Can Cancer be Stopped?

By Mark Lappé

Over a decade ago, I warned in my book Chemical Deception (Sierra Club Books, 1991) that a number of cancers appeared to be increasing unrelentingly: these included melanoma, brain cancer, non-Hodgkin's lymphoma, kidney, liver, lung, breast and testicular cancer. While no one wants to be proved right about such disturbing news, the latest statistics on cancer incidence appear to bear this prediction out: seven of the eight cancers that were increasing the fastest in the period 1973-1987 again increased the most in the period from 1983-1999, based on National Cancer Institute/National Tumor Registry data. Melanoma, with a 155% increase tops the list, followed by prostate and liver cancer (105 and 103%, respectively), non-Hodgkin's lymphoma (87%), testicular cancer (67%), brain cancer (50.2%) and breast cancer (41%). Perhaps most disturbingly, in spite of overall leveling of increases overall (largely because of declines in lung cancer), childhood cancer was up a disturbing 26% between 1975 and 1999.

So what is going on? Are these increases simply due to an aging population? No, they are "age-adjusted," meaning they are corrected for the age of the people who get cancer. Some of the increase for breast cancer is attributable to a 10% increment in new breast cancers among women who are less than 50 years old. And the childhood tumors that are included in the registry data are also increasing. While numerous factors almost certainly come into play in setting when and how cancer arises, certain exposures to known or suspected carcinogens are almost certainly implicated in these tumor types. For instance, some 21 agents are listed by the National Toxicology Program as being able to produce breast cancer in animals: another 29 are suspected of being mammary carcinogens. Many of these same agents are encountered in the workplace by over a million women. While some carcinogens have been eliminated, such as the toluene diamine based hair dyes, others are now recognized as being harmful and likely human carcinogens, such as diethylstilbestrol (DES). A disturbing number of chemicals capable of producing cancer remain in commerce. These include methylene chloride, benzene, ethylene oxide and phenylenediamine dyes.

Overall, the common denominator in the major cancers increasing in incidence today is that they all have strong environmental links to chemicals or other agents. Non-Hodgkin's lymphoma for instance is linked to chemical solvents that are unusually prevalent in drinking water near Superfund and other hazardous waste sites. Similarly, brain and testicular cancer are associated with work in the chemical industry and to exposure to certain pesticides and related chemicals.

Of course, diet also plays a role as suggested by data that show women of Asian ancestry have only a fraction of the cancer that affects some 1 of 8 Americans. (The age-adjusted incidence overall for breast cancer is 139 per 100,000 women, taking into consideration the young average age of the populaton). When Japanese women move to Hawaii and adopt American diets their incidence rate rises to a point between Asian and American levels.

But the real picture behind these increasingly disturbing and common cancer patterns likely reflects certain basic truths about carcinogenesis. Repeated episodes of cell growth can put tissues at risk for becoming cancerous. Diets high in fat and calories predispose animals to cancer, as do naturally occurring hormones like insulin-like growth factor that may be present in excess in milk from hormone stimulated cows. Pregnancy in some animals increases breast cancer risk dramatically. But paradoxically, if human pregnancy is followed by nursing, the breast cancer risk plummets. Why?

Some researchers believe that at-risk cells may be shed in the milk. Others, that the cycling of hormones is somehow protective. But the real difference may be in the type of agent associated with breast cancer in animals. A form of virus distantly related to the HIV/AIDS virus called the mammary tumor virus causes breast cancer in animals. And it does so in an insidious way. It is transmitted from mother to offspring in the milk. Once in the body, the mammary virus targets the immune system and depresses possible reactions against it, just as the AIDS virus does. It then travels to the breast ducts and their lining where it sets up shop and creates the conditions the predispose the animal to cancer. A few drops of milk passed to a nursing pup sets in train the cancer process anew. If extra chemicals which themselves can cause cancer are added to such breast tissue, cancer occurs with alarming frequency. This model provides a tantalizing clue to some forms of cancer in people.

