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It is now altogether fitting and proper that we attend to cancer, which in the hierarchy of mortality is the uncontested occupant of second place. It has been set apart as the very word strikes fear, and for over the past 30 years the so-called war on cancer, initiated by President Richard Nixon, has not been won, and continues unabated. However, new knowledge of the malignant process is beginning to turn the tide of battle. That horizon is coming into view. But let us first consider cancer and its nature.

At the outset, two portentous questions require consideration. Is there a cancer epidemic abroad in the land, as some would have us believe, and, are cancer numbers, cases, and deaths all soaring?

The Chinese scholar who said a good picture is worth 10,000 words, would be pleased with Figures 1.2 and 1.3, which convey literally gobs of information. In seven distinct trendlines, representing major cancer sites, Figure 1.2 conveys the cancer death rates for men over the 72 years 1930-2001. Of the seven major sites, lung cancer makes the most powerful statement. Not only did it rocket upward between 1940 to a peak in 1990, taking many lives with it, but also clearly evident is its decline since 1990. Antismoking campaigns can take well-deserved credit. The stomach cancer trendline tells another wonderful story. If there is a cancer epidemic across the country, stomach cancer surely hasn't contributed, as it has been dropping steadily for 70 years; by 2000 it had the lowest death rates of the seven trendlines. Colorectal cancer, holding steady for 30 years between 1950 and 1980, has also been declining. After a 5-year blip upward, when new screening tests for prostate cancer appeared, it, too, has declined steadily. Hepatic and pancreatic cancers and leukemia have held steady at 5-10 deaths per 100,000 (people) over the past 70 years.

The scenario is much the same for women. From Figure 1.3, we learn that lung cancer is the leading cause of cancer deaths, and still rising. But stomach, uterine, breast, and colorectal cancers have declined sharply, while ovarian and

1930 1940 1950 1960 1970 1980 1990 2001

Note: Due to changes in ICD coding, numerator information has changed over time. Rates for cancers of the liver, lung & bronchus, and colon & rectum are affected by these coding changes.

Source: US Mortality Public Use Data Tapes 1960-2001, US Mortality Volumes 1930-1959,

National Center for Health Statistics, Centers for Disease Control and Prevention, 2004. American Cancer Society, Surveillance Research, 2005

Figure 1.2. Age-adjusted cancer death rates (per 100,000 people, age - adjusted to the 2000 US standard population), males by site, United States, 1930-2001.

Note: Due to changes in ICD coding, numerator information has changed over time. Rates for cancers of the lung & bronchus, colon & rectum, and ovary are affected by these coding changes.

Source: US Mortality Public Use Data Tapes 1960-2001, US Mortality Volumes 1930-1959,

National Center for Health Statistics, Centers for Disease Control and Prevention, 2004. American Cancer Society, Surveillance Research, 2005

Figure 1.3. Age-adjusted cancer death rates (per 100,000 people, age - adjusted to the 2000 US standard population), females by site, United States, 1930-2001. Uterine cancer death rates are for uterine cervix and uterine corpus combined.

pancreatic cancers have resisted change over 70 years. The answer to the first question seems self-evident. If a cancer epidemic is among us, it is limited to lung cancer in women. We will deal with this shortly. But what is an "epidemic" of any illness or condition? Simply stated, it is a sudden outbreak of an illness above the expected number. Yes, every disease has an expected number of new cases or deaths for each week and month of the year. Should that number be exceeded, it is understood to be of epidemic proportions. Obviously with cancer deaths there have been no sudden increases, and other than lung cancer deaths in women there has been no unusual increase in numbers.

Considering the sweep of time from 1930 to 2001, there appears to be yet another story behind the numbers. Prior to World War II, and well into the 1960s, the United States could be described only as an agriculturally based society. The unprecedented shift to an industrial society, and a giant one at that, was yet to occur. That remarkable shift has occurred over the past 45 years. Yet in these undeniably different environments, most cancer rates have either declined or remained steady. The only soaring cancer rate in sight has been that for lung cancer for both men and women—the result primarily of cigarette smoke.

