47
48 Prevention of Cancer

in wartime, was beautiful and I think that most of us navy trainees

considered it a wonderful opportunity to study and learn. We were
indeed appreciative for this opportunity. The reason for bringing this up
is that Notre Dame had an elegant facility called the Rockne Memorial
located at the end of a huge quadrangle. The Rockne had a fantastic
swimming pool where swimming coach Gil Burdock taught me how to
swim—and not far from that pool was a solarium. The solarium had a
large ultraviolet lamp and after a swim, we trainees if we wished could
take a “sun bath” in that warm and bright room. It was so soothing and
gave us what we thought was a “healthy” tan.
I am an old man now. Old people often have skin problems, and
many, including me, have had skin cancer. I sometimes wonder if the
assorted spots and blemishes that I carry around as an old man may
be due, in part, to that wonderful solarium. Both before and after my
Notre Dame experience, I swam for recreation and often, worked out of
doors without sun protection. Far be it from me to blame the University
of Notre Dame for skin changes that occurred due to my repeated sun
exposure since that time more than 60 years ago. I describe the experi-
ence to illustrate that few people now and even fewer people then knew
of the hazards of exposure to ultraviolet light and to the Sun. Much is
now known about how to protect against skin damage, aging, and skin
cancer. You will learn about that in this chapter.

A Note for Dark Complexioned People

This chapter is focused on preventing cancer in the most vulnerable

population: people of light complexion. Readers of a darker hue should
read the chapter nevertheless—you are extraordinarily fortunate to be
at a notably lower risk for skin cancer; but the risk is not zero. Further,
 Skin Cancer—Do Not Risk It! 49

malignant melanoma in people with dark skin is often diagnosed at

a later stage than in people with light skin. Late diagnosis of melanoma
leads to a cancer that is much more deadly.

How Common is Skin Cancer?

The occurrence of considerably more than 1 million skin cancers per

year make skin cancer the most common cancer in the United States.
That is the quick answer. While the death rate for skin cancer is low,
nevertheless 10,850 people, mostly men, are predicted to die in 2007
(American Cancer Society, Inc. data)—almost all needlessly. Most of the
victims who die of skin cancer will die of malignant melanoma. Perhaps
a shocking bit of information is that in the United States, the probability
of developing invasive (not superficial) malignant melanoma in women
from birth to age 39 is second only to that of breast cancer. It follows that
the probability for developing invasive malignant melanoma exceeds the
probability for developing leukemia, lung cancer, cancer of the uterine
cervix, and non-Hodgkin lymphoma during those years.
The prevalence of skin cancer increased by 300 percent from 1973
to 2001, and it is still increasing. This chapter will tell you how to avoid
skin cancer and be a part of an enlightened group who may yet turn the
tide and finally decrease this deadly cancer.

Who Gets Skin Cancer?

We are all equal under the law but we are not all equal in our vulnerabil-
ity to specific cancers. White people with fair complexions who freckle
and burn easily are far more likely to get skin cancer than their African
American friends—or their friends from India. Pigmentation is protective.
This is true not only in the United States but also worldwide. Male citizens
50 Prevention of Cancer

of Mumbai, India, are 100 times less likely to have skin cancer than white
male citizens of Australia and New Zealand. Blonde and red-haired, white
citizens with blue eyes are more vulnerable than their dark-haired, dark-
eyed fellow citizens; people of Scandinavian or Celtic origin are more
likely to develop skin cancer than people of Mediterranean origin.
Of course, lightly pigmented skin does not cause skin cancer. As
suggested in the introductory paragraphs of this chapter, exposure to
ultraviolet radiation causes skin cancer. It makes no difference if the
ultraviolet radiation comes from a lamp in a solarium, a lamp in a tan-
ning bed, or from the sun at the seaside—it is the ultraviolet radiation
that damages the skin and causes skin cancer. People who are exposed
to ultraviolet radiation are the population at risk. Some exposure is on
purpose. Note the number of people who sun themselves at the beach
to get their desired skin color. But perhaps of greater concern are babies
and small children, often of blonde hair with blue eyes, frolicking in the
sun while being watched by careless or ignorant parents—the young
ones have not chosen to be unprotected and some of them will pay a
high price for their exposure.

Various Forms of Skin Cancer

Automobiles come in diverse models, colors, horsepower, etc. Most

people do not become perturbed or confused when they read of a
2005 6-cylinder, 4-door, Buick LaCrosse CXL sedan and they distinguish
that car with ease from a 2002 4-cylinder, 4-door Ford Focus SE station-
wagon. All cars are not alike and accordingly they have different names
and designations. As cars differ, so too do skin cancers. Three kinds of
skin cancer will be described briefly—they differ from each other in
significant ways—including lethality.
 Skin Cancer—Do Not Risk It! 51

Basal Cell Carcinoma

The most common cancer in the United States is basal cell carcinoma.
More than 3 of every 4 skin cancers are basal cell carcinomas. Since there
are more than a million cases of skin cancer in the United States each
year, that makes for a huge number of basal cell carcinomas.
A bit of terminology is in order. The descriptive “basal cell” refers to
the deep (basal) layer of epithelial skin cells and it is these cells, which
have become malignant. Carcinoma is a cancer of epithelial cells. Thus,
the term “basal cell carcinoma” tells the knowledgeable reader exactly
what kind of skin cancer is under discussion.

FPO
Figure 3.1 Basal cell carcinoma is the most common form of skin cancer in the
United States. (National Cancer Institute/U.S. National Institutes of Health)
52 Prevention of Cancer

The cure rate for basal cell carcinoma is probably 95 percent or

even higher. The high cure rate is a result of the cancer’s slow growth
and slowness of spreading (metastasis), which gives a good opportunity
for removal by a skin doctor. The excellent cure rate also relates to the
fact that most people do not want an ugly skin growth. They see skin
cancer and when doing so, most seek its removal. An extremely ugly
form of this cancer known as “rodent ulcer,” which occurs if the basal
cell carcinoma is not eliminated in a timely manner. The rodent ulcer
has the potential to destroy a large part of the face including an eye and
all or part of the nose and/or an ear resulting in horrible and permanent
disfigurement. The message here is do not ignore a skin growth.

Squamous Cell Carcinoma

About a fifth of skin cancers are squamous cell carcinomas. This form
of skin cancer is the second most common cancer in the United States.
It derives its name from the outer layer of the skin epithelium plus the
term carcinoma. Squamous cells are scale-like cells that ordinarily flake
off and are lost. An individual with repeated exposure to ultraviolet
radiation is vulnerable. People with transplanted organs who are on
immunosuppressive drugs have an increased risk for both the cancer
and its spread (metastasis).
Sometimes basal cell carcinomas and squamous cell carcinomas
are lumped together as “non-melanomas.” This is probably due to the
fact that both are considerably less lethal than malignant melanoma.

Malignant Melanoma
This form of skin cancer was once thought to be rare. Malignant
melanoma is no longer rare and it is increasing. While melanoma is
less common than either basal cell or squamous cell carcinomas, it
accounts for about 75 to 80 percent of skin cancer mortality (deaths).
 Skin Cancer—Do Not Risk It! 53

Melanoma, as the other two skin cancers discussed here, is believed

to be caused by exposure to ultraviolet radiation. The adjective “ma-
lignant” is indeed appropriate. Pigment cells in the skin are the cells
that become malignant. Early detection of a melanoma is absolutely
essential for survival. Localized melanoma has a high cure rate. Cures
plunge precipitously if metastasis has occurred. It is far better to pre-
vent melanoma than to attempt treatment because survival rates of
metastatic melanoma are grim.
Prevention efforts for these three kinds of skin cancer have been
mostly ineffective. Failure in prevention is obvious because, while the

Figure 3.2 A malignant melanoma of the skin that shows asymmetry, an

irregular border, several colors, and a diameter greater than a pencil eraser. Its
evolving state cannot be shown in a single photograph. (National Cancer Institute/
U.S. National Institutes of Health)
54 Prevention of Cancer

cause is known, skin cancers continue to increase in number. The often

lethal malignant melanoma is largely preventable, but it is still increas-
ing in men (but not in women!).

What Is Ultraviolet light?

Visible light is but one portion of the electromagnetic spectrum. Elec-

tromagnetic radiation with wavelengths longer than X rays but shorter
than visible light are known as ultraviolet light. Ultraviolet radiation is
invisible to humans but some animals are able to see this part of the light
spectrum. The Sun is the chief source of ultraviolet radiation.
Of course, ultraviolet light has wavelengths of various lengths. The
longer wavelengths (320 to 400 nanometers) are known as ultraviolet
A (UV-A); the shorter wavelengths (280 to 320 nanometers) are known
as ultraviolet B (UV-B). A third wavelength (100 to 280 nanometers) is
called ultraviolet C (UV-C), but this radiation is almost entirely absorbed
in the ozone layer and doesn’t reach the skin. The DNA genetic material
of skin cells is damaged by UV-B radiation and it is the damaged DNA
that leads to skin cancer. While tanning lamps are designed to emit pri-
marily UV-A, users of these lamps should be aware that UV-A damages
skin elasticity and probably leads to cataract formation. Further, many
UV-A lamps inadvertently produce UV-B. The message here is beware!

Prevention

Avoid excessive exposure to ultraviolet radiation. Exposure to all forms

of ultraviolet radiation, whether from the Sun or manmade, causes skin
cancer. All forms include exposure to tanning beds in fitness centers and
in tanning salons. It includes sunlamps that can be used in the privacy of
the home. Ultraviolet is ultraviolet.
 Skin Cancer—Do Not Risk It! 55

The notion that tanned skin is healthy skin is simply not true. Many
people use tanning beds in spite of the known hazards. The obvious
reason is that they want their skin to appear more attractive, at least
for the present. Beauty is a culturally derived value. It was not long ago
when the fair skin of a blonde or redhead was prized as beautiful. Seek-
ing to be attractive is neither evil nor a trivial desire. However, beauty
is transient and exposure to ultraviolet radiation hastens wrinkles and a
loss of natural elasticity. Ultraviolet radiation accounts for the leathery
skin of the habitual sun worshiper, and it causes the brown “age spots”
of many elderly people, which are not due to aging but result from radia-
tion damage.

What to Wear

To retain a youthful skin later in life, avoid unnecessary exposure to the

Sun and artificial ultraviolet radiation. Wear protective clothing. A hat
with a broad brim that shades the eyes, ears, and face will protect. Base-
ball hats worn either frontward or backwards do not protect the ears.
As a result, skin cancer of the ears is becoming increasingly prevalent.
Wear dark, densely woven clothing when sun exposure is expected.
A quick measure of protection is how much of a shadow a piece of
clothing makes. If the shadow is not dark, obviously sunlight, including
ultraviolet radiation, is going through the fabric and the fabric provides
little protection. Even with protective clothing, reflected ultraviolet light
from snow or water can add to the burning effect of the harmful rays. Do
not forget eye protection and wear sunglasses that are known to protect
against ultraviolet radiation.
Babies should be protected from sun exposure at all times. Young
children, who enjoy frolicking in the sun, should be provided with
56 Prevention of Cancer

protective hats that shade the face and ears as well as long-sleeved shirts
and trousers. It is believed that childhood sunburns are related to adult
skin cancer of all types including malignant melanoma.
Time of day matters. Especially important is to avoid the summer
sun between 10 a.m. and 4 p.m. The summer sun’s rays are far more pow-
erful at noon than in early morning or late afternoon. Do not forget that a
cloudy sky filters out only a small amount of ultraviolet radiation; a bad
burn can be the result of exposure on an overcast day.

Figure 3.3 A grandmother applies sunscreen to her grandson before spending

time outdoors. Both are also wearing protective clothing to avoid excessive sun
exposure. (National Cancer Institute/U.S. National Institutes of Health)
 Skin Cancer—Do Not Risk It! 57

Sunscreen Lotions

Avoidance of ultraviolet radiation is the best way to prevent skin can-

cer. However, every drugstore has a shelf of sunscreen preparations,
which many people think protect from the harmful effects of the sun.
Sunscreens come in a variety of levels of protection. All provide some
protection from ultraviolet B and some protect from ultraviolet A. A
higher sun protection factor (SPF) provides greater protection from
ultraviolet B but indicates nothing about protection from ultraviolet A.
It is wise to find and use sunscreens that protects from both ultraviolet
A and B. Even with the best sunscreen, protection is never absolute. An
SPF of 15 indicates that when the preparation is applied correctly, the
user can be exposed to burning sun 15 times longer than without the
protection. An ample amount of sunscreen must be applied—about
one ounce is adequate to protect arms, legs, neck, and face for an
adult. Read the label and reapply as directed. Sweating and swimming
diminish the protection of most sunscreens and thus special water-
proof or water resistant sunscreens should be sought for these special
conditions. Apply well in advance before sun exposure. Most products
must be absorbed into the skin and this takes up to a half hour. A
check of the date on the bottle is necessary because many sunscreens
lose their potency with storage or with heat. If the sunscreen package
“use by” date has expired, your vulnerability is probably double: One
because perhaps you use too little (which is why you still have the
unfinished bottle) and two because of reduced protection potential of
the aged sunscreen itself.
Any user of sunscreen who is on a prescription drug may be par-
ticularly liable to sun damage. If you regularly take medication you have
58 Prevention of Cancer

a responsibility to check with your doctor or druggist to find out if the

drug you use increases your vulnerability to sun damage.
Even when applied properly, sunscreens provide less than total
protection against UV. Sunscreens support the illusion that the user is
fully protected. Prolonged exposure to ultraviolet light may be sought
because of this illusion. Light complexioned people are most vulnerable
to sun damage and it is these who are most likely to use sunscreen.
Dark complexioned individuals with dark brown eyes are less likely to
use sunscreen than blue eyed blondes or redheads. As a result, many
of those who are most vulnerable to ultraviolet damage are exposed
for prolonged periods with the notion that they will not fall victim to
premature skin aging and skin cancer. They hold this notion at their
own peril.

Excessive Exposure

The term exposure was coupled with “excessive” several times in the
preceding paragraphs. Vitamin D is the reason for this. Vitamin D is
believed to be related to reduced vulnerability to several cancers includ-
ing colon cancer, breast, ovarian, and prostate. Generally diet does not
provide adequate vitamin D. The radiation of the sun augments the
level of vitamin D in the body. The correct balance of sun exposure to
minimize melanoma hazard and maximize colon cancer prevention is
unfortunately unknown. Even the scientists who study cancer thought to
be related to inadequate vitamin D agree that exposure to summer sun is
hazardous and that protective clothing and sunscreen should be used. A
way around this dilemma is to increase vitamin D by oral supplements.
Even with this, the optimal amount of vitamin D supplementation is
unknown. It is best to remember that “excessive” exposure to ultraviolet
 Skin Cancer—Do Not Risk It! 59

radiation is a known hazard for skin cancer. It is wise to keep an eye on

vitamin D in the diet. I will not recommend how much vitamin D, but I
am confident that the recommended level of the vitamin will likely be
increased by our government soon to offset the reduced exposure to
sun as recommended by dermatologists.

How Do I Know If I Have Skin Cancer?

