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This report coincided with my anecdotal observations in the Philippines suggesting that children of families consuming the most protein upper socioeconomic class also were consuming peanuts that were heavily contaminated with the highly mutagenic hepatocarcinogen, aflatoxin commercial peanut butter 97 , suggesting an unusually high susceptibility to primary liver cancer. In retrospect, as I was later to learn, early mutation by the carcinogen aflatoxin did not, singularly, lead to cancer; it had to be promoted by a nutritional stimulus.

In short, cancer development was unusually responsive to nutritional exposure, forwards and backwards, at early and late stages of cancer development, presumably by non-mutagenic mutation events. The mechanism for this protein effect was presumably explained by not one but multiple mechanisms occurring both before and after establishment of the initial mutation.

As an aside, there seemed to be many foci of initiating mutations observed soon after carcinogen administration because, histologically, isolated clusters of pre-neoplastic clones appeared, each theoretically arising from a mutagenic event. Beyond the initiation period, low dietary protein also shifted energy calories away from its otherwise being used to support cancer growth. This is an excellent demonstration of biological pleiotropy wherein intervention with one nutrient, i.

These experimental animal studies were conducted 20—40 years before the human genome project was undertaken and at a time when methods were not yet available to investigate these events in greater genetic and molecular detail. Modern day methodologies should be expected to elucidate additional mechanisms, all supporting the same response, that is, control of cancer growth by nutrition. During the third, progression stage of cancer development, cancer cells become more aggressive, advance from their primary site of origin and wander around the body in search of a new home.

It is this activity, metastasis, which is responsible for almost all cancer deaths. Celia-Terrassa and Kang, when reviewing the cellular properties of metastasis, pointed out that only a very small fraction of cancer cells circulating in the lymphovascular system are able to successfully adapt to relatively foreign tissue environments. These cells do so by using a network of interrelated mechanisms to create a functional property called cellular plasticity, i. These mechanisms may include clonal cooperation, epithelial to mesenchymal cell transitions EMT or its reversal, MET , metabolic adaptation, cell proliferation, resistance to apoptosis controlled cell death , evasion of immune system attack and resistance to drug therapy, among other mechanisms.

A particularly fascinating question concerns how the circulating cancer cell uses its repertoire of aggressive mechanisms to successively counter the multitude of defensive mechanisms that allows residence to take place in foreign tissue. Metastasis is an exceptionally complex system, with countless moving parts. These authors raise the same question that I do as to how will it be possible to target the use of drugs against specific elements of a rapidly changing and complex environment—at least this is my interpretation of their hypothesis.

Nonetheless, these authors seem to remain optimistic. The mechanisms of metastasis represent an extraordinarily complex array of genes, gene mutations and gene expression mechanisms. Methodologies of ever increasing sensitivity and precision are being developed and used to identify mutations and combinations of mutations most critical for developing metastasis—as well as for cancer formation events that precede metastasis. Very large databases of somatic mutations, including, for example, a catalog of 21, genomes or exoms from cancer patients, are now available for more discriminating study of an almost infinitely complex system.

Although there are many challenging issues to be resolved when investigating such an enormously complex system, many believe that progress is being made and, by some accounts, it is substantial. For example, studies have identified subgroups of mutations having distinct functions, times when mutations occur during the cancer development process, causes of mutations by extrinsic or intrinsic factors, mutation derived protein products that may or may not lead to altered amino acid sequences, and mutation outcomes arising from inside or outside of the coding region of the genome, substantially summarized by Piraino and Furney The number of driver mutations, hence the number of driver genes per cell, seems to be growing as the discovery of each new mutation means discovery of yet another function that favors metastatic aggression.

This does not necessarily mean the accumulation of new driver mutations among cells on the pathway to metastasis. Then, there are the passenger genes with no known function as of yet that may be arising by the play of chance during normal cell proliferation. The goals of investigating mutations—their tissue origin, their causes and their effects—are certainly noteworthy and progressive. Such information, according to many researchers, may be crucial to the development of treatment protocols that enable potential drugs to be targeted to the offending events and cell components.

Perhaps a few quantitative estimates can illustrate the complexity and size of this task [the following citations refer both to the original finding and to the review that cited these observations]. Somatic mutations are highly variable between and within cancer classes, ranging from one to , mutations per trillion base pairs. Is it possible that these powerful genome sequencing and computational methodologies are revealing ever more complex patterns of somatic mutations, some of which may help identify tumor origin, tumor progression, and custom-made, targeted treatment options?