As for numbers, what we've been experiencing is a statistical artifact—an all-boats-rising phenomenon. Lung cancer is not only the leading cause of cancer deaths; its exceptionally high numbers absolutely skews the rates for all cancer sites combined—an excellent reason for not combining them. This skewing distorts the data and misleads interpretation by falsely implying that cancers of all sites are rising. Can numbers mislead? Indeed, they can. In fact, since 1993, death rates have decreased 1.1% per year—1.5% for men and 0.5% for women—and, perhaps most significantly, from 1950 to 2004, with lung cancer excluded from the total, the combined cancer death rate has dropped by 18%! That ' s the message the American public should have received, but didn ' t. That 's the message that requires national dissemination—a message that will help dissipate the widespread pall of fear, while bringing a message of hope.

The media totally missed the boat on this. They preferred to trumpet the overall increased rate, rather than explain the distorting effects of lung cancer on the combined rate. Readers, viewers, and listeners are not being served. The media appears to have lost touch with the public. Issues such as this are not of the complexity of the Patriot Act, Social Security reform, or free trade, requiring journalists to have in-depth knowledge of the subject in order to provide the public with comprehensible accounting. By comparison, the facts of life and death, the numbers, are both simple and direct.

Much of the discussion has focused on rates because rates bring unique insights and provide a firm basis for comparing populations, especially populations of diverse sizes. Figure 1.4 shows the estimated number of new cases of cancer for 2004, for each of the 50 states. Glancing east to west, west to east, north to south, or south to north, we see that California with 134,000 new cases is far and away the highest. At the opposite coast is Vermont, with some 3000

Rates are age-adjusted to the 2000 US standard population.

Estimated number of new cancer cases for 2004, excluding basal and squamous cell skin cancers and in situ carcinomas except urinary bladder. Note: These estimates are offered as a rough guide and should be interpreted with caution. They are calculated according to the distribution of estimated cancer deaths in 2004 by state. State estimates may not add to US total due to rounding.

Figure 1.4. Cancer deaths by state. (Figure courtesy of the American Cancer Society.)

Rates are age-adjusted to the 2000 US standard population.

Estimated number of new cancer cases for 2004, excluding basal and squamous cell skin cancers and in situ carcinomas except urinary bladder. Note: These estimates are offered as a rough guide and should be interpreted with caution. They are calculated according to the distribution of estimated cancer deaths in 2004 by state. State estimates may not add to US total due to rounding.

Figure 1.4. Cancer deaths by state. (Figure courtesy of the American Cancer Society.)

cases. Should you be looking for a place to drop anchor, Vermont seems a better bet than California. But is it? Table 1.8 compares five states with the highest number of cancer cases with five of the lowest. But now the populations of all states need to be introduced, and the rates per 1000 population calculated. Without rates per thousand, California appears cancer-prone. But Florida, New York, Pennsylvania, and Illinois (see Fig. 1.4) are not that far behind, and suggest avoidance compared to North Dakota, Idaho, and Montana. By considering their populations, and calculating rates per thousand, a much different picture emerges. California, with 134,000 new cases, is in fact the state with the lowest new-case rate, and Vermont, with 45 times fewer new cases, does in fact have a far higher case rate than does California. So, do you still prefer Vermont to California for setting down roots? California, with the nation's largest population, would be expected to have far more cases of anything simply because of its larger numbers. In order to appropriately compare California with 50 times the population of Vermont, calculating rates per 1000 provides a reasonable basis for comparison and interpretation.

Yet another concern about cancer is its predilection for the elderly. Indeed, as Figure 1.5 so clearly represents, cancer death rates soar with advancing age. Although cancer can occur at any age, it is primarily a disease of the elderly.

TABLE 1.8. Estimated Cancer Incidence, United States, 2004

Five Highest States

California

134,300

Florida

97,290

New York

88,190

Texas

84,530

Illinois

60,280

Five Lowest States

Alaska

1,890

Wyoming

2,340

Vermont

3,140

South Dakota

4,000

Delaware

4,390

Source: Cancer Facts and Figures, American Cancer Society, 2004.