This chapter is about how to prevent skin cancer. Prevention is the name
of the game for cancer in this book, but when primary prevention fails
for whatever reason, there is another form of prevention. The second
form relates to prevention of death by early detection and treatment of
a cancer.
It is my belief that diagnosis is the business of the doctor. So, why
intrude on the doctor’s business? For starters, you see yourself every day;
your doctor may see you only once or twice a year. Self-examination
for skin cancer in general and melanoma in particular costs nothing.
Your self-examination can become an early warning system to help your
doctor. In keeping with my stated belief, you may detect a change in
a “spot,” call it to the attention of your doctor, but your doctor makes
the diagnosis. In the end, your self-examination may be a lifesaver. You
should not be embarrassed if your doctor tells you that the spot that
concerned you is of no medical consequence; indeed, you should be
happy if that is what you learn.
A simple memory aid (otherwise known as a “mnemonic device”) is
the ABCDE scheme for detecting malignant melanoma (and other skin
cancers). All of us carry around common moles and benign pigmented
lesions—“spots,” in other words. The memory aid is designed to help
discriminate between the common benign mole and the less common
60 Prevention of Cancer

skin malignancy. The “spot” test will help to identify skin lesions that
your doctor should examine, and perhaps biopsy for diagnosis, and
perform surgery if required. The ABCDE test is

♦ A – Asymmetry; lack of similarity in shape of the halves of a spot

♦ B – Irregular Border

♦ C – Several Colors

♦ Diameter greater than 6 mm (about the diameter of a pencil

eraser)

♦ Evolving (changing) with respect to diameter, shape, color, surface

(bleeding), and onset of itching and/or tenderness

The ABCDE scheme is described further in an article by Abbasi and

his colleagues in a 2004 issue of the Journal of the American Medical
Association. The article has excellent color illustrations of the ABCDEs.
More information on self-examination can be found on the Web site of
the Skin Cancer Foundation ([Link] The Ameri-
can Cancer Society has a Web page on Skin Cancer Prevention and Early
Detection that can be accessed through Google. Self-detection should
be done while standing naked before a full-length mirror with a hand
held mirror for seeing your back. This should be done at least monthly.
However, detection of a new or growing spot is not a diagnosis of malig-
nancy but it does warrant examination and perhaps biopsy by a skilled
doctor. Obviously, consultation with a family doctor or dermatologist
will provide appropriate information whether a spot is not significant
or if it is pre-cancerous or in fact cancer. Remember, early diagnosis of
melanoma has the potential of a completely curable cancer; delayed
treatment may be lethal.
 Skin Cancer—Do Not Risk It! 61

Learn from History

Southern ladies about the time of the Civil War were known to wear
with inordinate pride broad-brimmed hats, fashionable long dresses,
long white gloves, and to carry parasols for style and for comfort in the
sun. I wonder if they knew that their fashion statement was protection
from the southern sun? To learn of this protection, they had to look no
further than the poor white farmers who labored in the hot sun and
who had aged, weather-beaten skin to show for their efforts. The white
workers were vulnerable to skin cancers. The ladies were vulnerable
mostly to boredom.

S umma ry

Skin cancer is generally caused by “excessive” exposure to ultraviolet B

(UV-B) radiation. Because the body requires vitamin D, which is provided
by sunlight, it’s important to remember that “excessive” is the key word.
Skin cancer occurs in three forms: basal cell carcinoma, squamous cell
carcinoma, and malignant melanoma. Basal cell carcinoma is the most
common, but malignant melanoma is potentially deadly. However, most
skin cancer is preventable through carefully guarding against exposure
to the sun and avoiding artificial sources of ultraviolet radiation.
 4
Cervical Cancer—Preventable?

Key Points

♦ Each year, there are about 11,000 new cases of cervical cancer in
the United States and approximately 500,000 worldwide. Of that,
about 3,700 in the United States and a quarter of a million women
worldwide die from cervical cancer each year.

♦ The human papillomavirus (HPV) causes cervical cancer. Most

women who are sexually active with several partners have (or have
had) an HPV infection. It is caught through intimate contact.

♦ Researchers have introduced a vaccine that produces immunity to

HPV infections and thus prevents cervical cancer.

Cervical cancer is one kind of cancer of the uterus. The uterus, also
known as the womb, is a pear shaped hollow organ in which a fetus de-
velops during pregnancy. The lining of the uterus is the source of blood

62
 Cervical Cancer—Preventable? 63

and other material lost during the monthly period (menstruation).

The upper portion of the uterus is known as the corpus and the lower
portion that extends into the vagina is known as the cervix, which is
another name for neck. A malignancy that occurs in the neck of the
uterus is thus known as cervical cancer.

Cervical Cancer in the United States

An estimated 11,150 new cases of cervical cancer are expected in the

United States in 2007. The death toll is predicted to be about 3,670. Virtu-
ally all of these cancers are preventable. Cervical cancer is rare among
young people, but young people should not be indifferent to what it is
and how it spreads. Inattention to this now may bring woe later.

Cervical Cancer Worldwide

About a half million new cases and a quarter of a million deaths from
cervical cancer occur worldwide each year. Mexico leads the world in
cervical cancer deaths with a rate more than 500 percent greater than
that of the United States. Close to Mexico in cervical cancer death rates
are Colombia and Venezuela. As in the United States, the vast majority
of these deaths are preventable. Finland is notable because it has the
lowest cervical cancer death rate in the world.
Cervical cancer is of great interest for two reasons. The first concern
is what causes the cancer (doctors refer to causation as etiology). The
second relates to the development of a vaccine that may protect from
this deadly disease. Both of these reasons are important to the readers
of this book.
64 Prevention of Cancer

Etiology

To understand cervical cancer etiology, one must consider who is vulner-

able and under what circumstances cervical cancer occurs; that is, one
needs to know something of cervical cancer epidemiology. Particularly
vulnerable are girls and women who had sexual intercourse early in
life, who have had many sexual partners, and whose sexual partners in
turn have had many sexual partners. Women who smoke, who have a
poor diet, or who have other sexually transmitted diseases are similarly
thought to be at increased risk. In contrast, cervical cancer is rare in
women younger than 20, among women who abstain from sex (such as
nuns with their celibate life) and women who have had but one sexual
partner who, in turn, had but one sexual partner. This pattern suggests
that cervical cancer is a sexually transmitted disease (STD). A more pre-
cise term is “sexually transmitted infection” (STI) because the disease is
not transmitted; rather, an infectious agent is transmitted. The infectious
“agent” that is transmitted is a virus.
The virus that gives rise to cervical carcinoma is the human papil-
lomavirus. Most women who are sexually active with several partners
have (or have had) an HPV infection. It is the most common venereal
(sexual) infection among college women in the United States. There is
no cure for the viral infection and frequently there are no symptoms.
While many women have had the infection, fortunately relatively few
will develop cervical cancer.
Human papillomaviruses come in an amazing variety. About 200
kinds are known. Fortunately, not all cause cervical cancer. The best-
known, cancer-associated human papillomaviruses are HPV-16 and
HPV-18, which are thought to cause about 70 percent of cervical cancer,
but others are also known to be associated with cancer.
 Cervical Cancer—Preventable? 65

Transmission of the noxious, cancer-causing HPV is by intimate geni-

tal contact. Intimate in this case means skin to skin, and actual sexual
intercourse is not necessary. The genital contact may be between same
sex couples or of different sex couples. Condoms are of limited value in
that they do not cover all of the skin adjacent to the penis and thus, skin-
to-skin contact is possible, which may lead to HPV infection. However,
many health experts still recommend the use of condoms because they
reduce the risk for other sex diseases and may possibly also reduce the
risk of HPV infection.
HPV as a cause of cervical cancer is a surprisingly useful discovery.
Why? To begin with, knowing what causes the cancer provides a way of
preventing the cancer. Prevention is simple. Avoid behavior that exposes
one to infection by HPV. Cervical cancer, certainly for the most part,
is a venereal disease. Avoid any sexual behavior that could lead to a
venereal infection. Avoidance of sexual contact has the happy added
feature of protection from many other STDs—or as more appropriately
suggested above—STIs. It is unfortunate that while prevention through
abstinence from promiscuity is easy to understand, it seems to require
Herculean effort on the part of many people, and that effort to avoid
promiscuous sex seems often to be imperfect. As a result, the HPV is the
most common sex disease among young people in the United States.

Detecting HPV

The primary method for detecting an HPV infection and hence, vulner-
ability to cervical cancer, is with a Pap smear. The term Pap smear is
derived from the name of George Papanicolaou, the doctor who devel-
oped this method of examination. Cells from the cervical portion of the
uterus are taken painlessly by swab and transferred to a slide where the
66 Prevention of Cancer

cells are stained and examined with a clinical microscope. The person
examining the cells sees exactly that: cells. Viruses are too small to be
detected with a clinical microscope. However, a trained cytologist
(the person who examines the cells) can recognize abnormal cells if
present. Certain of these cells indicate that an HPV infection is present.
When this occurs, there may be no other symptoms and no treatment
may be required other than a re-examination in another three to six
months. Alternatively, a doctor may seek further examination with a
colposcope. The examination, known as a colposcopy uses a bright
light and magnifying lens to detect abnormalities in or on the cervix.
The doctor may perform a minimally painful biopsy with subsequent
removal of infected tissue.
It is not the purpose of this book to describe treatment for cancer.
This is because, with proper medical attention, no cervical cancer
should ever develop. How to prevent infection is known: Do not engage
in activity that presents a risk for a sexually transmitted infection. If this
warning fails and a HPV infection occurs (as it does in the majority of
college women in America), then proper medical care can detect the
infection and abnormal cells can be removed. Note: The abnormal
cells are removed before they have a chance to become cancer. This is
prevention at its best.

A Vaccine to Prevent Cancer!

Knowing that a virus causes cervical cancer provided researchers with

the opportunity to develop a vaccine. The vaccine available in the United
States is known as Gardasil and the U.S. Food and Drug Administration
approved it for use on June 8, 2006. If, as stated above, death by cervi-
cal cancer is preventable, why bother with a vaccine? While modern
 Cervical Cancer—Preventable? 67

Figure 4.1 Cervical cells in a Pap smear are examined by a cytologist using a
compound (clinical) microscope. (Bill Branson/National Cancer Institute/U.S. National
Institutes of Health)
68 Prevention of Cancer

medical care is available in the United States, inattention to appropriate

prevention measures is far too common. Because of inattention, about
11,150 new cases of cervical cancer with 3,670 deaths are expected in
2007 (American Cancer Society, Inc., data). That death rate in the United
States is small indeed compared with the lethality of cervical cancer in
developing countries worldwide. Clearly, there was a need for a vaccine
and it is now approved for use.
Researchers who developed the vaccine are now conducting stud-
ies of who should be vaccinated and when that vaccination should take
place. The drug is licensed for females age nine to 27. Should young teen-
agers be vaccinated against HPV? Early vaccination is crucial because
the vaccine protects against future infection; it does not cure existing
infections. The vaccine should be administered prior to the onset of
sexual activity. Thus, the answer to the rhetorical question of whether
young persons should be vaccinated is “yes.” Some parents strongly
object to this, believing that immunity to HPV will encourage earlier sex
with an increased number of sexual partners. Other parents consider
protection against HPV infection to be a worthy goal and protection
against a cancer-causing infection overrides the fear of greater promis-
cuity. Then there is the question of gender. It may seem nonsensical to
vaccinate boys or young men against HPV infection—boys do not get
cervical cancer! Of course not, but where do girls get HPV infections?
The answer to that question is from boys. If young males do not have an
HPV infection, there is no way that they can spread the virus. Vaccina-
tion of boys has the potential to reduce HPV infection, and ultimately,
reduce cervical cancer.
Gardasil protects against cervical cancer caused by HPV-16 and
HPV-18 and what is especially valuable, it also protects against HPV-6
and HPF-11. The latter two HPVs cause genital warts. Genital warts, while
 Cervical Cancer—Preventable? 69

Figure 4.2 A 17-year-old woman gets a shot of Gardasil, the vaccine against
human papilloma virus and cervical cancer. ( AP Images)

not malignant are multiple, small, ugly growths that have been described
as “cauliflower-like” lesions that can occur in both males and females in
the genital area. Genital warts may also occur in the mouth and throat
of people who have oral sex with a person with an HPV-6 or HPV-11
infection—such infections are becoming much more common.
Perhaps protection from HPV-6 and HPV-11 in the American vaccine
will encourage parents to permit boys to be vaccinated—most parents
would not wish a case of venereal warts on their sons and daughters.
70 Prevention of Cancer

♦ A D iscovery of “ Exce ptio n a l Im po r ta n ce ”

P eyton Rous swam against the current. What does that mean? It means
that he had the guts to challenge accepted wisdom. He opened new doors
in medical research by doing so. The accepted wisdom of his time was that
cancer was “spontaneous.” Bacteriologists had sought in vain for a cause of
cancer. While bacteria were often isolated from cancers, careful study would
invariably show that the bacteria had secondarily infected the cancer and
therefore, the cancer was “without cause” (or so it was thought at the time).
That kind of work led to the generally accepted notion that cancer was truly
a spontaneous disease. Viruses had been considered as possible causes.
However, viruses were ordinarily associated with acute infections—cancer
is a chronic disease for the most part; untreated, it persists until the patient
dies. Thus, viral infections could also be lumped with bacterial infections as
not responsible for cancer—again, or so it was thought.
A Plymouth Rock chicken with cancer was brought to Rous’ laboratory
in 1909. A “soup” was made of the cancer by grinding up the tumor. The
soup was filtered to remove all intact cells of any kind (chicken, bacterial,
or other), and then, this filtered material was injected into other chickens.
It caused cancer in those injected chickens. Rous refrained from using
the term “virus.” Rather, he reported that there was a “tumor agent” in
the filtered “cell-free” preparation. He knew it was a virus and he knew
his experiment showed that a virus could cause cancer. He concluded in
his now famous 1911 scientific report, “. . . the fact of its transmission
by means of a cell-free filtrate assumes exceptional importance.” This was
the first demonstration that a solid cancer (not a leukemia) was caused
by a virus.
 Cervical Cancer—Preventable? 71

This discovery may have assumed “exceptional importance” in the mind

of Rous, but it did not in the mind of the scientific community. Viruses and
bacteria were not considered good candidates for the cause of cancer as
explained above. Further, chickens were clearly unfashionable as labora-
tory animals; mice, rats, and guinea pigs, yes, but chickens, no! Thus the
discovery by Peyton Rous of viruses as a cause of cancer was not given the
recognition it richly deserved until he received the Nobel Prize in medicine
in 1966—over a half century after his study of “exceptional importance.”
It should be noted that Nobel Prizes are not given posthumously. Peyton
Rous was 87 when he received his Nobel Prize. Had he not lived so long,
he would never have received this recognition.
After Rous showed that a virus could cause cancer in a chicken, many
other animal cancers were similarly shown to be virus related; these
included Lucké’s frog kidney cancer, Shope’s rabbit papilloma, Bittner’s
mouse mammary cancer, Gross’s mouse leukemia, and others. Much later,
some human cancers were shown to be related to, or caused by, viruses and
an important example of that are the human papillomaviruses (HPVs).
Francis (he did not use his first name) Peyton Rous was born October
5, 1879; he grew up in Baltimore where he attended medical school at
Johns Hopkins University. He cut his hand during an autopsy during his
student years and became infected with tuberculosis (TB). He went to
Texas seeking a rest-cure from TB and lived for a while in Quanah near the
Oklahoma border. His many talents were such that he was hired as a cow-
boy and participated on horseback in roundups of cattle. In later years,
he recalled with pleasure his memory of sitting around the campfire with
fellow cowboys. Somehow this outside work must have helped cure his TB

(continues)
72 Prevention of Cancer

(continued)

for he returned to Hopkins to finish medical school in 1905. It was not

long after he was invited to the Rockefeller Institute for Medical Research
(which later became Rockefeller University) where he did his famous work
with chicken cancer.
Peyton Rous died February 16, 1970, at the age of 90 of metastatic
cancer. He wrote over 300 scientific articles, 60 of which were written
after he retired. Perhaps staying busy, as well as his early life as a Texas
cowboy, permitted him to live longer—at least long enough to collect the
Nobel Prize in medicine.

The sons and daughters who are protected from HPV strains that cause
cervical cancer are at the same time protected from the HPV strains that
cause venereal warts. The vaccine is truly a double-whammy!
It is at least possible that in the lifetime of all who read this chapter,
cervical cancer will disappear. Thanks to continued medical research
and good public health measures, the end of cervical cancer may be
in sight!