Or are these alleged opportunities offset by somatic mutation combinations that work for one type of cancer but not another, making almost insurmountable the development of broad-scope treatment protocols, especially if cancer is considered to be more than distinct diseases, as believed by some?

Ignoring nutrition as a means of cancer control, first proposed around , , has left a trail of undesirable consequences since that time. Contemporary understanding of nutrition has traditionally relied on investigations of individual nutrient activities, as when they are investigated in isolation in laboratory experiments, in clinical trials in humans and when adjusted for confounding in human observation studies. These are classic examples of reductionism.

When reductionist information on individual nutrients is aligned with reductionist cancer research on individual gene mutations, both being infinitely complex processes, I believe that a fundamental understanding of the association of nutrition with cancer will never be possible, even when assuming the increasing power of sophisticated methodologies and computational procedures to sort out complex systems.

It is vitally important to acknowledge that these complex systems are not static; they are infinitely dynamic. It is widely believed that, in addition to our understanding that mutations initiate cancer, there are the uncertain functions of mutations which accumulate in parallel with the rising rates of cancer with age. Although this project has provided a treasure trove of data for investigating the endless combinations of mutations related to cancer causation and progression, it has been running a very serious risk of overlooking other factors and events that may be even more important than genes and their mutated derivatives.

These authors claimed that two-thirds of these mutations and their cancer outcomes are random, a play of chance, with no known cause. This provocative finding generated a number of rebuttals — that mostly challenged the idea that cancer is a play of chance that infers a hopeless inability to prevent this disease. These rebuttals also are limited because they, too, assume that mutations are the core events that initiate and sustain cancer development.

The mutation theory of cancer is so firmly established that virtually any new discoveries in cancer research almost reflexively adds new support for this belief. To restate, the U. Accepting the prominence of the mutation theory of cancer very likely will continue into the future because of its widespread, mostly unchallenged support. But in spite of this enthusiasm for the future of genetic mutation research as the principle means to understand and control cancer, there are disquieting opinions—voiced from within the genetic mutation research community.

I believe that the hypothesis of this paper focused on a nutrition theory of cancer is this new paradigm. To be fair to the mutation theory inferences, many authorities believe that establishing mutation locations and functionality in the genome may lead to 1 the clinical application of better, more targeted pharmaceuticals for disease treatment, 80 , , , , 2 more refined screening of otherwise healthy individuals for future disease , — and 3 discovery and control of mutagens in our environment. When more than one molecular target participates in the final disease outcome and needs to be treated, unique drugs can be combined, as in the proposal for the polypill.

Also, the decades old emphasis on environmental mutagens as the main causes of cancer also labors under this reductionist philosophy. The role of nutrition as a non-mutagenic agent in cancer etiology is, however, mostly ignored if mentioned at all. I believe that the assumption that human cancer is mainly caused by mutations is substantially over-emphasized.

I agree that cancer begins with a mutation and, further, that there is convincing evidence that mutations accumulate as cancer advances toward metastasis but this does not mean that cancer is primarily or even solely caused by a series of subsequent mutations. Contemporary research practices, policy development, clinical practice and public knowledge await an answer to this question.

It has long been accepted that a mutation is an extremely rare event, perhaps one mutation occurring every 10 7 cell divisions. This suggests that, except for extremely rare occasions, cancer development cannot be reversed. As a consequence, the only way to treat this disease is to kill cancer cells according to Robert Gatenby, as quoted cited by Kaiser, especially when these cells, now endowed with thousands of mutations, may have metastasized.

This is traditionally accomplished by cytotoxic chemotherapy or radiotherapy, targeted, if possible, to the cancer cells so as to avoid damage to neighboring tissue. More recently, efforts have focused on energizing our immune system to use its innate ability to kill cancer cells, a strategy that may prove to be especially useful for older people whose immune system is in decline.

Given this abundant acceptance of the mutation theory of cancer development, I therefore pose a highly provocative question: Research designed to test this nutrition-reversal-of-cancer hypothesis undertaken in my laboratory in the early s showed an opposite answer. It was prompted, in part, by the observations on the effect of smoking on lung cancer risk cited above. It was well established at that time that smoking increases lung cancer risk, presumably due to mutagenic chemicals, and further, that lung cancer risk decreases to baseline within 5—10 years upon cessation of several years of smoking.