Source: Cancer Facts and Figures, American Cancer Society, 2004.

http://seer. gov.)"/>
Figure 1.5. Cancer cases by age in the United States. (Source: http://seer. gov.)

cancer.

As indicated in Figure 1.5, the numbers rise after age 40, and began their steep ascent to the 80s, then decline as the number of available folks over 85 disappear, and cancer along with them. One explanation for the fact that cancer occurs more frequently at the older ages may be that for a tumor to develop, cells must accumulate gene alterations, (mutations), which can occur with each cell division and thus accumulate with advancing age. Before raising the question "Why cancer?" a brief discussion of its nature will buttress our perceptions.

Cancer is a group of diseases. More than 100 types are well documented, each with a distinct character and a different trigger. Ergo, lumping them together gains no understanding, nor does it serve any useful purpose other than gathering numbers. The only commonality among these diseases is that the abnormal cells that they produce have no intention of slowing their runaway division.

Tumors are classified as benign or malignant. Benign tumors are not cancer, and do not spread or metastasize to a new site. They are just lumps. A malignant tumor can and often does enter the bloodstream or lymphatic system to be carried to a site far removed from its original site. Most tumors are named for the organ or cell type in which they began their uncontrolled growth, such as stomach, lung, liver, and breast. Others, such as melanoma, are not as clear. Melanoma is a cancer of melanocytes that produce blue -purple pigments. Melanomas often develop on the skin or in the eyes. Leukemias are cancers of blood cells, and lymphomas are tumors of the lymphatic system.

Around the country, the most common cancers are carcinomas, cancers that develop in the epithelial tissue lining the surfaces of the lung, liver, skin, or breast. Another group of cancers are the sarcomas, which arise in bone, cartilage, fat, connective tissue, and muscle. No tissue or organ has a free pass. Any can become cancerous. And then there is the question "Why?" Why does cancer occur?

We humans have 44 autosomal chromosomes in 22 corresponding pairs. One of each pair is contributed by each parent—which differ in their gene content. In addition to these 22 pairs, normal human cells contain a pair of sex chromosomes. Women carry a pair of X chromosomes, men have an X and a Y, for a total of 23 pairs and 46 chromosomes. A chromosome consists of the body's genetic material, the DNA (deoxyribonucleic acid), along with numbers of other proteins. Within each chromosome, DNA is tightly coiled around these proteins, allowing huge DNA molecules to occupy a tiny space within the cells nucleus. Figure 1.6 shows the tightly coiled DNA strands, which carry the instructions for making proteins. Each chromosome is divided into two segments or "arms"—the short or "p" arm (from the French petit, meaning small) and the "q" or long arm. The symbol "q" was chosen simply because it followed "p" in the alphabet and is below the "p" arm The sections are linked at the centromere, the junction where the chromosome attaches during cell division.

Genes are the subunits of DNA. A single chromosome can contain hundreds of protein- encoding genes. Chromosome 16 has 880 genes, including those implicated in breast and prostatic cancers, Crohn 's disease, and adult polycystic disease. Chromosome 19, has over 1400 genes, including those that code for cardiovascular disease, insulin-dependent diabetes, and migraines. Cells containing an abnormal number of chromosomes are called aneuploidic. It is now evident that cancer cells have either gained or lost entire chromosomes. This loss or gain—this instability, this mutation in chromosome number—can result in cancer. Indeed, the destabilization of a cell's genome is known to initiate cancer. But most cancers are not hereditary, which doesn ' t end the search for other causes. So, for example, it is also

Changed From Cancer
Figure 1.6. The tightly coiled strands of DNA that carry the instructions allowing cells to make proteins are packaged in chromosomal units. (Figure adapted from Cancer and the Environment, National Cancer Institute, publication 03-2039.)

known that alterations in oncogenes, can, as shown in Figure 1.7, signal a cell to divide uncontrollably, rather than repair the DNA or eliminate the injured cell.

One of the cell' s main defenses against uncontrolled cell growth is the protein p53. Apparently cancer can occur only when the p53 protein, produced by the p53 gene, is damaged. As p53 may be the key that unlocks the riddle of cancer, we shall consider p53.