Summary

Human papillomavirus (HPV) types 16 and 18 cause about 70 percent

of cervical cancer. The risk factors for becoming infected with HPV and
developing cancer are well-known, making cervical cancer one of the
most preventable forms of this disease. Yet, cervical cancer still causes
many unnecessary deaths in the United States each year and even
 Cervical Cancer—Preventable? 73

♦ The Pap T est

T he young couple arrived in the United States almost broke and unable
to speak English. They got jobs at the Gimbels Department Store in
New York City; she sewed buttons on clothing and he sold rugs. Not an
auspicious start for either. Things got better. At the end of his career, he
was credited with the greatest medical discovery for cancer prevention
in modern medicine—she was his loyal coworker throughout all of their
married life. But, that is getting ahead of the story.
He was born George Papanicolaou on May 13, 1883, in the village of
Kymi on the island of Evia (aka Euboea) very close to mainland Greece.
His father was a doctor and a politician. After being mayor of Kymi, the
father was elected to the National Assembly of Greece. The family moved
to Athens, where George finished high school and studied medicine at the
University of Athens. He graduated as a doctor with high honors at age 21.
While he greatly loved most academic subjects—he was an “A” student in
medical school—he was not excited about medicine as a career. He went
to Germany to study biology where he received a Ph.D. from the Zoological
Institute of Munich. In time, he became an underwater life biologist on an
oceanographic research vessel with Prince Albert of Monaco. Opportunities
were limited for research in Greece at the time so he and his young wife
came to the United States in 1913.
Life was not particularly rewarding either intellectually or financially
working at Gimbels doing buttons and carpets. George jumped at the op-
portunity for a research position at Cornell University Medical School.
Before long, he was doing reproductive studies using guinea pigs. He was

(continues)
74 Prevention of Cancer

(continued)

annoyed at the prospect of killing many guinea pigs in order to find just
a few with eggs at the proper age. He reasoned that female guinea pigs
might have a reproductive cycle somewhat similar to humans so he started
examining cells taken from the guinea pig vagina. Papanicolaou found that
he could detect exactly what part of the reproductive cycle the animals
were in by cells obtained on a swab of the reproductive tract. He was
delighted because this saved the lives of many guinea pigs. One might call
his guinea pig study the original Pap test.
Papanicolaou then extended his studies to humans, and he was ex-
cited indeed not only to find normal but also premalignant and even
cancer cells on slides prepared from the swabs. Intense study with his
coworker wife (she was his first human “guinea pig”) eventually led to
the Pap test as it is known now. The medical term for loose cells that
will adhere to a swab or soft brush is “exfoliated.” A cytologist examines
exfoliated cells from the woman’s cervix using a clinical microscope. The
test has the potential of detecting premalignant cells or “precursor”
cells of cervical cancer. The test identifies who is in need of subsequent
examination and treatment prior to the time that the abnormal cells
become actual cancer. Those who died of cervical cancer were those
who were not screened regularly with the Pap test. As a result, cervical
cancer death rates plummeted in countries where the Pap test was regu-
larly used. Literally millions of women are alive because of Dr. George
Papanicolaou and his coworker wife Mary. Their screening procedure has
been justly called the most significant advance in the prevention of
cancer in the 20th century.
 Cervical Cancer—Preventable? 75

more around the world. A vaccine against HPV is available, and regular
screening through Pap tests can detect precancerous cells early enough
to prevent cervical cancer. These methods, combined with proper at-
tention to this disease, may greatly reduce and perhaps even eliminate
deaths due to cervical cancer.
 5
Childhood Cancer Survivors:
A Paradox

Key Points

♦ Chemotherapeutic agent(s), or radiation, or a combination of che-

motherapeutic agent(s) and radiation are responsible for effectively
curing some cancers. However, these same therapies may cause
second cancer decades later in life.

♦ Despite the risks of chemotherapy and radiation, those with cancer

should opt for cancer therapy. The therapy, however risky, is better
than any alternative at this time.

♦ Survivors of childhood cancers should reduce the risk of developing

a second cancer by avoiding smoking and excessive sun exposure.
Survivors should also make sure to get regular checkups.

76
 Childhood Cancer Survivors: A Paradox 77

What a strange world it is in which we live. Modern medicine (in

this case “modern” means, for the most part, post-World War II but
especially the 1970s and onward) has developed the very remark-
able capability of curing many individuals afflicted with cancers. As
stated by our government’s Centers for Disease Control and Prevention
(CDC), the numbers of people alive who ever received a diagnosis of
cancer has increased steadily to an amazing 9.8 million in 2001—they
are alive because of advances in early detection and treatment. Can-
cer has become a curable disease for some and a chronic illness for
others. This statement applies to cancer in both children and adults.
What a boon that is to those who are saved! Words cannot be written
that appropriately express the appreciation and gratitude that we owe
to the many researchers who have made cancer cures possible. How
many are saved? Currently, it is estimated that three of every four who
suffer from childhood cancer will become survivors.
Some of the cancers of young people that respond well to therapy with
a high rate of cures are: acute lymphoblastic leukemia, testicular cancer,
Wilms tumor, non-Hodgkin lymphoma, and Hodgkin’s disease.
So, what is strange about this world? It is the paradox of the con-
tradictory properties of cancer therapy. Chemotherapeutic agent, or
radiation, or a combination of chemotherapeutic agent and radiation
have the very real potential of converting a cancer patient into a survivor.
That potential has already translated into more than a quarter million
young cancer survivors in the United States. However, with survivorship
there is risk. The risk is for the development of a second cancer unre-
lated to the first. The appearance of the second cancer in many, if not
most cases, is due to the effects of the successful treatment. The second
cancer is a long-term complication of treatment. Because the chemical
78 Prevention of Cancer

Figure 5.1 Children receiving chemotherapy for acute lymphatic leukemia.

The child on the left is receiving chemotherapy into her neck and the other
child is receiving her chemotherapy into her arm. (Bill Branson/National Cancer
Institute/U.S. National Institutes of Health)

agents and radiation used to kill cancer cells also affect healthy cells,
the agents and procedures that cure also have the potential for causing
cancer. That is the paradox.
Is the vulnerability to a second cancer limited to young people? Of
course not. Older people are similarly vulnerable. However, it may take
several decades for cancer to occur after exposure to a cancer-causing
event. There is not much remaining time for a cancer to appear when
an 80-year-old person is cured of cancer. Contrast that narrow “window
 Childhood Cancer Survivors: A Paradox 79

of opportunity” to the years of life that a teenaged survivor expects.

Because of the much greater life expectancy of the young person, there
is a long window of opportunity for a second unrelated cancer. Hence,
there is concern for the survivors of childhood cancer.
In this chapter will be listed specific second cancers and their re-
lationship to chemotherapy and radiation. Here are my views on the
paradox. In facing a potential life-threatening cancer in me or a loved
one, I know that I would opt for the most effective treatment available as
recommended by my doctor. While I have spent a lifetime in the study of
cancer, I have neither studied the clinical aspects of cancer nor do I have
experience with response to treatment. Thus, I will assume whatever risk
that goes with the treatment in the hope that I, or my loved one, might
become a survivor. To me, the possibility of becoming a survivor is far
preferable than becoming an occupant of a grave. The development of
second cancers attributed to therapy is due only to the success of that
initial therapy—there are no secondary cancers with therapeutic failure.
To repeat, second cancers are a complication of successful therapy; they
do not result from poor medical management. This message translates
into the following: Do not forgo lifesaving therapy because of the fear of
a possible second cancer. Nothing in this chapter is written to suggest
one should decline or delay proper treatment of cancer.

Not All Second Cancers Are Due to Therapy

Second cancers are those that are not related to the first cancer. First
cancers, as all cancers, will metastasize in time. The metastatic colonies
of cancer are located at anatomically distant sites from the first cancer—
the metastases are colonies of the first and are not considered “second”
cancers. The metastases are comprised of cells that are identical with
80 Prevention of Cancer

the first cancer. Prostate cancer that is metastatic to bone is not bone
cancer; it is prostate cancer that has colonized bone. Second cancers
are different in every way from the primary cancer.
The term iatrogenic means caused by medical treatment. Are all
second cancers iatrogenic? The quick answer to that question is “no.”
Consider life expectancy in the new millennium. It is longer now than
ever before. Cancer frequency increases with age. With long life, there
are more years for a totally separate cancer to develop for quite different
reasons than the first. For example, a childhood survivor of a leukemia
may take up smoking in his or her 20s; clearly lung cancer, should it oc-
cur in later years, can not be attributed to the medicine and procedures
of the physician who brought about the cure of the first cancer. Tobacco,
not the physician, is the culprit. Other cancers occur for reasons not yet
understood and a second cancer may occur purely as a chance event.
Some individuals have a genetic susceptibility for multiple cancers,
and those multiple cancers would likely occur regardless of treatment.
However, many second cancers are due to therapy and some will be
discussed, along with what is known about preventing the noxious ef-
fects of second cancers.

Specific Causes of Second Cancers

There are several causes of second cancers among survivors of an initial

cancer. These include:

Genetic Predisposition
While retinoblastoma is relatively rare it is nevertheless the most
common eye cancer of children. There is no known strategy for the
prevention of the hereditary form of retinoblastoma. Hereditary means
that the disease is a genetically-inherited trait passed down from one’s
 Childhood Cancer Survivors: A Paradox 81

parents and may develop regardless of external cancer factors. The pres-
ent book is about prevention. Why then is retinoblastoma discussed? It
is considered here as an example because about half of the children
with the hereditary form of the eye cancer will develop another cancer
not related to the retinoblastoma. This ratio compares with perhaps one
in 20 children who develop a second unrelated malignancy who have
the nonhereditary (or non-inherited type of) retinoblastoma. Clearly,
there is a genetic predisposition for a second, unrelated cancer in the
hereditary form of retinoblastoma and this is not the fault of modern
medical treatment.

Chemotherapeutic Drugs
Etoposide, teniposide, and VP-16 are drugs that have been used to
treat several kinds of cancers. They are derivatives of podophylotoxin,
which in turn is derived from the underground roots of an herbaceous
plant. These plant derivatives are recognized as inducers of leukemia in
some individuals who survived their first cancer with successful therapy.
Another chemotherapuetic drug is doxorubicin, an antibiotic derived
from Streptomyces peucetius, with a potency to treat a wide spectrum
of cancer types. Unfortunately doxorubicin, like the podophylotoxin
derivates, also has the potential to cause leukemia as a second cancer.
A whole group of very reactive and potent chemical agents (includ-
ing chlorambucil, cyclophosphamide, busulfan and others) are
chemicals that cause leukemia. The platinum complex drug cisplatin,
perhaps in interaction with other chemotherapeutic agents, also causes
leukemia. The list could be continued. This is not to denounce or con-
demn specific drugs. The point is to make the reader aware that not one
but most cancer drugs can cause cancer. Powerful drugs have powerful
side effects. Cancer is an awesome disease requiring powerful drugs. It
82 Prevention of Cancer

is unfortunate that cancer is a side effect, but remember, the side effect
of a second cancer is a potential hazard only to those who have survived
a first very lethal disease.
Emphasis here has been on leukemias as second cancers. Ordinar-
ily, it takes solid cancers longer to develop than leukemia and thus, less
is known about solid tumors as second cancers. However, some solid
cancers thought to result from prior treatment of primary cancers are
bladder cancer, bone sarcoma, and lung cancer. This list is clearly not

Figure 5.2 Powerful chemotherapeutic agents not only have the potential
to cure cancer but may cause, in some cases, a second cancer. Shown here is a
health care worker hanging bags of chemotherapeutic agents to be used in the
treatment of cancer. (Bill Branson/National Cancer Institute/U.S. National Institutes
of Health)
 Childhood Cancer Survivors: A Paradox 83

exhaustive. The leukemias that occur after successful chemotherapy

are mostly acute myeloid leukemia (AML) and acute lymphoblastic
leukemia (ALL).

Radiation Therapy
X rays were discovered in 1895 by Wilhelm Conrad Roentgen (1845–
1923). Roentgen received the Nobel Prize for this discovery because of
its immense value in medicine. Workers in the factories that produced
X-ray machines used their own hands to test the machines. Primitive X-
ray films of the time were slow (insensitive) and thus, the workers’ hands
received multiple, high doses of X rays—with cancer resulting. The
atomic bomb survivors of Hiroshima are known to have an increased
prevalence of cancer. Many people fear nuclear reactors. What does all
of this tell us? The message is that radiation can cause cancer. It can
also cure cancer. Radiation in this regard is not unlike chemotherapeu-
tic drugs—i.e., radiation to cure a first cancer has the potential to cause
some second cancers.
Most kinds of cancer can be caused by exposure to ionizing radia-
tion. For example, thyroid cancer is a frequent complication of the treat-
ment of Hodgkin’s disease. Other second cancers following therapeutic
radiation include cancers of the central nervous system, bone sarcoma,
and breast cancer. As before, nothing stated here is to suggest that a
cancer patient avoid potentially lifesaving therapy.

Strategy for Survivors of Cancer

For a successful strategy, those who are at risk must be informed

that they are at risk. For whatever reason, a significant number of
childhood cancer survivors are unaware that they are indeed survivors,
perhaps because they were judged too young to understand potential
84 Prevention of Cancer

♦ The Discovery of a C hem o t h e rapy D r ug

I t was so cold the water pipes froze and burst. That was the night in
1918 (January 23 to be specific) when Gertrude Belle Elion was born.
Fortunately, her mother chose to give birth in a hospital rather than sub-
jecting her newborn to a shower of cold water. Both of Gertrude’s parents
were immigrants. Her mother was born in a part of Russia that is now
Poland; her father was born in Lithuania. During the Great Depression the
Elions were less than affluent. Gertrude attended her local high school
in the Bronx, in New York City. She won admission to Hunter College,
New York City, from whence she graduated in 1937 with high honors in
chemistry. Hunter College was a tuition-free college at the time (it is no
longer) and Gertrude Elion attended it because, for among other reasons,
money was scarce.
Students of today know that grades are the ticket to professional school.
Gertrude wanted to get an advanced degree in chemistry. Therefore, as an
honors graduate of Hunter, she applied to the chemistry departments of
15 universities. Rejection letters came from all 15. One of the departments
wrote: “You’re qualified. But we’ve never had a woman in the laboratory
before, and we think you’d be a distracting influence.”
Among the jobs she took was that of a substitute teacher in high school
chemistry at $7.50 per day. In 1944 she was hired by Burroughs Wellcome,
a pharmaceutical company, and she worked for them for the next 39 years.
It was her job to study DNA in disease and attempt to find a metabolic
“Achilles heel.” DNA replicates in cell division and she speculated that if
she could interfere with the metabolism of one of the components of DNA
(in this case a purine), she might discover a means of blocking cell division.
 Childhood Cancer Survivors: A Paradox 85

With persistence, she was

able to synthesize 6-
mercaptopurine (6-MP)
which did indeed interfere
with cell division—to the
extent that it became a
major component of the
treatment of leukemia.
For sophisticates of
chemistry, please note
that Elion’s studies were
done before the double-
helix structure of DNA was
known. Despite that fact,
she discovered a way to
block DNA replication and Figure 5.3 George Hitchings (left) and Ger-
therefore, cell division. trude Elion (right) won the Nobel Peace Prize
for designing drugs that could fight pathogens
All of the 15 chemistry
without harming healthy human cells. ( AP
departments that rejected Images)
Gertrude Belle Elion must
have been shamed when
she received a Nobel Prize in medicine in 1988. Regardless of her lack of
the Ph.D., she received 23 honorary doctorates.
Gertrude Elion probably was not pleased, nor surprised, to learn that
her powerful 6-mercaptopurine is, with probably most other chemothera-
peutic agents, implicated in some second cancers. I would speculate, that

(continues)
86 Prevention of Cancer

(continued)

were Elion still alive, she would be at work to develop a gentler chemo-
therapeutic agent to use instead of the 6-mercaptopurine. And, knowing
how devoted she was to her scientific work, I feel certain she would in
time, have been successful. Would that she were still alive! She died Febru-
ary 21, 1999.

complications of their cancer treatment. This is unfair to the survivor. It

is unfair because the survivor must marshal every available procedure
to minimize the chances or severity of a second cancer. As most would
say, “one is enough.” It is said that lightning never strikes the same place
twice, but the young survivor must realize that is not true in the case of
cancer. Being aware will protect to a very real extent; properly managed
awareness clearly reduces risk.
The survivor must become knowledgeable about established and
newly developed screening procedures so that he or she may work in
close collaboration with his or her doctor for early detection of a second
cancer should one occur. Screening for cancer should not be viewed as
a morbid preoccupation. There should be a significant degree of hap-
piness each time a screening procedure reveals no new cancer. And,
if there is an unfortunate second cancer, the survivor will know it was
detected early for the best treatment.
Smoking avoidance should be a personal high priority for survivors.
Of even greater importance is smoking cessation, if the survivor has
taken on this habit. Survivors must not use tobacco in any form. Further,
the survivor must avoid secondhand smoke. Smoking cessation is
 Childhood Cancer Survivors: A Paradox 87

discussed in Chapter 2. Other prevention strategies include attention to

a proper diet and exercise (see Chapter 7) and protection from the sun
(see Chapter 3). Regular physical checkups are essential as a part of the
screening procedures described in the preceding paragraph.

Honor the Doctors Who Saved Your Life

Survivors of cancer may become apprehensive about a second cancer

and develop an antagonism for the medical team that saved his or her life
after reading this chapter. Do not become angry. Cherish your life and give
your doctors the appreciation that they deserve. You are at an increased
risk for a second cancer and that cannot be denied. But there are well
known ways of minimizing risk for that cancer and they are described
above. Give prevention your best effort and strive to make something use-
ful and beautiful of your life. Only a few short years ago, your life would
not have been spared. Knowledge of your new life expectations should
be a message for personal achievement—keep your doctors informed on
how well you are doing. They will appreciate hearing from you.