This was the evidence, however valid it was, that led to the laboratory rodent studies on dietary protein and liver cancer mentioned earlier. The results were striking. Decreasing animal-based protein consumption completely prevented the development of a type of cancer hepatocellular carcinoma initiated by the most potent mutagen known at that time aflatoxin. Also, tumor development could be turned on and off, quite rapidly, simply by increasing then decreasing the consumption of animal-based protein.

Although not studied in the same depth, the same on-off switch existed when adjusting dietary fat during the development of experimental pancreatic cancer initiated by azaserine and for mammary cancer initiated by dimethylbenzanthracene DMBA. This non-mutagenic nutritional effect of animal protein became even more convincing when searching for its explanatory mechanism s. Not one but several innate, normal mechanisms seem to work simultaneously to control cancer development, some of which enhances and some of which prevents cancer development.

In each case, increased consumption of animal protein altered these mechanisms to favor cancer development, elevating mechanisms that promote cancer development and corrupting innate mechanisms that prevent cancer development. Now, thirty years later, with much more sophisticated methodology many more mechanisms can be envisioned. On the likelihood that these animal protein-specific effects on cancer development apply to humans, it is necessary to add the cancer enhancing effects of simultaneously consuming less whole plant-based foods.

Total calorie consumption is mostly a zero-sum game, thus consuming more calorie-containing animal-based protein as food means less consumption of whole plant-based foods, which are lower in protein and fat and richer in antioxidants, complex carbohydrates and vitamins. Like the cancer enhancing mechanisms of animal-based protein, similar arrays of cancer repressing mechanisms exist for countless nutrients of plant-based foods.

In order to appreciate the full significance of these networks of mechanisms, whether caused by nutrients of animal or plant-based foods, it should be noted that nutrient function, in its totality, is not a simple summation of individual nutrient activities studied in isolation, but the highly dynamic contribution of countless nutrients of whole foods, as described elsewhere.

There are many plant substances that exhibit this pleiotropic effect. As summarized elsewhere, 54 , genistein, which is an anti-cancer estrogen-like isoflavone of soy products, , engages a large number of mechanisms to produce its effect. Genistein also appears to lower cardiovascular disease risk and prevents osteoporosis, very likely joining other isoflavones and related components in soy and other legume products that very likely play similar roles with genistein.

This is but one of many plant-based substances that employs pleiotropy to lower breast cancer risk while engaging related soy phytochemicals to minimize risks for cardiovascular disease and osteoporosis, as in epitropy. Another example of a potential cancer preventive agent for prostate cancer is lycopene, a red carotenoid pigment in tomatoes, which has strong antioxidant activity and which is hypothesized to prevent prostate cancer and its predecessor, benign prostatic hyperplasia, although this evidence is not convincing when lycopene is consumed as a supplement.

Many plant nutrients and related phytochemicals are well known antioxidants that counterbalance the oxidative stress largely created by reactive oxygen species ROS. As brilliantly summarized by Reuter et al, reactive oxygen species are endogenously produced in the body, mostly during mitochondrial respiration, and they play a vital physiological role, as in their attack and destruction of invasive disease producing organisms. Prolonged tissue excess of these highly reactive molecules leads to chronic inflammation that encourages aging and associated chronic diseases like cancer, cardiovascular disease and diabetes, among others.

The breadth of effect of this infinitely complex system cannot be overemphasized and food choice plays a vital role in keeping this oxidant-antioxidant system in balance. Within the context discussed here, the ROS system illustrates both the pleiotropy and epitropy concepts of nutrient function. In this case, there are pro- and antioxidant members of these contrasting families that illustrate the relative nutritional properties of whole plant-based foods from animal based foods and highly processed food fragments.

Both groups involve an exceptionally large number of substances, reactions and activities and it is this complexity and this contrast which must be acknowledged in any cause-and-effect hypothesis. The relative proportions of disease risk specifically attributable to the direct effects of animal-based protein as food compared to the effects of declining consumption of whole plant-based foods, however, is difficult to assess. Almost no human studies—except for a very few studies on heart disease — and prostate cancer 86 —have included individuals using a whole food plant-based WFPB diet with little or no added fat and refined carbohydrates.