According to David Lane [40] ' director of a cancer research group at the University of Dundee, Scotland, and discoverer of p53 in 1979, p53 may just be "The most important molecule in cancer." He believes, as others now do, that faults in this protein or the processes that it oversees may be the cause of all tumors. Lane also gave the chemical its name: "p" for protein and 53 for its molecular weight of 53,000. It is because of p53 ' s presence and vigilance that cancer is so rare [40]. Who would believe that cancer is rare? In his brief and comely book, One Renegade Cell, Robert A. Weinberg, director of MIT's Whitehead Institute, asserts that "One fatal malignancy per hundred million billion cell divisions does not seem so bad at all" [41] . He ' s not saying that anyone's tumor is okay; rather, he's making the momentous point that with

Figure 1.7. DNA—the molecule of life. In double-stranded DNA, the strands are wound about one another in the form of a double helix (spiral) and held together by hydrogen bonds between complementary purine and pyramidine bases. (Figure adapted from Genetic Basics, National Cancer Institute, publication 01-662.)

Figure 1.7. DNA—the molecule of life. In double-stranded DNA, the strands are wound about one another in the form of a double helix (spiral) and held together by hydrogen bonds between complementary purine and pyramidine bases. (Figure adapted from Genetic Basics, National Cancer Institute, publication 01-662.)

the body ' s astronomical number of cells (75-100 trillion) and the ongoing addition of new cells as we live and grow, it is simply remarkable how few cancers actually develop. Given the tremendous number of cells available, one can only gasp and wonder at the incredible fact that we do not get cancer soon after we're born. The stark fact is that youngsters with Li-Fraumeni syndrome, a condition caused by inherited mutations, are prone to develop cancer as young as 2 or 3 years. However, this is an extremely rare condition. It is also known that cancer-associated viruses produce proteins that can shut down p53, leaving cells defenseless.

p53 keeps the process of cell division in check by suppressing cancerous growth. p53 was, and still is, a tumor suppressor gene (TSG). When it was added to cells in culture, those that contained genetic errors made cells cancerous. The normal p53s suppressed cell division. But this protein, which could suppress tumor development, was also the target of cancer-causing viruses and, curiously enough, was found to be mutated in about half of all tumors. It is also odd to find that virologists investigating these unimaginable intracellular events talk of a protein molecule with "godlike properties deciding whether individual cells should live or die." How does this play out? If a cell becomes damaged beyond repair, p53 will force it to self-destruct. Cell suicide or programmed cell death is referred to as apoptosis (from the Greek, a "falling off," as leaves from trees) a normal process in which cells perish in a controlled manner. This ability to cause cells to self-destruct is p53's way of protecting us against runaway cell division.

As noted earlier, DNA damage destabilizes genes, promoting mutations. Collections of proteins are constantly traversing genes checking for faulty bases. As shown in Figure 1.6 , DNA consists of long, spiral helices—twisted chains—made up of nucleotides. The order of these bases along a strand of DNA is the genome sequence. Each nucleotide contains a single base, one phosphate molecule, and the sugar molecule deoxyribose. The nitrogenous bases in DNA are adenine, thymine, cytosine, and guanine. All instructions in the coded book of life, telling cells what to do, are "written" in an alphabet of just four letters—A, T, C, and G. These bases are strung together in literally billions of ways, which means that billions of coded instructions can be sent to cells. Consider, then, if billions of coded instructions are possible, doesn't this help explain how a single faulty instruction is not only possible but also inevitable? Only a single mutation in the enzyme tyrosinase, an enzyme involved in cat coat color, gives the Siamese cat its dark ears, face, paws, and tail.

So genes do their work by stimulating chemical activity within cells. How? Via proteins, the large complex molecules that require folding into intricate three-dimensional shapes before they can work correctly and provide another possible source of error. (This protein folding ability and requirement will loom large in Chapter 2, during the discussion of several diseases).