S umma ry

Using chemotherapy and radiation treatments, doctors can cure many

types of cancer, but these treatments, which affect healthy cells as well
as cancerous cells, bear the risk of inducing second cancers later in the
patient’s life. For this reason, anyone who has been successfully treated
for cancer must be extremely vigilant in taking preventive measures and
following proper screening practices to protect against the development
of a new cancer.
 6
Breast Cancer—Preventable?

Key Points

♦ Breast cancer in women is second only to lung cancer as a cause of

death by malignancy in the United States.

♦ Women who had their first child under age 18 had only a third to
40 percent of the breast cancer of women who delayed having a
child until after age 35. Any delay in age at pregnancy and first
birth will slightly increase breast cancer risk, including having no
children at all.

♦ Other risks of breast cancer include genetic mutations such as those

to the BRCA1 and BRCA2 genes, obesity, family history, race, and age
of first menstruation.

♦ Risk reduction includes moderating consumption of alcohol, exer-

cise, and breast-feeding for at least one year after giving birth.

88
 Breast Cancer—Preventable? 89

Bernardino Ramazzini (1633–1714) was born in the northern Italian

town of Carpi. He received a doctor of philosophy and medicine degree
in 1659 from the ancient and distinguished University of Parma. At some
time in his career he became interested in the relationship between
how people made a living and the diseases from which they die. He is
mentioned at the beginning of this chapter because he observed that
nuns in Italy of that time had more breast cancer than women who
were not nuns. The breast cancer was caused, Ramazzini wrote, “in my
opinion, by their celibate life . . . every city in Italy has several religious
communities of nuns, and you seldom can find a convent that does not
harbor this accursed pest, cancer, within its walls.” His book on occupa-
tional cancer, De Morbis Artificium, which included the nun story, was
published in 1700.
If an occupational group, in this case nuns, are found to have a dif-
ferent prevalence of breast cancer from other women, then one may
ask what it is about the occupation that causes the difference. Can
understanding what causes the difference be useful in reducing cancer
rates in the special group and in the general population who are at a
different risk?
Ordinarily, nuns are women who take vows of chastity—in other
words, they have a celibate life. Ramazzini believed that it was their
celibate life that was causing their breast cancer. Celibacy means doing
without sex for religious reasons. Surely, abstaining from sex should not
cause cancer. What else is related to celibacy? Among other things, no
sex means no children. Nuns forego having children their entire lives.
Before proceeding further, perhaps the epidemiological breast cancer
data should be updated. After all, Ramazzini published his book in 1700,
which makes the nun story a bit dated. Perhaps for clarity, instead of
90 Prevention of Cancer

focusing on celibacy it would be informative if we considered the nuns

as nulliparous (from the Latin nullus, meaning “none” and parere,
meaning “to bear”) women, or women who never became pregnant and
bore children. Let us now compare not just nuns but other nulliparous
women with women who do have children. Fortunately, this has been
done. And, it seems that in general, Ramazzini was correct. Multipa-
rous (from the Latin multi, meaning “many” and parere) women have
less breast cancer than do women who are nulliparous. Having a large
number of children requires starting the pregnancy business early.
Because of that fact, investigators decided to study the age of women at
the birth of their first child.

The Mother’s Age and Birth of Her First Child

A study was published in 1970 in the Bulletin of the World Health Orga-
nization called, “Age at first birth and breast cancer risk,” that looked at
the age of women at the birth of their first child and their relative risk for
breast cancer. The investigators studied women of different geographical
sites and ethnic groups; these included women of Boston, Massachu-
setts; Glamorgan, Wales; Athens, Greece; the Republic of Slovenia; Sao
Paulo, Brazil; Taipei, Taiwan; and Tokyo, Japan. They found a striking
relationship between their age and incidence of breast cancer. Women
who had their first child under age 18 had only a third to 40 percent of
the breast cancer compared to women who delayed having a child until
after age 35!
This is one kind of epidemiological data that could be exploited
for prevention, at least in theory. The theory would suggest a massive
decrease in breast cancer prevalence if all women had their first child
before age 18. I can hear some college-destined (or medical school,
 Breast Cancer—Preventable? 91

law school, engineering, theological seminary, or you name it) women

thinking, “Great! Just exactly how am I to enter college and medical
school while caring for one or more small children?” The real mes-
sage here for prevention is not to have children early; it is to look at
epidemiology to seek practical clues to cancer prevention. Are there
any for breast cancer?

Risk Factors

Breast cancer is second only to lung cancer as a cause of death by malig-

nancy in the United States (perhaps this will stimulate a reexamination
of the significance of smoking in those women who enjoy tobacco—you
smokers, go back and reread Chapter 2). While lung cancer kills more,
the toll on women by breast cancer is sufficiently great that preventive
measures of this terrible disease must be considered. The American
Cancer Society, Inc. estimates that there will be 178,480 new cases and
40,460 deaths of women by breast cancer in the United States in 2007.
For comparison, about 16,000 to 17,000 Americans are expected to die
of AIDS in 2007.
A risk factor is any condition that increases one’s chance of getting a
particular disease. Here, we consider breast cancer risk factors. It must
be remembered that “chance” is just that: A woman may have a breast
cancer with no known risk factors or she may have several risk factors
and be disease-free. Risk factors are presented to inform readers about
causes of cancer; most cannot be changed but some can.

Risk Factors That Cannot Be Changed

Gender. The reader may think, “Duh, what a no brainer!” Obviously,
women have breasts and thus are vulnerable. But, it is not as simple as
all that. About 2,030 (less than 1 percent of the female rate) new cases
92 Prevention of Cancer

Figure 6.1  AP Images

of breast cancer in males will be diagnosed in 2007 according to the

American Cancer Society. Thus, female sex is judged as a significant
risk factor but males, at a far lower rate, are also vulnerable.
Age. Women between 20 and 29 have only a fraction of a percent
chance of developing breast cancer. More than three-fourths of breast
cancer is diagnosed in women over the age of 50. Of course, a particular
woman’s risk will be higher or lower depending upon other known and
unknown factors.
Age at the Birth of First Child. For practical reasons, most women
in the United States delay having children beyond the age of 18. Any
 Breast Cancer—Preventable? 93

delay in age at pregnancy and birth will slightly increase breast cancer
risk including the ultimate delay, having no children at all. This is still
true for nuns as it was 300 years ago.
Genetics. Several specific mutations affect breast cancer vulner-
ability; these include mutations to BRCA1 and BRCA2 (the “BR” stands
for breast, “CA” indicates cancer, and the number refers to the par-
ticular gene. One of these genes, BRCA1, accounts for about 5 percent
of breast cancer. That number translates to 1 in 20, which does not
seem like many until it is realized that nearly 41,000 women die of
breast cancer in the United States each year. Five percent of the an-
nual toll is more than 2,000, a not inconsiderable number. Mutations
to BRCA1 are particularly common in the breast cancers of Ashkenazi
women (Ashkenazim is a Hebrew word meaning “Germany” and it
refers to Jews who lived in the Rhineland valley and nearby areas
of France prior to moving to Russia and the Ukraine and then else-
where). Women who have mutations to either BRCA1 or BRCA2 have a
lifetime risk for breast cancer of 60 percent to 80 percent. That should
be compared with the lifetime risk of women who do not have those
mutations of only 12 percent.
Human epidermal growth factor receptor gene 2, better known as
HER2, is a gene that is overexpressed in breast cancer. Overexpression
of a gene means that the gene is producing too much of its gene prod-
uct. This occurs in somewhat more than a quarter of all breast cancer
patients. Overexpression of HER2 leads to a more aggressive form of
breast cancer with rapid cell growth and a high metastatic potential.
Women with overexpression of the gene are known as HER2 positive.
Most cancer chemotherapy involves control of cancer growth by
killing cells. This is known as cytotoxic chemotherapy and losing hair
and nausea are recognized as two of the many toxic side effects. Many
94 Prevention of Cancer

people hope that chemotherapy will advance from conventional chemo-

therapy (which generally fails to distinguish between normal and cancer
cells) to a more cancer-cell-specific therapy. This seems to be the case
in breast cancer treatment with an antibody that targets cancer cells
that have overexpression of the HER2 gene. The exact mode of action of
the antibody is not yet known but what is known is exciting indeed. The
antibody with the proper name of trastuzumab (Herceptin is the trade
name) inhibits cancer cell proliferation in HER2 positive women. Other
genes are known to be involved in breast cancer growth.
Family History. My brother has prostate cancer. That fact elevates
my risk for prostate cancer. I am completely powerless to sever my blood
relationship with my brother even if I wanted to (which I do not—at least
most of the time). In a somewhat similar fashion, women who have blood
relatives, such as daughters, mothers, sisters, referred to as “first-degree
relatives,” who have had breast cancer are at twice the risk compared to
women who do not. Risk is increased further if two or more blood rela-
tives had breast cancer, or if they had both breast and ovarian cancer, or
if the cancers occurred prior to the age of 50, or if a male blood relative
has breast cancer, or if there are Ashkenazi Jewish relatives. Obviously
these risk factors are not subject to change.
Personal History. A woman who previously had breast cancer is at
a significantly higher risk to develop a second breast cancer. The risk is
more than three times that of a woman who has not had breast cancer.
Race. White women have a slightly increased risk compared with
African American women. Asian and Native American women have a
reduced risk compared with white women.
Menstruation. Girls who have their first monthly period at an early
age (before 12 years of age) are at an increased risk, as are women who
are more than 55 years old when they undergo menopause.
 Breast Cancer—Preventable? 95

Radiation Therapy to the Chest. Young women who received

radiation therapy to the chest for another cancer are at elevated risk
for breast cancer. This statement does not pertain to the breast cancer
screening technique called mammography. Mammography obvi-
ously involves radiation. Note that therapeutic radiation involves a much
greater dose of radiation than does mammography. Ordinarily, young
women are not given routine mammographic evaluation.
Other Risk Factors. Because breast cancer has been studied so
extensively, it should not come as a surprise that a multitude of other
correlates have been described. One example is that previous benign
breast disease and/or previous abnormal breast biopsy increases risk
(this does not include fibrocystic breasts). During World War II and
for a decade or so thereafter, pregnant women at risk of a spontane-
ous abortion (miscarriage) were given a drug called diethylstilbestrol
(DES) to save their babies. Those now grown babies have a slightly
increased risk for breast cancer. Some women at menopause have a
variety of symptoms (hot flashes, mood swings, reduced sex drive, etc.)
and treatment for these and other menopausal symptoms may involve
hormone replacement therapy (HRT). HRT decreases coronary heart
disease and osteoporosis risk, but when HRT involves both estrogen
and progesterone, there is an increased vulnerability to breast cancer.

What You Can Do to Reduce Risk

Consumption of Alcohol. It is estimated that having several (two
to five) drinks a day results in women who have 1.5 times the risk of non-
drinkers. This risk factor can be easily controlled by all women other
than those who suffer from alcoholism. Accordingly, women who wish
to minimize their risk for breast cancer should consider limiting alcohol
consumption—if they consume alcohol at all. The term that is important
96 Prevention of Cancer

here is alcohol, i.e., ethyl alcohol. Ethyl alcohol in any form: beer, wine,
brandy, whisky (bourbon, scotch, Irish or “the white lightning” of the
Missouri Ozarks; it makes no difference; all contain much alcohol)
taken in excess will increase risk for breast cancer.
Maintenance of a Proper Weight. Many epidemiological stud-
ies have shown that obesity is related to breast cancer but the relation-
ship is controversial. Weight gain after age 18 seems to increase breast
cancer that occurs after menopause. Obesity results from an intake of
dietary calories in excess of those burned or as a result of inadequate
physical activity.
Exercise. Sedentary women are thought to have an increased risk
for breast cancer. An impressive alternative to the sedentary lifestyle is
jogging, but walking is easier. How much walking? The Women’s Health
Initiative, a study of 161,808 women, reported that brisk walking for 1.25
to 2.5 hours a week will reduce breast cancer risk by 18 percent. Walking
for 10 hours reduces the risk to an even greater extent. Think of it. No
special equipment. No drugs. No expensive athletic attire or “running”
shoes. No painful workout. Just walk. Get started now!
One may ask ,“How does exercise affect my breasts?” Good question!
It was noted earlier that onset of menstruation at an early age increases
breast cancer risk. Young women who participate in vigorous athletic
activity have a delay in onset of menstruation and lowered serum estro-
gen. These are in turn are thought to result in a reduced risk. Exercise
also may lead to a leaner body—obesity is a correlate of breast cancer;
exercise and lose that body fat!
Breast-feeding. “The longer women breast-feed the more they are
protected against breast cancer. The lack of or short lifetime duration of
breast feeding typical of women in developed countries makes a major
contribution to the high incidence of breast cancer in these countries.”
 Breast Cancer—Preventable? 97

Figure 6.2  AP Images

A rhetorical question: Can the risk for breast cancer be quantified? The
answer is “yes” for group averages; the answer is “no” if one seeks the
exact risk for a particular individual. What are the risk factors with nurs-
ing? “The relative risk for breast cancer decreased by 4.3% . . . for every
12 months of breast-feeding in addition to a decrease of 7.0% . . . for
each birth.” These findings were reported by Beral in 2002 in The Lancet.
The ellipses indicate deleted statistical material, which makes this data
reliable—for those who seek the statistical information, the full citation
for this article appears in the Further Resources section. The authors of
this monumental (about 147,000 women) study further stated: “These
relations are significant and are seen consistently for women from devel-
oped and developing countries, of different ages and ethnic origins, and
with various childbearing patterns and other personal characteristics.”
The reader must bear in mind that the data are averages of groups;
the data cannot be extended to individuals with any validity. Neverthe-
less, I cannot help but be reminded of my long-dead mother who had
98 Prevention of Cancer

three children and nursed each for one year. A calculation: 3 times 7
percent (21 percent) for bearing each child plus 4.3 percent times 3 (12.9
percent) for nursing each child one year. If these reductions in breast

♦ What D o Chimpanzees an d B r ea s t Can c e r

Have in Comm on?

A first answer to the question posed by the title of this essay is “not
much.” However, in reality, the cancer and the small primate do have
a few things in common. For starters, it should be stated that the DNA (the
genome) of the chimpanzee was studied by Professor Mary-Claire King.
King also identified the first gene, BRCA1, known to be related to breast
cancer. So, the monkey and the cancer have in common that they were
studied by the same distinguished scientist. For one person to work on
such disparate projects and to make profound and major contributions to
both is unusual to the extreme.
Mary-Claire King, and her coauthor A.C. Wilson, showed in a study that
the genetic material DNA and its products in chimpanzees and humans are
nearly identical. Nearly identical here means about 99 percent. The issue
here is that subtle DNA differences can result in vast dissimilarities in
organisms.
King began a study looking for a single gene that would be related
to breast cancer. The gene in its normal form would, among other things,
suppress the formation of cancer. Cancer would likely develop if the gene
were found in a mutant form. The DNA genetic material of a human is vast
indeed—to look for a single gene mutation that would account for cancer
was thought to be an endeavor not likely to succeed. But Dr. King and her
 Breast Cancer—Preventable? 99

cancer are cumulative as the data suggest to some, then that calculates
as a whopping 33.9 percent reduced risk for breast cancer—my mother’s
group average. She would have been pleased to inform readers that, as

colleagues found a single gene difference, which is now known as BRCA1.

BRCA1 in its mutant form(s) causes a hereditary form of breast cancer in
a small group of women—but in that small group, it has the potential for
inducing cancer in the majority of those who have the gene.
King showed that subtle changes in DNA characterize the differences
between a monkey and humans; perhaps in a somewhat similar fashion,
the mutation of BRCA1, which changes only a tiny fraction of the total
genomic DNA, has the potential to alter normal cells and to render them
malignant. Minute variations to DNA can pack an immense wallop!
It is now possible to screen for the presence of mutant BRCA1 and
thus detect who is at a very high risk for breast cancer. Does this help
in the prevention of cancer? No. But the detection of who is at high
risk saves lives. And, by knowing more about how mutant genes brings
about cell transformation to cancer will enable scientists and doctors
to understand the process. Understanding cancer holds the promise of
preventing cancer.
Mary-Claire King was born February 27, 1946, in Evanston, Illinois.
She attended Carleton College in Northfield, Minnesota, and graduated
in mathematics cum laude. She received her Ph.D. in genetics from the
University of California, Berkeley, and she has received many honorary
doctorates since that time. She is currently American Cancer Society pro-
fessor in the departments of medicine (medical genetics) and of genome
sciences, University of Washington, Seattle.
100 Prevention of Cancer

many of her group, she did not die of breast cancer. My daughters nursed
even longer—it is my hope that they too will be spared.
It is my desire that the women readers of this chapter will consider
breast feeding of their children yet to be born and join my mother’s
group in enjoying a reduced risk for breast cancer.
Tamoxifen and Women at High Risk. Tamoxifen is a drug given
to some women to prevent the recurrence of breast cancer. It is not an
elective for most women. It is given by prescription only to women at
high risk whose breast cancer expresses estrogen and progesterone
receptors. Strictly speaking, it does not prevent occurrence of cancer;
rather as indicated, its role is to prevent recurrence.
Reduction of risk for breast cancer is possible for many women as
discussed in this section. The future may hold even more promise.