My own view is that the key to understanding breast cancer and other rapidly increasing tumor types is linked to understanding the dynamics of the tissue itself. Chemicals that induce cell proliferation can "set up" the breast for chemical or viral damage and lead to mutations that result in cells with deranged metabolism and lost growth control leading to cancer. It has long been noticed that cancer is more likely in rapidly cell-dividing tissues than in quiescent or resting ones. Breast cancer risks may increase as cells in the breast epithelium, especially the lining of the milk ducts, proliferate. This cellular growth occurs late in adolescence and during the early stages of pregnancy, and can be exacerbated by prior treatment with dioxins and the presence of estrogens. If the hormone stimulation proceeds unabated, cells are progressively at higher and higher risk of carcinogenic transformation, especially if chemicals in the environment that concentrate in the fatty tissues of the breast impact on the dividing cells.

This latter likelihood is underscored by findings that proliferating tissues are at greatly increased risk of DNA or genetic damage from ionizing radiation or chemical mutagens. But there is an evolutionary model at work here as well. If cancer occurs early and life and kills its host (as it is now doing in an inordinate number of children in developed countries), any genetic predisposition to getting cancer will "die off" with the cancer patient. But, if people live long enough to pass along their genes - or the viruses that cause cancer - to their offspring or their spouses (as may occur in the human papilloma virus that causes some types of cervical cancer), the genes that "cause" or at least predispose to cancer will proliferate in the population. This phenomenon is particularly likely if people are simultaneously ingesting or being exposed to chemicals in their diet or environment that increase their vulnerability to cancer by depressing their immune system - or by setting up their tissues for further damage, as is likely the case for estrogens that can induce or accelerate breast cancer.

The creation of environmentally "at-risk" tissues is likely to extend back to the womb. Researchers have shown that early exposure to potent toxicants like dioxin at extremely low levels can increase the number of proliferating end-buds in the milk ducts of breast tissues. While the dioxin itself does not necessarily "cause" a resulting tumor, it can increase the likelihood that one or more cells in the breast tissue will react with a chemical agent that will cause genetic damage precisely because there are so many more cells available for being harmed by that chemical after adolescent breast development has proceeded.

A case in point is the increase in breast cancer now being seen among younger women. While an age-related increase in breast cancer risk is well known, no one expected or predicted that younger women would be getting breast cancer at an increasing rate. Whether or not this is due to exposure in early adulthood to suspect environmental agents such as the dry cleaning fluid known as perchloroethylene, or if it is the result of estrogens or estrogen-like substances in the diet or drugs women take, or some entirely unknown factor is still a mystery. Many such substances, like dioxin, have as their secret power, the ability to induce unexpectedly high levels of cellular turnover and division. During cell division, as we have seen, such cells may be more vulnerable to attack by chemicals with gene-damaging ability.

While the true cause (if there is any single one) of the increase in cancer rates among our population remains unknown, the common denominator of damage, cell growth and replacement provides a general backdrop against which to gauge the vulnerability of our tissues and organs. Almost any potential cancer site is usually one that is vulnerable to stimulation and excessive cellular growth and proliferation. For instance, the damage done by the ultraviolet rays in sunlight to skin will increase cell proliferation and likely genetic damage.

An additional factor to "successful" skin cancer induction is depression of the immune system - which ultraviolet also does. If we consider skin cancer as a model, the following sequence can be observed: damage, cell growth and replacement, excessive proliferation if the stimulus remains, and ultimately certain genetic mutations that predispose to freeing up a cell to become malignant. This model may be found to be applicable to other organs in the body and may help explain why so much cancer occurs in populations of well nourished and chemically-dependent populations such as those in the United States and the developed world generally. It is probably no accident that the rise in cancer incidence follows a trajectory that mimics the curve of increasing chemical production generally and pesticide production specifically, in the last four decades. If these and all of the remaining factors that impinge on the vulnerability of children and immunologically damaged people generally are not considered, it is unlikely that a solution to the cancer problem will soon be found.