Findings of occasional studies on self-proclaimed vegetarians and vegans as experimental subjects certainly are indicative of these effects but they are not especially relevant for fully assessing the effects of a WFPB diet. Most vegetarians consume generous amounts of dairy and some eggs and fish. Vegans, although consuming no animal-based protein, still consume substantial amounts of fat and refined carbohydrates.

These findings on the apparent effects of animal-based protein on cancer development, as observed in correlation studies on humans, become much more significant when nutritional function is viewed as the comprehensive, epitropic effects of virtually countless nutrients, nutrient-like substances and their interactions during their consumption, digestion, absorption and metabolic disposition.

Additional evidence for a comprehensive nutrition-based effect on reversal of chronic, degenerative disease not obviously mutagenic is the evidence showing the ability of a whole food plant based diet in intervention studies to dramatically reverse heart disease. Similar results were earlier reported by Ornish et al at one and five years , after onset of treatment.

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That study, which also included stress management and exercise , was one of the first to publish peer-reviewed findings on the effect of the whole food plant-based on cardiovascular disease. The etiology of heart disease is not like that for cancer because it has not yet been shown to be the result of mutations but, like cancer, it is a degenerative multifactorial disease forming over many years, also involving a similarly comprehensive effect of nutrition.

I am also aware of the fascinating discoveries tethered to genetic function and the many ways that it might complement newer treatment modalities. I submit that what has been done and what is still being planned for future cancer treatment protocols is over-simplistic, relatively ineffective, extremely costly and likely to be encumbered with unintended and counterproductive side effects. Such a strategy is over-simplistic because it ignores the infinitely complex biology that underlies, respectively, cancer development and nutritional function.

Cancer cannot primarily be the consequence of a series of mutations. Back-mutation of mutated cells to normalcy is too improbable. Yet, experimental animal evidence shows that cancer development can be reversed by nutritional means. Nutrition, in turn, cannot be ascribed to the effects of individual nutrients operating independently and in isolation because single nutrient supplements do not faithfully mimic their biological activities in food.

That is, these combined observations, each representing infinitely complex but still highly integrated phenomena, support the hypothesis that cancer is primarily a nutrition-responsive disease. These phenomena, considered independently or together, represent what might be called Nature.

There is only one way to affirm or deny this hypothesis and this is to conduct an intervention trial in human cancer patients. Evidence is already available showing that a whole food plant-based diet reverses heart disease remarkably effectively while similar but less robust evidence supports the same effect on other chronic illnesses.

Given the evidence showing that cancer could be considered primarily a nutrition-based disease, instead of a genetic disease, it is therefore reasonable to assume that the same nutritional effect on cancer may also exist. It should be noted, however, that an association of diet and nutrition with cancer or other disease outcomes is far more than a single nutrient functioning through a single mechanism that produces a single outcome. It is time that we recognize the complexity of these systems, then use this information to chart a more efficacious pathway to future cancer care practices which, not so incidentally, are similar to those for other illnesses as well.

I also acknowledge four clinicians whose work with patients came to my attention at a critical time 37 years ago that encouraged my interpretation of the results that we had obtained in the laboratory. Alphabetically, they are Caldwell Esselstyn, Jr. National Center for Biotechnology Information , U.

Author manuscript; available in PMC Oct The publisher's final edited version of this article is available at J Nat Sci. See other articles in PMC that cite the published article. Abstract Cancer is traditionally considered a genetic disease. Introduction A new perspective is needed on the failed War on Cancer begun 46 years ago by President Nixon because there is little or no convincing evidence that this project has specifically decreased the all-important rates of cancer.

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Diet, Nutrition and Cancer Initiation Convention among experimental researchers holds that there are three somewhat arbitrary stages of cancer development, initiation, promotion and progression although these stages blend from one stage into the next. Diet, Nutrition and Cancer Promotion This second stage of cancer, promotion, traditionally begins with an already mutated cell which clones itself into a multicellular tissue mass that eventually becomes billions, even trillions of cancer cells.

Diet, Nutrition and Cancer Progression During the third, progression stage of cancer development, cancer cells become more aggressive, advance from their primary site of origin and wander around the body in search of a new home. Comprehensive Effects Ignoring nutrition as a means of cancer control, first proposed around , , has left a trail of undesirable consequences since that time. Footnotes Conflict of Interest: The contribution of cytotoxic chemotherapy to 5-year survival in adult malignancies. Clin Oncol R Coll Radiol ; Doll R, Peto R. The causes of cancer: J Natl Cancer Inst.