What Does the Future Hold?

The answer to the question, “Is breast cancer preventable?” is: “Well,
to some extent but not by much.” That’s not to say there is no hope for
a better future. It is worth mentioning here that while breast cancer is
certainly and reasonably to be feared, most women do not get breast
cancer (7 of every 8 women will not get that cancer during their entire
life) and most of those who do will survive (the lifetime risk of dying from
the dreaded malady is 1 in 28). Those statistics are encouraging but we
must do better. Of that, there is no choice. Epidemiology is a branch of
science that holds the potential of reducing breast cancer prevalence.
Mentioned in this chapter is the astonishing conclusion that breast
cancer risk could be deeply cut if women breast-fed their children
for the length of time that women do (or used to do) in developing
countries. That data shows the power of analytical epidemiology. Are
 Breast Cancer—Preventable? 101

there other modes of behavior yet to be discovered that, if exploited

by all or most women, would similarly decrease breast cancer? If so,
epidemiologists will discover those preventive factors sooner or later. I
hope it is sooner. In the meantime, young mothers might well consider
breast-feeding as a practical, inexpensive, non-drug procedure for
reducing breast cancer risk.
Another kind of research involves genetic analysis. The discovery
of specific mutant genes that cause breast cancer (or any other can-
cer for that matter) holds the promise that knowing the variant gene,
its product, and how the gene product causes cancer, will permit
molecular biologists to devise ways of replacing the mutant gene, or
blocking the production of the mutant gene product, or introduction
of another gene or its product that will abrogate (block) the effects
of the mutant gene. That sounds complex, but all of the procedures
requisite for these genetic manipulations are available, waiting to be
exploited, and beginning efforts are underway and promising. Now,
molecular biology is focused primarily on treatment but in the near
future, modes of prevention with these marvelous tools of science
will emerge.

S umma ry

Breast cancer is not readily preventable, but there are many steps
women can take to reduce their risk of developing it. These include
lifestyle changes, such as keeping fit and getting regular exercise as
well as either not drinking alcohol or having no more than one drink
per day. Other major factors are pregnancy, childbirth, and breast-feed-
ing; women who have children and have breast-fed them reduce their
breast cancer risk significantly. Some breast cancer is hereditary, and
102 Prevention of Cancer

specific genes related to breast cancer have been identified. While this
doesn’t allow the prevention of cancer, it does help in screening and
monitoring those women at high risk, so that if cancer develops it can
be treated early.
 7
Diet and Exercise
Do Make a Difference

Key Points

♦ Many cancer researchers believe that diet is related to perhaps 30 to

40 percent of all cancers. These cancers are believed to be related
primarily to high fat, low fiber, and fried food. A healthy diet consists
mostly of plant sources and limited consumption of meat.

♦ Even though the link between diet and cancer is controversial, those
who follow nutrition guidelines will enjoy better health and put
themselves at a lower risk for coronary heart disease and diabetes.

♦ Obesity is a significant threat to life expectancy. Diet and exercise

help reduce the threat of obesity.

Several years ago, I received an honorary doctor of science degree

from Drury University in Springfield, Missouri. There is a required talk

103
104 Prevention of Cancer

that goes with receiving the degree. I chose to speak about cancer
and diet. As I described what I thought were appropriate foods that
might reduce risk for that abominable disease, I reflected that the
recommended meals were very close to the meals my mother gave
me when I was a small boy. I remember well her telling me to eat my
greens and other veggies, to eat the whole wheat bread on my plate,
and to enjoy the fresh fruit she put out as a dessert. I remarked to the
graduating students that nutrition scientists could have saved a lot of
research money by just listening to my mother. I suspect that most
mothers similarly encourage a good diet for their offspring, a diet that
is not only good for growing boys and girls but a diet that is believed
by many to be good for helping to prevent cancer. If you hear similar
words from your mother, listen to her.
Contrast what my mother advocated with the fast-food fare that many
people choose today. A fast-food meal may be made up of sugar water
with caramel coloring and some flavoring (a “cola” drink), potatoes
deprived of their skin and treated with hot oil (french fries), and cooked
fatty hamburger meat served on bleached white flour baked in the form
of a soft, bland bun. I wouldn’t feed that concoction to a pet dog—or to
any other pet—much less a child of my own.

What You Eat May Save Your Life

Nutrition and food are thought by many cancer researchers to be re-

lated to perhaps 30 percent to 40 percent of all cancers. These cancers
are believed to be related primarily to consumption of high fat, low
fiber, and fried food. The principal cancers related to these dietary fac-
tors are cancers of the colon, breast, pancreas, prostate, ovary, kidney,
and endometrium. Inadequate levels of fruit and veggies are thought
 Diet and Exercise Do Make a Difference 105

by some to be related to stomach and other cancers. I agree with Gary

M. Williams and Ernest L. Wynder that “definitive proof of causation
is difficult to establish . . . Nevertheless, public health action does not
have to await irrefutable evidence of causality.” I shall take the view
that recommended “cancer preventing” diets could enhance other
aspects of good health and just may protect against cancer—what is
there to lose?
The significance of diet extends beyond simply eating the right foods.
It must also include a serious consideration of caloric intake (how much
one eats) and the amount of physical exercise that one gets. Together,
the amount of good food and the extent of physical activity will result
in either a proper weight throughout life—or the very real possibility of
the pathological effects of obesity. The last paragraph of this chapter ad-
dresses the dire consequences of an obese America—if you do nothing
else, read and remember that last paragraph.

Fight Cancer with Your Knife and Fork

Wendy Demark-Wahnefried, a professor in the department of surgery at
Duke University Medical School, wrote in the magazine, Coping, “Fight
cancer with your knife and fork by eating plenty of vegetables, fruits
and whole grains, and eating less red meat and fatty foods (especially
saturated fat from animal sources).” Dr. Demark-Wahnefried’s remarks
were directed to cancer survivors—her recommendations are just as
appropriate to people who wish to prevent cancer.
Regarding mega doses of vitamins and antioxidants sometimes
consumed to protect against cancer: A balanced diet of vegetables, fruit,
cereals, and fat-free dairy products contains everything that an ordinary
person needs for good nutrition. Seeking to enhance that good diet
106 Prevention of Cancer

Figure 7.1 Fight cancer by eating plenty of vegetables, fruits, and whole
grains, as illustrated here, is the advice of Dr. Demark-Wahnefried. (National
Cancer Institute/U.S. National Institutes of Health)

by large doses of vitamins and antioxidants is unnecessary, and, if an

undetected cancer is present, might even enhance the growth of that as
yet to be discovered malignancy. Many oncologists discourage cancer
patients from using antioxidants during chemotherapy and radiation
treatment because the very antioxidants that ordinarily protect normal
cells might encourage cancer cells. For any cancer patient who happens
to read this, the author urges that patients consult with their oncologist
and heed the advice of the person in charge of therapy.
 Diet and Exercise Do Make a Difference 107

Nutrition Is Not
Without Controversy

Controversy abounds in the modern world. Many people believe in

special creation; others favor evolution. Some citizens wish to build
football stadiums; others seek funds for art museums or university can-
cer centers. Cigar and cigarette smokers want their freedom to light up
in restaurants, while others demand clean air and a ban on smoking
in eating places. I focus on controversy to make it perfectly clear that
there is no unanimous view about the role diet plays in cancer. One
needs only to refer to the enormous tome (2,898 pages not including
a 300+ page index) of Cancer, Principles & Practice of Oncology, 7th
edition, edited by V.T. DeVita Jr., S. Hellman, and S.A. Rosenberg,
published in 2005 by Lippincott Williams & Wilkins, to find statements
such as: “. . . any conclusions should be regarded as tentative” with
regard to fat in the diet (on page 511); as to fiber, “observational data
presently available do not indicate an important role for dietary fiber
in the prevention of cancer” (on page 517); and concerning fruits and
veggies (my mother would not like this), “doubts have been cast on the
protective association between fruit and vegetable consumption and
cancer” (on page 518).
However this may be, my view of nutrition and cancer is in harmony
with the American Cancer Society (ACS) Guidelines on Diet and
Cancer Prevention, which, incidentally, are essentially identical with
the recommendations of the American Institute for Cancer Research
(AICR) and are similar to the recommendations of the National Cancer
Institute and the American Heart Association. The ACS guidelines for
cancer prevention are thought to offer the best nutrition information
currently available to the citizens of the United States. They are offered
108 Prevention of Cancer

Figure 7.2  AP Images

in this chapter with the thought that the readers who abide by the
recommendations may profit from a reduced risk for cancer. Even if
this ultimately proves not to be the case, those who follow nutrition
guidelines will enjoy better health and put themselves at a lower risk
for coronary heart disease and diabetes.
 Diet and Exercise Do Make a Difference 109

An aspect of nutrition that is not a matter of controversy is obesity,

which is a subject of grave concern for all epidemiologists. That will be
discussed in the last paragraph of this chapter.

Be Physically Active

When I was young, we were not couch potatoes. What has changed in
America to result in a generation of obese kids and their fat parents? My
life many years ago may reveal a little of what has changed. As a boy,
I had a bat made of wood and a ball. That was all it took to get a few
kids out playing baseball. When not engaged in baseball (or football),
we hurried to our bikes and covered many miles finding new territory
to explore. We raked leaves, mowed lawns, and shoveled snow with
muscle power. We walked to and from school. Many of us had paper
routes—newspapers in those days were delivered on foot and on time.
Desktop computers would not appear for another half century—so,
there was no sitting watching figures move about on a small screen. I
could go on and on, but the point is that exercise came naturally, and it
was just what we did those many years ago.
Television was yet to come into homes, and junk food was either not
available or we did not have the cash to buy it. I do not remember kids
who were overweight. Clearly, we kept our caloric intake pretty much
balanced with our energy output. This is not the case today. What is the
solution? The American Cancer Society recommends exercise. I agree.

Exercise and Weight Affect More Than Cancer Risk

Weight gain and reduced physical activity characterize our way of life
in America. About two thirds of U.S. adults are overweight, and nearly
110 Prevention of Cancer

a third of these are classified as obese, according to the World Health

Organization. Obesity and lack of physical activity are associated with
increased risk for cancer. What is the solution to this problem? The
solution is simple enough: retain a healthy weight and get involved in
exercise.
What is the incentive to watch weight and exercise? People who
have occupations that involve daily physical activity have lower rates of
colon cancer. Colon cancer is the third largest cancer killer in the United
States. An expected 52,180 Americans will die of cancer of the colon
and rectum in 2007, about three times the number of people expected to
die of HIV/AIDS during the same period. I think that vigorous exercise is
little enough to pay to reduce the possibility of colon cancer. A number
of studies suggest that vigorous exercise reduces the risk of breast can-
cer, which is the second leading cause of cancer death to women in the
United States. Again, exercise is a modest cost for reduced vulnerability
to breast cancer. Men who have occupations that involve vigorous physi-
cal activity have a reduced risk for prostate cancer, which is the second
leading cause of cancer deaths in men. Death is but one of the problems
associated with prostate cancer. Incontinence, erectile dysfunction,
fatigue, hot flashes, loss of libido also accompany prostate cancer. It is
irrelevant whether these symptoms are due to the cancer per se or due
to treatment. The problems are real—and enough to make me want to
exercise now! Graham Colditz and Kathleen Yaus Wolin wrote in 2005:
“A strong and consistent relation has been reported between obesity
and mortality from all cancers [italics added] among men and women.”
Exercise makes one feel better—why not feel better and reduce the risk
for a killer cancer at the same time.
There are health benefits other than cancer risk reduction with
exercise, weight control, and a healthy lifestyle. There is now a “common
 Diet and Exercise Do Make a Difference 111

agenda” for the American Cancer Society, the American Diabetes

Association, and the American Heart Association. These health
organizations seek to stimulate improvement in primary prevention for
cancer, diabetes, and cardiovascular disease. Two-thirds of all deaths
in the United States are due to these diseases. Yet prevention efforts are
not well funded. Dr. Harmon Eyre and his associates wrote: “Despite
the incontrovertible evidence supporting the medical and economic
benefits of prevention and early detection, current disease control
efforts are underfunded and fragmented.”

A Decreased Life Expectancy

in the New Millennium?

Life expectancy in the Western world has been gradually increasing for
many hundreds of years. It is something that we have grown to expect.
Many people are perhaps unaware that the amount of increase per unit
time (decade or year or whatever) is now decreasing. The big incre-
ments in increased life expectancy were due to prevention of childhood
diseases and more and better public health measures. Chapter 8 of this
book chronicles diseases that were formerly rampant killers, but are
no longer, at least to most citizens of the United States. So where are
we going to get the extra years of life that accrue with enhanced life
expectancy? Well quite frankly, it does not seem that we will have an
increased life expectancy in the near future—and perhaps there may
even be a loss in life expectancy in this big and rich country of ours. The
important killers of today, cardiovascular disease, diabetes, and cancer
are not going away in the near future. And what is ominous indeed is
the fact that today’s big killers may become even bigger killers. Why?
Because of obesity.
112 Prevention of Cancer

Figure 7.3  AP Images

A potential decline in life expectancy is the subject of an important

article in the March 17, 2005, issue of the prestigious New England
Journal of Medicine. The source of the article is not listed to stimulate a
 Diet and Exercise Do Make a Difference 113

mass run of high school students to the nearest medical library. Rather,
the source is indicated to advise students that serious and thoughtful
medical doctors and scientists view with alarm the epidemic of obesity
and its effects on health and life expectancy. While this book is about
preventing cancer, bear in mind that preventive measures for cancer
apply to coronary heart disease and diabetes as well. Take home the
message that exercise and proper diet will enhance the possibility of

♦ Ameri can Cance r So ci e t y (A C S)

Guide lines, 2005

T he ACS states, and I concur, that “no diet can guarantee full protection
against disease.” The following recommendations were first published
in 1984, reviewed in 1991, reviewed again in 1996, and were current as of
September 2005.
1. Choose most of the foods you eat from plant sources
♦ Eat five or more servings of fruits and vegetables each day
♦ Eat other foods from plant sources, such as breads, cereals, grain
products, rice, pasta, or beans several times each day
2. Limit your intake of high-fat foods, particularly from animal sources
♦ Choose foods low in fat
♦ Limit consumption of meats, especially high-fat meats
3. Be physically active: Achieve and maintain a healthy weight
♦ Be at least moderately active for 30 minutes or more on most days
of the week
♦ Stay within your healthy weight range
4. Limit consumption of alcoholic beverages, if you drink at all.
114 Prevention of Cancer

a long and healthy life. The good doctors and scientists who wrote the
2005 article in the New England Journal of Medicine agree.

S ummary

The question of whether or not a proper diet can prevent cancer has no
easy answer. What is clear is that a good diet and regular exercise have
extensive health benefits and minimize the risk of numerous diseases.
For the first time after many decades of rising life expectancy, people in
the United States may be facing a decline in how long they can expect
to live. This is due primarily to obesity. It is crucial to make a healthful
diet and exercise a part of your life.
 8
A Final Word on Prevention

Key Points

♦ At least half of all, and probably much more, cancer diagnoses can
be prevented.

♦ Far less money is spent preventing diseases than on treating them in

the United States.

♦ History shows that many terrible diseases have been controlled or

even eradicated through prevention.