These proteins twist and buckle, and only when they settle into their final shape do they become active. Because proteins have many diverse roles, they come in many shapes and sizes. Proteins consist of chains of 20 interlinked amino acids. These chains contain 50-5000 of the 20 amino acids, each with its own amino acid sequence. It is in this sequence that yet additional trouble brews, as an error in just a single amino acid can spell disease. An error, or mutation, can result in an incorrect amino acid at one position in the molecule. So, collections of proteins are searching for faulty bases or breaks in the double helix. If found, they signal p53, which springs into action with an electrifying effect—slamming the brakes on cell division, allowing DNA repair to proceed. As David Lane makes clear, "p53 has earned the title, guardian of the genome." Nevertheless, it can and does malfunction. A variety of triggers can do it. Cigarette smoke and ultraviolet light, among other factors, can damage p53 by twisting the protein out of shape so that it cannot function correctly. Current research seeks to discover ways of blocking the processes that break down p53, or restoring its shape and thereby its function.

An approach taken by a Chinese biotech company was to use gene therapy—adding back normal p53 via injection of viruses primed to reinsert the healthy gene. When combined with radiotherapy, the gene treatment actually eliminated tumors in a number of patients with head and neck tumors, an authentic and epoch- making achievement. Indeed, the creativity of current research is itself mind-boggling. For example, another route of manipulating faulty p53, should its shape be the problem, like humpty-dumpty, it can be brought back together again [42]. Once p53's power source is revealed, there is every reason to believe that cancer will become little more than a chronic illness. The new approaches, based on intimate knowledge of cell mechanisms, will no longer be a one-size-fits-all, shotgun approach, but more akin to a single bullet fired at a specific cellular element. Consequently, I find it quite reasonable to believe that in the fullness of time, 5-7 years down the road, it will have been worked out, incredible as it sounds.

As if this were not sufficiently exciting, recent research at Baylor College of Medicine, in Houston, by Dr. Lawrence A. Donehower and his team, has taken p53 to new heights [43].

In 2002, the Princes of Serendip passed through Houston. As a consequence of a failed experiment, instead of making a protein that Donehower's group wanted, the mice were making tiny fragments of p53. They noticed, too, that the mice were unusually small and were aging prematurely, getting old before their time. As if that weren ' t startling enough, these mice appeared to be almost cancer-free—highly unusual for mice. As it turned out, the mouse cells contained an unusually high level of p53, which was vigorously suppressing tumors. Dr. Donehower had some 200 mice that were at once innately protected against cancer, but growing old and decrepit well before their time. A reviewer commenting on the Donehower publication in the journal Nature said that the condition of the mice "raise[s] the shocking possibility that aging may be a side effect of the natural safeguards that protect us from cancer" [44] t The possibility was suggested that the Baylor mice with extra p53 may be aging prematurely because too many cells are becoming apoptotic and their tissues cannot function properly. These mice do force the issue as to whether human longevity can be increased? In addition to this issue, there is wonderment as to why we can't maintain p53's cancer-fighting potency and also forestall the aging process. A double whammy if ever there was one. So there appears to be a gene that can limit cancer and accelerate aging. Is aging the price to be paid for a cancer-free life?

Can the next development be the outrageous possibility of manipulating p53 to control both cancer and aging? Are we not living in the best of times? In the most exciting time. We need only live long enough to see this all bear fruit. Just down the road, previously inconceivable cancer therapies are being developed. Truly, the tide is running with us. Stay tuned.

TABLE 1.9. Probability (Chance) of Developing Breast Cancer by Specific Ages among US Women

By Age

1in

15

763,328

20

76,899

30

2,128

45

101

50

53

60

22

70

13

80

9.1

90

7.8

Source: Ries, L. A. G., Eisner, M. P., Kosary, C. L., eds, SEER Cancer Statistics Review, 1975-2002, National Cancer Institute, Bethesda, MD, 2005.

Source: Ries, L. A. G., Eisner, M. P., Kosary, C. L., eds, SEER Cancer Statistics Review, 1975-2002, National Cancer Institute, Bethesda, MD, 2005.