Committee on Diet Nutrition and Cancer. Diet, Nutrition and Cancer. Food, nutrition and the prevention of cancer, a global perspective. Present trends in cancer epidemiology. Proc Can Cancer Conf. Drasar BS, Irving D. Environmental factors and cancer of the colon and breast. The epidemiogy of large bowel cancer. Progress in Biochemical Pharmacology: S Karger; New York: Armstrong D, Doll R. Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices.

Diet and breast cancer. Hosp Pract Off Ed ; The role of a high-fat diet in enhancing the development of mammary tumors in ovariectomized rats. Bingham SA, et al. Metabolic epidemiology of colorectal cancer. Dietary fibre and regional large-bowel cancer mortality in Britain. Epidemiology of cancer of the colon and the rectum. The great cranberry scare.

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Chemical carcinogens and human risk assessment. Methods in cancer research. Academic Press; New York: Estimation of risks of irreversible, delayed toxicity. J Toxicol Environ Health. Prog Exp Tumor Res. History of chronic toxicity and animal carcinogenicity studies for pharmaceuticals.

Difficulties in extrapolating the results of toxicity studies in laboratory animals to man. The correlation of experimental carcinogenesis and cancer in man. The limits of two-year bioassay exposure regimens for identifying chemical carcinogens. Human carcinogenic risk evaluation: A decision tree approach to the regulation of food chemicals associated with irreversible toxicities.

CA Cancer J Clin. Dietary carcinogens and anticarcinogens. Effect of a low-fat diet on hormone levels in women with cystic breast disease. Serum steroids and gonadotropins. Diet, serum breast fluid growth hormone and prolactin levels in normal premenopausal Finnish and American women. Dietary fiber and breast cancer. High-fiber diet reduces serum estrogen concentrations in premenopausal women. Am J Clin Nutr. J Nat Cancer Inst. Calories and chemically induced tumors in rodents. Caloric restriction and cancer.

J Nutr Sci Vitaminol. Prevention of chemical carcinogenesis by vitamin A and its synthetic analogs retinoids Fed Proc. Can dietary beta-carotene materially reduce human cancer rates? Dietary protein enhancement of N-nitroso-methylurea-induced mammary carcinogenesis, and their effect on hormone regulation in rats.

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Effect of protein diet on release of prolactin and ovarian steroids in female rats. Effect of dietary protein on morphoplogic development of rat mammary gland. Madhavan TV, Gopalan C. The effect of dietary protein on carcinogenesis of aflatoxin. Effect of high and low dietary protein on the dosing and postdosing periods of aflatoxin B1-induced hepatic preneoplastic lesion development in the rat.

Dietary protein intervention during the post-dosing phase of aflatoxin B1-induced hepatic preneoplastic lesion development. Inhibition of aflatoxin-initiated preneoplastic liver lesions by low dietary protein. A plant based diet and animal protein: Nutrition renaissance and public health policy. Studies of migrant populations. Haenszel W, Kurihara M.

Studies of Japanese Migrants: Contribution of the environment to cancer incidence: The decline in gastric cancer: Epidemiology of an unplanned triumph. Diet, nutrition and cancer: National Academy Press; Washington, D. Obesity, preventing and managing the global epidemic: World Health Organization; Geneva: Department of Health and Human Services and U.

Nutrition monitoring in the United States: Committee on Diet and Health; p. Superintendent of Documents, U. Cancer facts and figures Diet, life-style and mortality in China A study of the characteristics of 65 Chinese counties. Campbell TC, et al. Policy implications of the epidemiological transition. Ecology of Food and Nutrition. Uber die Wirbung des tierischen eiweiss auf die aorta und die parenchymatosen organe der kaninchen.

Kritchevsky D, Czarnecki SK. Animal and vegetable proteins in lipid metabolism and atherosclerosis. Gibney MJ, Kritchevsky D, editors. Newburgh LH, Clarkson S. The relation between atherosclerosis and ingested cholesterol in the rabbit. The effect of quantity and quality of dietary protein on drug metabolism.

Role of nutrition in the drug metabolizing system. DNA methylation and chromatin remodeling: Human cancers express a mutator phenotype. Multiple mutations and cancer. Sjoblom T, et al. The consensus coding sequences of human breast and colorectal cancers. Relative contribution of dietary protein level and aflatoxin B1 dose in generation of presumptive preneoplastic foci in rat liver. Dietary protein level and aflatoxin B1-induced preneoplastic hepatic lesions in the rat. Ornish D, et al. Effect of comprehensive lifestyle changes on telomerase activity and telomere length in men with biopsy-proven low-risk prostate cancer: The cocarcinogenic action of croton resin.