“Despite the incontrovertible evidence supporting the

medical and economic benefits of prevention and early
detection, current disease control efforts are underfunded
and fragmented.”
Eyre, Kahn, and Robertson, 2004

115
116 Prevention of Cancer

“. . . a conservative estimate is that at least half of all

cancer deaths could in principle be avoided by the ap-
plication of existing knowledge.”
Cancer Prevention & Early Detection
Facts & Figures, 2005

The United States spends less than 3 percent of its total health budget
on prevention studies—consider this in light of Secretary of Health and
Human Services Margaret M. Heckler who, over two decades ago, gave
voice to the notion of the simple truth that we can prevent most cancer.
How long will it be before we believe Heckler’s “simple fact,” or the per-
suasive statement of the American Cancer Society, and do something
about it? Governments may tarry but as individuals, we can endeavor
to place ourselves and our loved ones at a reduced risk for cancer now.
The readers of this book are urged to do just that.
Is a cure only a pill away? Most of us have gotten used to the idea that
penicillin and the other “miracle” antibiotics can cure almost any disease
and that it is simply a matter of time before cancer will be cured with a
pill. As it is now, much cancer is cured—but at a cost. The cost includes
damage to the individual who receives chemotherapy (see Chapter 5).
Unquestionably, the cures are worth the profoundly powerful treatment.
It is far better to have a survivor grandchild than one who ceases to live.
Although Chapter 5 concerns survivors among young cancer patients,
the painful lessons pertain to adults also. But would it not be preferred
to prevent cancer in the first place?
A disease of self is a major part of the problem. Let us consider again
the reference to penicillin and other antibiotics. Antibiotics are designed
to kill invaders of the body. Example: The streptococcus bacteria group,
which includes bacteria that cause scarlet fever and bacterial pneumonia.
Streptococci are foreign to us. Their cells are constructed differently than
 A final word on prevention 117

are ours; for example streptococci have no nuclear membrane and they
have a rigid cell wall. Beginning biology courses point out that human
cells have nuclear membranes and no cell wall (a plasma membrane
encloses our cells).
Differences in cell structure can be exploited to kill the invader (the
bacteria) and not the host (the patient). Clever and immensely bright
scientists have sought for differences in many of the pathogenic bacteria
and have developed effective drugs that target the differences with the
result that they are killers of noxious bacterial invaders. Penicillin inter-
feres with the synthesis of a substance essential for cell wall formation.
No cell wall results in bacterial death. Death not only for streptococci
but also staphylococci, pneumococci, meningococci, and a number of
other disease-causing organisms. However, because human cells lack a
cell wall, human cells survive treatment with penicillin.
Contrast a bacterial invader with a human cancer cell: The cells of
the cancer are the patient’s own cells. Accordingly, the cancer cells have
a distinct nuclear membrane as do all normal cells of the patient (with
the notable exception of mature red blood cells, which lack a nucleus
altogether). None of the cancer cells have a rigid cell wall, which of
course is lacking in all normal host cells. One can go further and note
that the cancer cells have mitochondria, cellular organs that power cells,
as do all normal cells. The DNA of the cancer cell is identical to the DNA
of normal body cells except for minute changes in the cancer cell DNA
due to mutation or other genetic events. The list of similarities of cancer
cells to normal cells could be extended to fill a textbook.
Now consider a drug that may become useful in treating cancer. It is
likely that the drug, designed to kill cancer cells, will be toxic to normal
cells as well. Without going into too much detail, consider cell division
in cancer cells. They divide when they should not. Several chemothera-
peutic agents have been designed to attack dividing cells. They work.
118 Prevention of Cancer

The dividing cells of the cancer will respond to the drug by not divid-
ing. But unfortunately, so too will normal cells that are dividing—and
these include the cells of hair follicles, the lining of the gut, and bone
marrow where blood cells are made. With some chemotherapy, hair
falls out, the gums bleed as do parts of the gut, and infection-fighting
white blood cells drop in number. The reader already knows that not
all cancer can be prevented (see Chapter 1). But much cancer can be
prevented—there is no question it is much gentler to prevent than to
cure. And cheaper, too.
Another problem is that cancer often works as a “silent” disease. Our
bodies are wondrous indeed. We receive the gift of capacity greater than
need. Our brains are competent to learn far more than we actually learn.
We have excess kidney capacity and can survive with only one. We live
with lungs that can exchange carbon dioxide with oxygen using only a
small part of their capacity.
Why is excess capacity a problem? If a cancer begins to grow in the
lungs, it may be years before it is detected. It grows “silently.” The indi-
vidual with a lung cancer feels no less well and experiences no difficulty
in breathing for years. Those years of undetected cancer growth permits
much time for metastasis to occur—without the patient even being
aware that he or she harbors a malignancy. It is believed that metastasis
occurs in at least 75 percent of cancer prior to detection. Metastasis is
difficult to treat and metastasis often causes death. Again, prevention is
far more preferable than the agony of treatment.

Prevention Is the Name of the Game

My maternal grandparents’ cemetery plot includes the graves of four chil-

dren who died in early childhood during the latter part of the 19th century.
 A final word on prevention 119

A similar situation is found in my paternal grandparents’ cemetery plot.

This is absolutely typical for the time. There have been no deaths among
the offspring of my sibling and myself and our grandchildren. Why the
difference? Prevention, not cure, of disease accounts for most of the lives
saved. My children and my children’s children did not have to endure and
survive the diseases described below. There is a message here.

Diseases That Are Preventable in the Modern World

Smallpox. Pandemic means that a disease is epidemic over a vast

area and affects many people. Smallpox, aka variola, was pandemic
in Western Europe in 1614, and only a few years later, it was epidemic
in England. It was a leading cause of death at the time. Smallpox, an
acute, often fatal, viral disease, was a scourge that elicited unsurpassed
fear. Vaccination, developed initially by Edward Jenner (1749–1823), is
credited for both prevention of the disease and the eradication of the
pestilence. The last case in the United States was in 1949. The World
Health Organization declared smallpox eradicated from the world in
1980. A specific treatment for this catastrophic lethal malady was never
developed. Jenner did not cure—he prevented smallpox.
Cholera. Cholera (see Chapter 1) is a gut infection caused by the
bacterium Vibrio cholerae. The disease results in massive diarrhea of up
to four gallons a day. Dehydration follows. Body temperature and blood
pressure fall. Gut pain is so intense that, if the patient is not already
in a coma, death is sought as relief from the illness. Death can occur
within hours of infection. Cholera is still found in India and Southeast
Asia, and it can occur in any country without basic sanitation. John
Snow (1813–1858) discovered the mode of transmission of cholera
prior to even knowing what it was in contaminated water that caused
the disease. Snow discovered that cholera is spread by consumption of
120 Prevention of Cancer

fecal-contaminated water and food. Many millions of lives in the United

States have been saved by treatment of public water supplies that separate
drinking water from sewage and which has been treated with chlorine
to kill Vibrio and other pathogens. The utterly devastating lethal disease
of cholera is not found where good public health measures are strictly
enforced—treatment of water renders treatment of cholera patients un-
necessary—by prevention.
Typhoid fever. The bacterium Salmonella typhi causes this acute
infectious disease. Fever of 104° to 105° is often followed by enlargement
of the spleen and frequent bowel movements occur. These symptoms
may be followed by twitching of the body, delirium, and a profound stu-
por. Fatalities are frequent. Clearly, typhoid is something to be avoided.
It is spread by contaminated food and water. Filtration and chlorination
of water supplies and other public health measures to ensure safe food
have effectively prevented this noxious disease.
Measles. Measles, aka rubeola, was a common, highly contagious,
mostly childhood, viral disease. It formerly was a deadly disease but
mortality declined in the twentieth century. A vaccine for its prevention
was introduced in the late 1960s.
Typhus. The Greek word typhos is the origin of our word typhus
and translates as “stupor originating from a fever.” Typhus refers to
several acute infectious diseases including epidemic (louse-borne)
typhus, scrub (mite-borne) typhus, and murine endemic (flea-borne)
typhus. The different types have in common high fever, chills, terrible
headaches, and ultimately delirium. Epidemic typhus has an especially
high mortality rate. Epidemic typhus is caused by Rickettsia prowazekii
transmitted by the bite of a louse. Similarly, the other typhus diseases
are caused by bacteria transmitted through the bites of mites or fleas.
 A final word on prevention 121

The insecticide DDT (dichlorodiphenyltrichloroethane) was

used during World War II to kill lice and thus to prevent spread of
epidemic typhus. DDT was also useful in containing plague, malaria,
and yellow fever. Many people who fear the ecological effects of
DDT forget the thousands (perhaps millions) of people whose lives
were spared during World War II because of DDT. A thankful postwar
world was pleased indeed that Paul Hermann Müller (1899–1965), the
Swiss industrial chemist who developed a commercial process for the
synthesis of DDT, was awarded the Nobel Prize in 1948. Cleanliness,
in addition to the DDT, was absolutely necessary to prevent body
lice. Probably few, if any, of the readers of this book personally know
of anyone who has had epidemic typhus. The rule of thumb here is
that no body lice means that typhus is prevented. DDT had an equally
spectacular effect on malaria prevention—by controlling the mosqui-
toes that spread the disease.
Pellegra. The term is derived from the Italian and means literally
“rough skin.” The disease was especially deadly in the southern United
States where 100,000 deaths occurred in the first third of the 20th century.
Pellagra’s four “Ds” describe this devastating and deadly disease: derma-
titis, diarrhea, dementia, and death. Pellagra has virtually disappeared
due to the insight and hard work of Dr. Joseph Goldberger (1874–1929)
of the United States Hygienic Laboratory (a predecessor of the National
Institutes of Health). Goldberger showed that pellagra is not contagious
and not caused by a virus or bacterium. It is caused poor diet. Pellegra
is prevented by a diet of red meat, fish, beans, nuts, and whole wheat
bread. That diet was shown by others to contain the water soluble vita-
min niacin. No one is cured of pellagra with drugs. Pellagra is prevented
by a well-balanced diet containing niacin.
122 Prevention of Cancer

Scurvy. This disease results in weakness, anemia, swollen and

bleeding gums, loose teeth, great fatigue, and eventually death. Sailors
were particularly vulnerable. The Scot James Lind (1716–1794) was
determined to find the cause of death of sailors who died of scurvy
in greater numbers than were lost in battle. He suspected it was due
to their limited diet of bread and salted meat. Lind found that citrus

♦ The Pitiful Pli ght of Y oun g C h i m n e y Sw e eps

P ercivall Pott was one of the first writers to describe a specific cancer,
the cause of the cancer, the occupation group vulnerable for the can-
cer, and treatment for the cancer. In the London of 1775, Pott described
scrotal cancer in clinical terms that are completely understandable to the
modern reader. The scrotum is the bag or pouch of skin that contains the
testes. Pott noted that chimney sweeps were more likely to have a skin
cancer of the scrotum than other people. Further, he wrote that scrotal
cancer “in these people [chimney sweeps], seems to derive its origin from
a lodgment [i.e., the retention] of soot in rugae [rugae: wrinkles or folds
of skin] of the scrotum.
Charles Dickens many years later described the plight of the English
working classes. Pott was a near match to Dickens in writing about the
difficulties of working people and perhaps social consciousness should be
added to Pott’s list of achievements. An example, taken from his scrotal
cancer essay: “I never saw it under the age of puberty, which is, I suppose,
one reason, why it is generally taken, both by patient and surgeon, for
venereal. . . . The fate of these people seems singularly hard; in their early
 A final word on prevention 123

fruits cured the disease and that lime juice added to the diet prevented
scurvy. Lind published his report in 1753, and more than 40 years later,
the British Navy ordered a daily dose of lime juice added to the diet,
with the result that British sailors are known as “limeys” to this day. It
was later learned that citrus fruits contain, among other things, vitamin
C. It is the vitamin C that prevents scurvy. A bit of history: Only the

infancy, they are most frequently treated with great brutality, and almost
starved with cold and hunger; they are thrust up narrow, and sometimes
hot chimneys, where they are bruised, burned, and almost suffocated; and
when they get to puberty, become peculiarly liable to a most noisome,
painful, and fatal disease.”
Pott was English and lived at a later time than the Italian Ramazzini
(see Chapter 6) Yet, Pott knew of Ramazzini and referred to him in the
context of occupational disease even though online indices (computer-
generated bibliographic services—or Google for that matter) were not
available in 1775. Ramazzini will be remembered for breast cancer and
nuns; Pott will be remembered for scrotal cancer and chimney sweeps.
Pott’s never-to-be-forgotten chimney sweep cancer essay made possible
behavior (bathing) that would prevent a loathsome and lethal cancer. The
article on chimney sweep disease is only three pages long and is described
in The Surgical Works of Percivall Pott, 1775.
Pott was born in London in 1714. At age 15 he became an apprentice
for the study of surgery and by age 22 was admitted into the Company of
Barber Surgeons. He became a distinguished surgeon with many famous
patients and was knighted. Sir Percivall Pott died in 1788.
124 Prevention of Cancer

English ordered that citrus juice be added to the diet of their fighting
men. During the American Civil War (1861–1865), United States and
Confederate soldiers were dying of scurvy because of vitamin C defi-
ciency. Note that drugs were not required to cure scurvy. A proper diet
prevented the lethal disease.
Beriberi. Beriberi is found in Southeast Asia, including Sri Lanka.
Beriberi in Sinhalese (the language of Sri Lanka) means “I cannot.” The
word refers to the totally wiped-out feeling and the inability, because of
illness, to do anything. The disease involves inflammation of peripheral
nerves, heart failure, edema, and diarrhea. It results from eating too
much polished rice (white rice) in place of whole grains, nuts, pork, and
fish. These other foods contain the B vitamin thiamin, which prevents
beriberi. Eating foods containing adequate amounts of the thiamin
prevents the beriberi.
Among the people to thank for many disease-prevention efforts
are water treatment chemists who provide pathogen-free water and the
plumbers who keep sewage and polluted water separated. Included also
are the immunologists who fashion vaccines that prevent disease—and
the epidemiologists who keep track of who gets a disease, where they
live, their occupations, etc. These people are responsible for the preven-
tion of many diseases and are, to a large extent, the reason why we
enjoy an enhanced life expectancy.
Let’s hope that cancer—or at least some cancers—can be added to
the list of preventable diseases. For now, start by stopping smoking, stay-
ing out of the sun, protecting yourself against HPV, eating a balanced
diet, and exercising.
 A final word on prevention 125

S ummary

Too little effort is put into preventing cancer. Many forms of cancer can
be prevented, yet most medical resources are spent in treating disease
after it occurs. Historical efforts to wipe out or control diseases such as
smallpox and typhus show that preventive approaches are effective. With
so many of the risk factors for cancer subject to personal and lifestyle
choices, it is important for individuals to make well-informed choices to
improve their health and avoid unnecessary diseases.
 Glossary
♦

6-mercaptopurine (6-MP) An anticancer drug that acts as a substi-

tute for a normal precursor of DNA; this blocks DNA synthesis result-
ing in cell death. Elion and Hitchings received the Nobel Prize in
1988 for the development of 6-mercaptopurine.

acute lymphoblastic leukemia (ALL) Malignancy of immature

white blood cells, specifically activated lymphocytes. It is the most
common acute leukemia of children. Acute refers to rapid onset and
not long duration.

acute myeloid leukemia A malignancy that usually occurs in adults

characterized by proliferation of white blood cells of the bone mar-
row. Acute refers to rapid onset and not long duration.

AIDS Acronym for acquired immunodeficiency syndrome; loss of im-

munity leaves the victim vulnerable to infection and some forms of
cancer.

antibody A molecule in the blood that tags, destroys, or neutralizes

bacteria, viruses, or other harmful toxins.

antidepressant A drug used in the treatment of severe feelings of

gloom, hopelessness, sadness, and despair.

basal cell carcinoma The most common skin cancer derived from
the basal layer of epidermal skin cells. It is rarely metastatic and
grows slowly. If not properly treated, it can become locally invasive
with much tissue damage. It now afflicts young people although it
formerly occurred primarily in older adults.