Breast cancer in women (men are not immune) is the most frequently diagnosed nonskin cancer. Some 216,000 new cases were estimated to have occurred in 2004. The risks of being diagnosed with breast cancer increases with age, and the risk increases steadily by decade as shown in Table 1.9. Unfortunately the media also got that one wrong. Recent headlines across the country trumpeted the news: "Cancer now the top killer of Americans" and "Cancer passes heart disease as top killer." The implication is that the war on cancer was lost. What the media so glaringly failed to acknowledge, or failed to understand, was that in their most recent annual report (2005), but whose data were limited to those of 2002, the authors extracted deaths by age, which they had never done before [45]. In doing so, they found that although death rates from all cancer sites combined have been falling steadily since 1993 (by 1.1% per year), the rate of death from heart disease, as shown in Figure 1.8, has been declining since the mid-1970s. Nevertheless, in 1999, for those people under age 85, who constitute 85% of the country's population, cancer deaths surpassed heart disease only because heart disease continued its unflagging descent [45]. As for breast cancer (and here the confusion mounts), another severely abused number is the often cited statistic that over a women's lifetime, the risk (the chance, the odds) of her getting breast cancer, on average, is one in eight, or about 13%. Far too many believe that this number is a woman's current risk. No. The risk involved is in fact a woman's lifetime risk, at age 85, and it works this way. If eight women are followed for their entire lives, one of them, on average, is likely to develop breast cancer. Also recall that with a 1 in 8 chance of developing breast cancer, there remain 7 in 8 chances that it will not occur. Again, as we've seen, cancer is a disease of advancing age, and breast cancer is strongly age-related, as Table 1.7 shows. At age 35, as noted in the table, it is 1 in 99, and at age 45 it is 1 in 101, or a 1% chance of developing breast cancer. Perhaps

Year of Death (a)

Year of Death (b)

Figure 1.8. Cancer and heart disease death rates (age-adjusted to 2000 US standard population) for individuals younger than (a) and older than (b) age 85. (Figure adapted from American Cancer Society, CA: A Cancer Journal for Clinicians.)

Year of Death (a)

Year of Death (b)

Figure 1.8. Cancer and heart disease death rates (age-adjusted to 2000 US standard population) for individuals younger than (a) and older than (b) age 85. (Figure adapted from American Cancer Society, CA: A Cancer Journal for Clinicians.)

more importantly, it is essential to recall that not all women live on to the older ages when breast cancer risk becomes greatest [46].

Much has been made of the fact there are inherited breast cancer susceptibility genes—BRCA1 and BRCA2. But these are responsible for no more than 1 in 10 cases of the disease. Yes, 9 out of 10 cases are not inherited. Of additional importance is yet another number: 0.2% the number of women in the United States whose BRCA genes have mutated. These numbers offer a good deal more than cold comfort.

Furthermore, breast cancer activists have consistently flailed their physical environment as the carcinogenic trigger(s) for breast cancer. One of the most politically active areas has been Long Island, New York, where, as in other areas of the country, breast cancer is commonly reported. In 1993, concerned residents got their Congressional representative to push for legislation requiring epidemiologists to investigate a possible environmental carcinogen/ breast cancer link. After a decade of study, the Long Island Breast Cancer Study Project (LIBCSP) began publishing its findings. Among the possible carcinogens under their purview were the polycyclic aromatic hydrocarbons (PAHs). Although the PAHs are potent mammary carcinogens in rodents, their effect on development of human female breast cancer has been equivo cal. The LIBCSP wanted to determine whether currently measurable PAH damage to DNA increases breast cancer risk. PAHs are byproducts of the combustion of fossil fuels, cigarette smoke, and grilling of foods and are found in smoked foods. As PAHs can be stored in fatty breast tissue, they were deemed a realistic candidate. The study did not find a relationship between PAH blood levels and exposure to smoked or grilled foods or cigarette smoke, and "no trend in risk was observed" [47] . In addition to PAH, the project studied the relationship between breast cancer and organochlorine pesticide blood levels [48] . Again, no dose-response relationship was uncovered. Nor could they find any support for the hypothesis that organochlorines increase breast cancer risk among the Long Island women.

In another venue, researchers at Maastricht University, in the Netherlands examined the relationship between stressful life events and breast cancer risk [49] . They reported no support for stressful life events and risk of breast cancer.