126
 glossary 127

Bence Jones proteins Abnormal proteins found in the blood plasma

and the urine in cases of multiple myeloma, named for Henry Bence
Jones, an English physician (1813–1873).

busulfan An anticancer drug that reacts directly (binds with) DNA

thereby blocking cell division.

cachexia Severe loss of weight.

carcinoma A cancer affecting epithelial (q.v.) cells.

celibate To abstain from marriage or sexual intercourse.

cervix Neck; when used as uterine cervix, the term refers to the por-
tion of the uterus that opens into the vagina.

chemotherapeutic agent A chemical designed to cure a disease. In

this book, it refers to drugs designed to cure cancer.

chlorambucil An anticancer drug known as a “nitrogen mustard”

that acts to prevent cell division by binding with DNA.

cholera A disease of the small intestine caused by water or food

contaminated with the bacterium Vibrio cholerae. It is often fatal
because of vomiting and diarrhea.

chronic obstructive pulmonary disease (COPD) A persisting con-

dition of airway blockage. Asthma and emphysema are examples.

cisplatin A platinum-containing anticancer agent that targets and

binds with DNA to block cell division. It is considered curative in
testicular cancer (q.v.).

colposcope An instrument used for a magnified examination of the

cervix.

colposcopy The examination of the cervix and vagina with a

colposcope.
128 glossary

coronary heart disease The coronary arteries supply the muscle of

the heart with essential oxygen and nutrients. Coronary heart dis-
ease results in a decreased blood supply to the heart due to partial
or complete blockage of one or more of the arteries.
corpus A word meaning body; when used with uterus, the term refers
to the main upper portion or body of the uterus; the isthmus con-
nects the uterine corpus to the cervix (q.v.).
cyclophosphamide An anticancer drug known as a “nitrogen mus-
tard” which blocks cell division by binding with DNA.
cytologist A person trained to detect changes from the normal in cells
observed under the microscope.
cytotoxic A term used with chemotherapy to indicate that the drug is
toxic and probably lethal to cells.
endometrium The term for the interior lining of the uterus. The lining
consists of a single layer of epithelium, which covers a layer of con-
nective tissue. The epithelium form glands that extend through the
connective tissue to the muscular layer of the uterus. The epithelium,
much of the glands, blood, and some of the connective tissue is lost
during the monthly menstrual cycle. The young embryo attaches to
(implants in) the endometrium if pregnancy occurs.
epidemiology The science of the distribution and prevalence of
disease.
epithelial Epithelial cells cover the internal and external surfaces of
the body and line hollow structures such as the gut. Epithelial cells
form many glands.
erectile dysfunction Inability to maintain a penile erection sufficient
for sexual intercourse.
etiology The cause(s) of a disease.
 glossary 129

etoposide A large molecule derived from podophylotoxin (q.v.) which

blocks cell division by interfering with an essential enzyme.
fibrocystic The term as used in breast disease refers to nonmalignant
lumps in the breasts that vary with the monthly cycle. About one
half of all sexually mature women have these nonmalignant lumps
from time to time.
herpesvirus A member of a large group of DNA-containing viruses
that infect many kinds of animals and humans.
Hodgkin’s disease A cancer of lymph nodes, spleen, and other lym-
phoid tissue. The disease is named for the English doctor Thomas
Hodgkin (1798–1866).
iatrogenic Illness or adverse outcome of a disease caused by the phy-
sician. The word is derived from the Greek iatros meaning physician
plus genesis, which means mode of origin.
immunosuppressive drugs Drugs designed to block the immune
response; generally given to patients after organ transplantation to
prevent immune rejection of the transplanted organ.
incontinence Inability to retain urine (or feces) voluntarily.
Jurassic The second period of the Mesozoic era, about 200 to 150
million years ago, when giant reptiles dominated and birds first
appeared.
leukemia A type of cancer or malignancy that involves the white blood
cells.
libido Sex drive; loss of libido means loss of interest in sex.
lymphoma Cancer involving the lymphocytes, or cells of the immune
system.
malignant melanoma A cancer of melanocytes, which are cells that
produce the dark pigment melanin. The cancer is also known simply
130 glossary

as melanoma. It occurs not only in the skin but may also occur in the
eye, mouth, throat, anal canal, and other places.
mammography The process of taking an X ray of the breast.
menstruation The loss of blood and other material from the uterine
lining that occurs about once per lunar month in women after the
onset of puberty.
metabolic The products resulting from the breaking down of sub-
stances by the body.
metastasis Colonies of cancer cells that grow distant from the original
cancer. Metastasis is unequivocal proof that a growth is cancer.
mortality The number of deaths from a disease.
multiparous The description of a woman who has borne more than
one child.
multiple myeloma A malignant tumor composed of plasma cells,
which are ordinarily found in the bone marrow. The tumor cells will
provoke the formation of characteristic multiple holes in bone.
mutant, mutations A mutant is an organism that has undergone a
change in its genetic material, the DNA. Mutations are permanent
changes to the DNA that have occurred.
nanometers One-billionth (10 -9) of a meter.
nasopharyngeal carcinoma Cancer of the nose and pharynx, af-
flicting primarily males of China and other parts of southeast Asia. It
is related in a causal way to a herpesvirus, among other factors.
nicotine An important component of tobacco used as an agricultural
insecticide. It is used in veterinary medicine to kill parasites. It is
addictive similar to heroin and cocaine and is probably the major
reason that it is difficult for smokers to quit.
 glossary 131

non-Hodgkin lymphoma There are many kinds of lymphoma in-

cluded in this term. Non-Hodgkin lymphomas (q.v.) are much more
common than Hodgkin disease (q.v.). White blood cells known as
lymphocytes divide without control resulting in enlarged lymph
nodes in the neck, armpits, and groin.

nulliparous The description of a woman who has borne no children.

osteomas Non-malignant, slow growing, tumors of bone.

osteoporosis A loss of bone density with fractures that occur after

minimal trauma; the condition is associated with the elderly, per-
haps because of a decline in exercise and inadequate diet.

osteosarcomas Malignant bone cancers affecting primarily young

adults.

paleopathology The branch of medicine dealing with ancient (fossil)

disease.

papillomavirus Any of a number of viruses of the genus Papilloma-

virus. These viruses are found in many higher animals from birds
to mammals including humans. All are characterized with DNA as
genetic material. Genital warts and cervical cancer are caused by
human papillomaviruses.

Pap smear Also known as Pap test. Named for George Nicholas Pa-
panicolaou who developed a method for examination of exfoliated
(detached) cells from the cervix as well as other organs. The exfoli-
ated cells are placed on a slide, fixed and stained, and examined
under the microscope for pathologic changes.

plasma cells Antibody-producing white blood cells.

132 glossary

podophylotoxin A toxic compound obtained from the roots of the May

apple whose scientific name is Podophyllum. The compound has sev-
eral derivatives (etoposide, teniposide, q.v.) used in cancer therapy.

prospective study An epidemiological study that starts with a popu-

lation of normal (healthy) individuals and follows them to see what
happens with respect to a particular disease. This is in contrast with
retrospective studies that start with the diseased individual and
endeavors to ascertain what led to the disease. Properly designed
prospective studies are considered to have more validity than retro-
spective studies, which depend to a large extent on memory.

recidivism Refers to resumption of an activity that was previously

stopped.

retinoblastoma A malignant cancer of childhood that occurs in one

or both eyes. It occurs either due to heredity (genetically deter-
mined) or spontaneously.

sarcoma A cancer of non-epithelial origin such as bone or muscle.

Epithelial (q.v.) cancers, known as carcinomas (q.v.), are more com-
mon than sarcomas.

solarium A room with one or more sun lamps for treatment with ul-
traviolet radiation.

squamous cell carcinoma Second most common skin cancer after

basal cell (q.v.) carcinoma. The cancer often has its origin in sun
damaged skin of light complexioned individuals. Keratinizing cells
(cells that turn horny and scale-like) of the skin form the cancer,
which may become invasive and ultimately form metastases.

STD Abbreviation for sexually transmitted disease.

 glossary 133

solarium A room with an ultraviolet light. These rooms were, and

some still are, used to obtain a tan but medical experts no longer
consider tanning healthy.
subsidy Public funds to artificially keep the price of an item low.
teniposide A large molecular weight derivative of podophylotoxin
(q.v.) that is chemically similar to etoposide (q.v.) but is much more
potent as an anticancer drug.
testicular cancer The testis is the male germ cell (sex cell) producing
organ. While children may have nonmalignant testicular growths,
generally the tumors are malignant in adults.
transdermal A method of administering a medication through the
skin, such as the nicotine patch.
ultraviolet Radiation with wave lengths shorter than visible violet
light and longer than X ray.
vaccine A substance that will assist the body in providing immunity
against a disease; usually a weakened or killed virus or bacterial
preparation, or an antigen derived from the virus or bacterium. The
word is derived from the Latin vaca meaning cow because of the
historic use of cowpox vaccine to prevent smallpox.
vibrio cholerae Rod-shaped bacteria, found in the intestines of nor-
mal and diseased humans and in water, which cause Asiatic chol-
era. The bacteria are motile as indicated by the Latin vibrare which
means to move rapidly.
Wilm’s tumor A kidney tumor of children that is rapidly growing
and composed of embryonic tissues; it is also known as
nephroblastoma.
 Further resources
♦

Bibliography
Abbasi, N.R., et al. “Early Diagnosis of Cutaneous Melanoma,” The Journal of
the American Medical Association 292(2004): 2771–2776.

American Cancer Society. Cancer Prevention & Early Detection Facts & Figures
2005. Atlanta: American Cancer Society, 2005.

Bendich,A., and R.J. Deckelbaum, eds. Preventive Nutrition:The Comprehensive

Guide for Health Professionals, 3d ed. Totowa, N.J.: Humana Press, 2005.

Beral, V. “Collaborative Group on Hormonal Factors in Breast Cancer,” The

Lancet 360 (July 20, 2002): 187-195.

Bourdelais, Patrice. Epidemics Laid Low: A History of What Happened in Rich

Countries. Translated by Bart K. Holland. Baltimore: The Johns Hopkins
University Press, 2005.

Crawford, D. The Invisible Enemy. New York: Oxford University Press, 2000.

Crawford, D., and R.W. Jeffery, eds. Obesity Prevention and Public Health. New
York: Oxford University Press, 2005.

D’Andrea, G.M.“Use of Antioxidants During Chemotherapy and Radiotherapy

Should Be Avoided,” A Cancer Journal for Clinicians 55 (2005): 319–321.

Hartmann, L.C., and C.L. Laprinzi. Mayo Clinic Guide to Women’s Cancers.
Rochester, Minn.: Mayo Clinic Health Information, 2005.

Hecht S.S., et al. “Similar Uptake of Lung Carcinogens of Regular, Light, and
Ultralight Cigarettes,” Cancer Epidemiology Biomarkers and Prevention
14 (2005): 693–698.

Hoh, Y.K., and H.K. Boo.“Prominent Women Biologists,” The American Biology
Teacher 65 (2003): 583–589.

134
 Further resources 135

Kluger, J. Splendid Solution. New York: Penguin, 2004.

Love, S.M. with L. Lindsey. Dr. Susan Love’s Breast Book, 4th ed. Cambridge,
Mass.: Da Capo Press, 2005.

McGinn, K.A., and P.J. Haylock. Women’s Cancers, 3d [Link], Calif.: Hunter
House, 2003.

McGrayne, S.B. “Portraits of Science. Damn the Torpedoes. Full Speed Ahead!”
Science 296, 5569 (May 3, 2002): 851–852.

McKinnell, R.G., et al. The Biological Basis of Cancer, rev. ed. Cambridge, UK:
Cambridge University Press, 2006.

Michalas S.P.“The Pap Test: George N. Papanicolaou (1883-1962), A Screening

Test for the Prevention of Cancer of Uterine Cervix,” European Journal of
Obstetrics & Gynecology and Reproductive Biology 90 (2000): 135–138.

Milholland, R.B.R., and S.D. Hines. “Tobacco Induced Mutations: A Fun, Visu-
ally Impressive Experiment,” The American Biology Teacher 66 (2004):
370–376.

Milne, Iain, and Iain Chalmers. “Documenting the Evidence: The Case of
Scurvy.” Bulletin of the World Health Organization 82 (2004): 791–796.

Okuyemi, K.S., et al. “Interventions to Facilitate Smoking Cessation,” American

Family Physician 74, 2 (July 15, 2006): 262–271.

Olshansky, S.J., et al. “A Potential Decline in Life Expectancy in the United

States in the 21st Century: A Special Report,” New England Journal of
Medicine 352 (2005): 1138–1145.

Pott, Percival. The Surgical Works of Percivall Pott. London: L. Hawes, W. Clarke,
and R. Collins, 1775.

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1879-1970. Rockefeller University Occasional Paper 16. New York: Rock-
efeller University Press, 1971.

Rous, Peyton. “Transmission of a Malignant New Growth by Means of a Cell-

free Filtrate,” A Cancer Journal for Clinicians 22 (1972): 397–411.
136 Further Resources

Stephens, F. The Cancer Prevention Manual. Oxford, UK and New York: Oxford
University Press, 2002.

Tulunay, O.E., et al.“Urinary Metabolites of a Tobacco-Specific Lung Carcinogen

in Nonsmoking Hospitality Workers,” Cancer Epidemiology Biomarkers
and Prevention 14 (2005): 1283–1286.

Vilos, G.A.“Dr. George Papanicolaou and the Birth of the Pap Test.” Obstetrical
and Gynecological Survey 54 (1999): 481–483.

Watson, R.R., ed. Functional Foods and Nutraceuticals in Cancer Prevention.

Ames, Iowa: Iowa State Press, 2003.

Wilds, J., and I. Harkey. Alton Ochsner: Surgeon of the South. Baton Rouge:
Louisiana State University Press, 1990.

Web Sites
The Web sites that follow contain information about all of the subject
matter contained in this book on prevention. The Web sites have been
judged to contain authentic information about cancer and are easy to
access.

American Cancer Society

[Link]
This is the Web site of The American Cancer Society (ACS) with an incred-
ible array of useful information about smoking, prevention of cancer, early
detection, treatment, and recent news.

Centers for Disease Control

[Link]
This the address of the Morbidity and Mortality Weekly Report (MMWR),
a weekly epidemiological digest for the United States published by the
Centers for Disease Control (CDC).

Cancer Information Service

[Link]
The Cancer Information Service (CIS) contains information for smokers
who wish to quit as well as cancer news, publications, and much more.
 Further resources 137

Harvard Center for Cancer Prevention

[Link]
Search the Harvard Center for Cancer Prevention and calculate your risk of
developing cancer.

Imaginis: The Breast Cancer Resource

[Link]
This Web site discusses the benefits and risks of mammography screening
in detecting breast cancer.

Lance Armstrong Foundation

[Link]
LIVESTRONG is the name of the Web site of the Lance Armstrong Founda-
tion, which has practical information and resources for cancer survivors.

Memorial Sloan-Kettering Cancer Center

[Link]
The Web site of the Memorial Sloan-Kettering Cancer Center of New York
City contains information for about specific cancers, research, and up-to-
date cancer news.

National Cancer Institute

[Link]
This Web site contains an almost inexhaustible source of cancer informa-
tion provided by The National Cancer Institute (NCI). Learn about types of
cancer, treatment, and screening.

Tobacco Free Kids

[Link]
This site discusses the benefits of a rise in tobacco tax and how it can help
deter people, especially teens, from smoking.

Tobacco Information and Prevention Source (TIPS)

[Link]
This Web site has a plethora of information for people who wish to quit
smoking. The site contains information on educational materials, tips for
youth, and even celebrities against smoking.
 index
♦

A biopsy, 60
Bittner’s mouse mammary cancer, 71
Abbasi, N. R., 60 Black, Shirley Temple, 13
ABCDE test for melanoma, 59–60 bladder cancer, 82
abstinence from sexual intercourse, 65 bone sarcoma, 82, 83
ACS. See American Cancer Society bone tumors, 6
acute lymphoblastic leukemia (ALL), Boston, MA, 90
19–20, 78, 83 BRCA1, 88, 93, 98–99
acute myeloid leukemia (AML), 83 BRCA2, 88, 93
addiction to cigarettes, 26–27 brain, lung cancer and, 34, 35, 37
African American, 49 breast cancer, 6, 13, 30, 49, 58, 88–90, 123
age and cancer, 7, 92 reducing risk, 88, 95
age at first birth, 88, 90–91, 92–93, 101 alcohol consumption, 88,
AIDS, 30, 91, 110 95–96, 101
Albert, Prince, 73 breast-feeding, 88, 96–100, 101
alcohol consumption and breast cancer, exercise, 88, 92, 96, 97, 101
88, 95–96, 101 tamoxifen, 100
alcoholism, 95 weight, 88, 96, 104, 108, 110
ALL. See acute lymphoblastic leukemia risk factors, 88, 91
American Association for Cancer age, 92
Research, Inc., 20, 22 age at first birth, 88, 90–91,
American Cancer Society (ACS), 20, 30, 92–93, 101
60, 91–92, 99, 109, 111, 116 family history, 88, 94
Guidelines on Diet and Cancer gender, 91–92
Prevention, 107, 113 genetics, 93–94, 101
American Diabetes Association, 111 menstruation, 88, 94
American Heart Association, 107, 111 personal history, 94
American Institute for Cancer Research race, 88, 94
(AICR), 107 radiation therapy to chest, 95
AML. See acute myeloid leukemia as second cancer, 83
antibiotics, 116 breast-feeding and breast cancer, 88,
antibody, 94 96–100
antidepressant, 41 breast tumors, 8
Ashkenazi Jews, 93, 94 Bulletin of the World Health Organization,
Athens, Greece, 90 90
atomic bomb, 19, 83 bupropion, 40, 41
Australia, 45, 50 Burdock, Gil, 48
Australopithecus, 6 Burkitt’s lymphoma, 6
Burroughs Wellcome, 84
B Buspirone hydrochloride, 41
busulfan, 81
bacterial pneumonia, 116
basal cell carcinoma, 47, 51–52, 61
Bence Jones proteins, 19 C
Beral, V., 97 cachexia, 13
beriberi, 124 California, 18

138
 index 139

caloric intake, 105 chlorambucil, 81

Canada, 45 cholera, 23–24, 119–120
cancer chronic obstructive pulmonary disease
age and development of, 7 (COPD), 30
childhood, 76–87 cigarettes. See smoking; tobacco
cure, 7, 77 cisplatin, 81
drugs, side effects of, 81–83. See Colditz, Graham, 110
specific drugs cold turkey and smoking cessation, 40
origins of, 6 Colombia, 63
past types of, 22–23 colon cancer, 31, 58, 104, 110
prevention, 115–125. See also specific colposcope, 66
types of cancer colposcopy, 66
control over, 15–24 Company of Barber Surgeons, 123
diet and exercise, 103–114 complexion and skin cancer, 48–49, 58
primary, 36 condoms, 65
screening for, 86 COPD. See chronic obstructive pulmo-
second. See second cancer nary disease
secondary colonies, 36 Coping magazine, 105
therapy, 76 Cornell University Medical School, 73
top cause of death, 32 coronary heart disease, 30, 95, 103, 108,
treatment, 7. See also specific 113
treatment corpus (upper portion of uterus), 63
types of. See specific types of cancer cyclophosphamide, 81
Cancer, Principles & Practice of Oncology, cytologist, 66, 67, 74
107 cytotoxic chemotherapy, 93
carcinoma, 51
cardiovascular disease, 111
Carleton College, 99
D
CDC. See Centers for Disease Control and DDT. See dichlorodiphenyltrichloroeth-
Prevention ane
celibate lifestyle, 64, 89 death, top causes of, 32
cell division, 7–8, 84 De Morbis Artificium (Ramazzini), 89
Centers for Disease Control and Preven- Denmark-Wahnefried, Wendy, 105, 106
tion (CDC), 30–31, 33, 77 deoxyribonucleic acid (DNA), 7, 84, 117
central nervous system, 83 breast cancer and, 98–99
cervical cancer, 62–63 double-helix structure, 85
detecting HPV, 65–66 skin cells, 54
etiology, 64–65 DES. See diethylstilbestrol
vaccine for, 62, 63, 66, 68–69, 72, 75 DeVita, V. T., Jr., 107
cervix, 63 diabetes, 103, 108, 111, 113
chemical pollution, 15, 17 diagnosis, 37, 49, 59
chemotherapeutic agents, 76, 77, 117 dichlorodiphenyltrichloroethane (DDT),
chemotherapeutic drugs, 81–83 121
chemotherapy, 37, 93–94, 116 Dickens, Charles, 122
Child, Julia, 13 diet
childhood cancer survivors, 76–79 cervical cancer and, 64
causes of second cancers, 79–83 controversy over, 107–109
strategy for, 83–87 importance of, 103–107
childhood leukemia, 8 lifestyle habit, 8, 87, 92
chimney sweeps, 122–123 vitamin D and, 58–59
chimpanzee and breast cancer, 98–99 diethylstilbestrol (DES), 95
China, 23 diseases, preventable, 119–124
140 index

District of Columbia, 33 cause, 16

DNA. See deoxyribonucleic acid predisposition, 8, 80–81, 93–94, 101
Dock, Dr., 42 retinoblastoma and, 80–81
Doll, Richard, 29–31, 38 genital warts, 68–69
doxorubicin, 81 Gimbels Department Store, 73
drugs, side effects of, 81–83. See also Glamorgan, Wales, 90
specific drugs Goldberger, Joseph, 121
Drury University, 103 Google search, 60, 123
Duke University Medical School, 105 Graham, Evarts A., 44
Gross’s mouse leukemia, 71
E group therapy for smoking cessation, 25, 40
Egypt, 6, 38
Elion, Gertrude Belle, 84–86 H
Elizabeth I (queen), 34 hair loss, 93
Elizabeth II (queen), 29 The Health Consequences of Smoking, 38
endometriosis, 37 heart damage. See coronary heart
endometrium cancer, 104 disease
England, 15, 18, 38 Hecht, Stephen, 27
epidemic typhus, 120–121 Heckler, Margaret M., 20, 116
epidemiology, 12, 100 Hellman, S., 107
epithelial skin cells, 51 Herceptin, 8, 94
Epstein-Barr virus, 23 heredity and cancer. See genetics and
erectile dysfunction, 38, 110 cancer
estrogen, 95 herpesvirus, 23
etiology, 63 HER2. See human epidermal growth
etoposide, 81 factor receptor gene 2
exercise Hitchings, George, 85
breast cancer and, 88, 92, 96, 97, 101 HIV, 110
importance of, 87, 109 Hodgkin’s disease, 77, 83
weight and, 109–111 Homo erectus, 6
eye cancer. See retinoblastoma hormone replacement therapy (HRT), 95
Eyre, Harmon, 111 hot flashes, 110
HPV. See human papillomavirus
F HPV-6, 68–69
family history and breast cancer, 88, 94 HPV-11, 68–69
fast-food meals, 104 HPV-16, 64, 68, 72
fatigue, 110 HPV-18, 64, 68, 72
fibrocystic breasts, 95 HRT. See hormone replacement therapy
Finland, 38, 63 human epidermal growth factor receptor
first-degree relatives, 94 gene 2 (HER2), 93–94
Florida, 18 human papillomavirus (HPV), 62, 64
Ford, Betty, 13 Hungary, 15, 18
Ford, Gerald, 13 Hunter College, 84
fossils, 15, 18–19, 22–23
I
G immunosuppressive drugs, 52
Gardasil, 66, 68, 69 incontinence, 110
gender and breast cancer, 91–92 India, 49–50
genetic analysis, 101 industrial pollution, 17
genetics and cancer Iran, 38
 index 141

Ireland, 20, 45 mortality, 52

Italy, 38 Müller, Paul Hermann, 121
multiparous, 90
J multiple myeloma, 15, 18–19
Mumbai, India, 50
James I (king), 34, 36–38 murine endemic typhus, 120
Jenner, Edward, 119 mutations in genes, 93, 101
Joe Camel, 45 myeloma, multiple. See multiple myeloma
Johns Hopkins University, 71–72
Journal of the American Medical Associa-
tion, 60 N
Jurassic period, 22 nanometers, 54
nasopharyngeal carcinoma, 23
National Cancer Act, 7
K National Cancer Institute, 7, 107
Kentucky, 18 National Institutes of Health, 121
kidney cancer, 31, 104 nausea, 93
King, Mary-Claire, 98–99 New England Journal of Medicine, 112, 114
Kunkel, Dale, 45 New York, 18
New Zealand, 45, 50
L Nicot de Villemain, Jean, 34
Nicotiana, 34
The Lancet, 97
nicotine, 27, 29
Leakey, Louis, 6, 31
patch, 39, 40–41
leukemia, 49, 81–82
replacement therapy, 41
libido, loss of, 110
and smoking cessation, 40
lifestyle habits, 8, 86–87, 101
Nixon, Richard, 7
Lind, James, 122–123
Nobel Prize, 71, 72, 83, 85, 121
London, England, 23–24
non-Hodgkin lymphoma, 49, 77
Lucké’s frog kidney cancer, 71
non-melanomas, 52
lung cancer, 22, 31, 43–44, 49, 88, 91 nortriptyline, 41
brain and, 34, 35, 37 Norway, 45
as second cancer, 82 nulliparous, 90
nuns and cancer studies, 89, 123
M nutrition. See diet
malaria, 121
malignant melanoma, 37, 47, 49, 52–54, 61 O
mammography, 95 obesity, 88, 96, 105, 109–114
Marin County, CA, 13 O’Brien, Gordon W., 12
measles, 120 Ochsner, Alton, 38, 42–44
Médicis, Catherine de, 34 osteomas, 22
meningococci, 117 osteoporosis, 95
menstruation, 63, 88, 94 osteosarcomas, 22
Mesozoic era, 22 ovarian cancer, 58, 94, 104
metabolic, 27
metastasis, 34, 36–37
Mexico, 63 P
Minnesota, 45 paleopathology, 22
miscarriage. See spontaneous abortion pancreatic cancer, 31, 104
Mississippi, 18 Papanicolaou, George, 65, 73–74
Missouri, 18 Papanicolaou, Mary, 73–74
mole (skin), 59–60 Pap smear, 65–66, 67, 73–74, 75
142 index

pellagra, 121 genetic predisposition, 80–81

penicillin, 116–117 radiation therapy, 83
personal history and breast cancer, 94 secondhand smoke, 27–28, 45, 86. See
plague, 121 also smoking
pneumococci, 117 sedentary lifestyle, 8
podophylotoxin, 81 sexual intercourse, 64
Pott, Percivall, 122–123 sexually transmitted disease (STD), 64
preventing cancer. See cancer, prevention Shakespeare, William, 12–13
prevention studies, 116 Shope’s rabbit papilloma, 71
progesterone, 95 6-mercaptopurine (6-MP), 85
prospective study, 30 6-MP. See 6-mercaptopurine
prostate cancer, 31, 58, 92, 94, 104, 110 skin cancer, 22, 47–48
public efforts smoking cessation, 25, 40, ABCDE test, 59–60
44–46 complexion and, 48–49, 58
Pyrenees, 15, 18 detecting, 59–60
forms of, 50–54
occurrence of, 49
R prevention, 54–59
race and breast cancer, 88, 94 vulnerability to, 49–50
radiation Skin Cancer Foundation, 60
exposure, 16, 19, 83 skin complexion and skin cancer, 48–49,
therapy, 76, 77, 83, 95 58
Ramazzini, Bernardino, 89–90, 123 skin lesion, 59–60
Reagan, Nancy, 13 Slovenia, Republic of, 90
Reagan, Ronald, 13 smallpox, 119
recidivism, 39 smoking, 25–26, 43. See also secondhand
rectal cancer, 31, 110 smoke; tobacco
retinoblastoma, 80–81 as deadly habit, 29–32, 91
Rickettsia prowazekii, 120 cervical cancer and, 64
Rockefeller, Margaretta (Happy), 13 cessation, 39–40, 76, 86–87
Rockefeller Institute for Medical cigarette advertisements, 45
Research. See Rockefeller University group programs, 40
Rockefeller University, 72 hooked on, 26–27
rodent ulcer, 52 lifestyle habit, 8
Roentgen, Wilhelm Conrad, 83 nicotine, use of, 40–41
Rosenberg, S. A., 107 other concerns, 38
Rous, Francis Peyton, 70–72 public efforts, 41, 44–46
rubeola. See measles Smoking and Cancer: A Doctor’s Report
(Ochsner), 44
Snow, John, 24, 119
S solarium, 48
Salmonella typhi, 120 SPF. See sun protection factor
Sao Paulo, Brazil, 90 spontaneous abortion, 95
Scandinavia, 50 squamous cell carcinoma, 47, 52, 61
scarlet fever, 116 staphylococci, 117
screening for cancer, 86 STD. See sexually transmitted disease
scrotal cancer, 122–123 Streptococci, 116–117
scrub typhus, 120 Streptomyces peucetius, 81
scurvy, 122–124 subsidy, 44
second cancer, 77–79 sun
causes, 79–80 excessive exposure to, 58–59, 76
chemotherapeutic drugs, 81–83 lifestyle habit, 8, 47
 index 143

protection from, 55–57, 87 uterus, cancer of, 62

sun protection factor (SPF), 57 UV light. See ultraviolet light
sunscreen lotion, 47, 56, 57–58
Surgery (medical journal), 42, 123 V
The Surgical Works of Percivall Pott, 123
survivors. See childhood cancer vaccine
survivors HPV, 62, 63, 66, 68–69, 72, 75
Sweden, 45 smallpox, 119
variola. See smallpox
venereal infection, 64
T Venezuela, 63
Taipei, Taiwan, 90 Vibrio cholerae, 24, 119–120
tamoxifen and breast cancer, 100 viruses and cancer, 70–72
tanning beds, 47, 50, 55 vitamin B, 124
tax on cigarettes/tobacco, 33, 34, 36–37, vitamin C, 123
41, 44 vitamin D, 58–59, 61
TB. See tuberculosis VP-16, 81
teniposide, 81
testicular cancer, 77 W
thyroid cancer, 83
tobacco, 22, 29. See also smoking Wangensteen, Owen, 42
low tar cigarettes, 27–29 Washington University in Saint Louis, 42,
origin of, 34, 36–38 44
tax on, 33, 34, 36–37, 41, 44 Wattenberg, Lee W., 20, 22
Tokyo, Japan, 90 wavelength of ultraviolet light, 54
transdermal patch, 40–41 weight. See also obesity
trastuzumab, 94 and breast cancer, 96
tuberculosis (TB), 71–72 and exercise, 109–111
Tulane University, 38, 42 Williams, Gary M., 105
typhoid fever, 120 Wilms tumor, 77
typhus, 120–121 Wilson, A. C., 98
Wolin, Kathleen Yaus, 110
Women’s Health Initiative, 96
U World Health Organization
ultraviolet (UV) light, 47, 48, 54 Bulletin, 90
ultraviolet radiation, 47, 50, 53, 54, 61 International Agency for Research,
United States Hygienic Laboratory, 121 29
University of Arizona, 45 smallpox eradication, 119
University of Athens, 73 weight classifications, 109–111
University of California, Berkeley, 99 World War I, 42
University of Minnesota, 20, 27, 42 Wynder, Ernest L., 105
Cancer Center, 27–29
University of Notre Dame, 47–48 X
University of South Dakota, 42
University of Washington, 99 X rays, 83
University of Wisconsin, 42
urinary metabolites, 27 Y
U.S. Department of Health and Human yellow fever, 121
Services, 20
U.S. Food and Drug Administration, 66
U.S. Surgeon General, 25, 32, 38, 44 Z
uterine cervix, 49 Zoological Institute of Munich, 73
 about the author
♦

Robert G. McKinnell was born in Springfield, Missouri in 1926. He served in

the United States Navy during World War II and the Korean War, attaining the rank
of Lieutenant. He and his now deceased and beloved wife of many years, Beverly,
are the parents of three children and the proud grandparents of five. He holds
undergraduate degrees from the University of Notre Dame and Drury University,
and a Ph.D. from the University of Minnesota. He was awarded a National Cancer
Institute Predoctoral Fellowship while at Minnesota. Following Minnesota, he be-
came a Postdoctoral Research Fellow at the Fox Chase Cancer Center, Philadelphia
from 1958 to 1961. He taught and did cancer research for nine years at Newcomb
College of Tulane University. He returned to Minnesota in 1970 where he was a
professor of genetics and cell biology and was designated a Morse/Alumni Distin-
guished Professor. He became a professor emeritus in 1999. He was the 1981–1982
recipient of the Royal Society of London Guest Research Fellowship in the Nuffield
Department of Pathology, Oxford University Medical School, Oxford, England.
He received the Prince Hitachi Prize for Comparative Oncology awarded by the
Japanese Foundation for Cancer Research, Tokyo, Japan, in 1998. He was a North
Atlantic Treaty Organization (NATO) senior scientist, Department of Radiotherapy
and Nuclear Medicine, Akademisch Ziekenhuis, Universiteit Gent, Belgium. He is
a member of the University of Minnesota Cancer Center, the Minnesota Academy
of Medicine and is an emeritus member of the American Association for Cancer
Research and the American Association for Cancer Education. He is a past presi-
dent of the International Society of Differentiation, Inc. He was a visiting scientist
in the Industrial Medicine Department at Dow Chemical in Freeport, Texas. He
has been the recipient of research grants from the American Cancer Society, Inc.,
the National Science Foundation, the National Cancer Institute, and the Damon
Runyon Memorial Fund for Cancer Research, as well as a number of other research
organizations. He has written several books on the subjects of cloning and cancer
including (with others) The Biological Basis of Cancer, 2nd edition, 2006, Cam-
bridge University Press. The Biological Basis of Cancer is also available in both
Chinese and Japanese editions. He is the author or co-author of more than 100
articles published in scientific journals.

144