Although we are most assuredly in an age of breast cancer awareness and breast cancer studies, thus far environmentally related breast cancer carcinogens remain to be discovered. The question at issue is whether heightened awareness and fear are desirable motivators for increasing screening behavior. Clearly the issue is debatable. But overemphasis on breast cancer may well be responsible for inattention to other illnesses. In fact, both heart disease and lung cancer carry greater risks and are greater killers of women than is breast cancer. Shocking though it may be, women worried about breast cancer continue to smoke. According to Dr. Barbara Rimer, Director of the Division of Cancer Control and Population Science at the National Cancer Institute, " We see smokers who are very, very worried about breast cancer, and yet they're continuing to smoke. They have a much better chance of getting and dying of lung cancer than breast cancer, but many women underestimate their chances of getting lung cancer" [50].

Lung cancer is the world' s number 1 cancer killer. In the United States, close to 100,000 men and women died of it in 2005. Cigarette smoke is the primary risk. However, another glance at Figures 1.2 and 1.3 shows that men have heeded the antismoking message and their declines in lung cancer deaths are striking whereas women have yet to respond to the messages. Despite the many warnings about the malign affects of smoke, fully 25% continue to do so. Women, especially young women, are the preferred target of cigarette advertisements. And they respond. As many as 20% smoke during their pregnancies. Are they really unaware of the deleterious effects of smoke on the developing fetus? Activists ought to zero in on this curious behavior.

Women and smoking, another cautionary tale that went by the boards, is being given short schrift by the media. However, several of Dr. David Satcher's numbers are devastating. To wit:

• An estimated 27,000+ more women died of lung cancer than breast cancer in 2000.

Figure 1.9. Age-adjusted death rates for lung cancer and breast cancer among women, United States, 1930-1997.

• Three million women have died prematurely because of smoking since 1980, and on average, these women died 14 years prematurely.

• For a never-to-be forgotten comparison the US Surgeon General has given us Figure 1.9, for which discussion may even be unnecessary [8].

It has been proposed that there is a higher rate of a specific mutation in the p53 gene in women's lung tumors compared to men. Perhaps. It has also been postulated that women may have a reduced capacity for DNA repair. There is, of course, much yet to be learned. Nevertheless, being female appears to be a factor for extended survival in lung cancer patients. What is not moot is that consequential differences do exist between men and women with lung cancer. Women who have never smoked are more likely to develop lung cancer than are men who have never smoked [51]. The "why" of this and other differences has researchers around the world scurrying for answers. That a number will be found in genes specific to men and in genes specific to women is emerging as a sure bet.

Even though colorectal cancer deaths have been declining over the past 50 years, over 150,000 deaths were expected to occur in 2004. Here again, the primary risk factor is age. Other proposed risks include smoking, alcohol consumption, obesity, and diets high in fat and/or red meats. On the other hand, frequent coffee consumption has been associated with reduced risk of color-

ectal cancer. Bear that word association in mind. We shall consider this possibility in some depth further along, as it can be easily misinterpreted.

Recently, researchers at Harvard University's School of Public Health probed the relationship between coffee, tea, and caffeine consumption and the incidence (new cases) of colorectal cancer ' 52] t Using data from the well' established Nurses' Health Study and the Health Professionals' follow-up study (physicians), which together provided 2 million person-years of follow-up and 1438 cases of colorectal cancer. They found that "regular consumption of caffeinated coffee or tea or total caffeine intake was not associated with a reduced incidence of colon and rectal tumors." But they did find that decaffeinated coffee did appear to reduce the incidence of these cancers, but also injected the caveat that this association requires confirmation by other studies. It's a start. Advertising by the tea and coffee producers, especially tea (particularly green tea), would have us believe that these are health-promoting beverages. Would that this were true. We shall see.

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How To Prevent Skin Cancer

How To Prevent Skin Cancer

Complete Guide to Preventing Skin Cancer. We all know enough to fear the name, just as we do the words tumor and malignant. But apart from that, most of us know very little at all about cancer, especially skin cancer in itself. If I were to ask you to tell me about skin cancer right now, what would you say? Apart from the fact that its a cancer on the skin, that is.

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