Berenblum I, Shubik P. Tomlinson I, Bodmer W. Selection, the mutation rate and cancer: Control of apoptosis by p These trials established lumpectomy plus radiation plus tamoxifen as standard of care for DCIS patients. Colorectal screening and polypectomy began in the s — and became standard practice even before they were established for preventing colorectal cancer by observational studies including the National Polyp Study In , colonoscopic screening and polypectomy were shown to effectively reduce colorectal cancer risk in Lynch syndrome hereditary nonpolyposis colorectal cancer patients Observational and clinical studies confirmed significant reductions in colorectal cancer mortality and, in some cases, incidence in the context of colorectal screening by stool blood—based tests or flexible sigmoidoscopy combined with colonoscopic adenomectomy , Smoking cessation and control.

Reports of smoking various materials including cow dung as treatment for melancholia date back to Herodotus in the 5th century BCE Tobacco is native to the Americas, however, and smoking tobacco began with native peoples of the New World long before it was known to Europeans, who adopted the custom as sailors began bringing tobacco plants home with them in the decades after Columbus discovered Cuba and Hispaniola in There is no better example of the important link between cancer prevention and cancer epidemiology than that reflected by lung cancer risk and its smoking-related epidemiology beginning as early as the s Seminal epidemiologic studies of Wynder and Doll fully demonstrated the long-suspected association between cigarette smoking and lung cancer risk in , Surgeon General's Report of established this association by adding the data of Auerbach showing the causal relationship between smoking and neoplasia in lung tissue to the compelling and later epidemiologic evidence, thus prompting major policy changes, media campaigns, cigarette taxation, and other measures to combat cigarette smoking, including the Federal Cigarette Labeling and Advertising Act requiring printing of warnings on cigarette packs and the U.

Public Health Cigarette Smoking Act banning advertising for cigarettes. Important tobacco biology studies of identified tobacco-specific nitrosamines After peaking for men in and for women in , the overall U. Studies of the addictive nature of tobacco use began in the early s , and studies of the biology of carcinogenesis induced by the numerous carcinogens in tobacco smoke seem to date back at least to the early s — The scientific name of tobacco is Nicotiana , and s research focused on the addictive component nicotine, examining its dependency-producing effects, pharmacokinetics, pharmacodynamics, self-administration, withdrawal, and tolerance , The early s suggestion of a genetic influence underlying tobacco dependence comes from several lines of research including twin studies and studies of the association between germ-line gene variants in neurotransmitter systems and tobacco dependence , , including germ-line variation studied by molecular epidemiology pioneer Spitz and colleagues and others in dopamine receptor genes The first nicotine replacement pharmacotherapy was nicotine gum , , which the U.

The first pharmacogenetic studies were reported in , Historically, the impact of behavioral trials on smoking behavior has been less than that of public policy measures, although many experts believe that clinical trials in targeted populations should play a bigger role going forward. As of , the overall age-adjusted U. In the s, Peto advanced the understanding of worldwide tobacco-related mortality, predicting 1 billion avoidable deaths in the 20th century if then-current smoking patterns persisted and with Doll showing in that half of all persistent smokers eventually die of their habit and can reduce this risk by quitting smoking , With a weaker effect, second-hand smoke exposure was more difficult to establish in causing lung cancer than was smoking.

This conclusion met with substantial skepticism because the epidemiologic data were somewhat limited and lung carcinogen metabolites were not yet reported in exposed nonsmokers. Then in , Hecht and colleagues published the first report establishing the presence of 4- N-nitrosomethylamino 3-pyridyl butanol and 4- methylnitrosamino 3-pyridyl butanol-glucuronide, metabolites of the potent tobacco carcinogen 4- methylnitrosamino 3-pyridyl butanone, in the urine of nonsmokers exposed to second-hand smoke This group followed with a series of studies firmly establishing the presence of these lung carcinogen metabolites in the urine of infants, elementary school children, women living with smokers, casino patrons, and restaurant and bar workers reviewed in ref.

The metabolites were not detected in nonexposed people. The link between second-hand smoke and lung cancer has spurred or strengthened legislation in many states to protect nonsmokers in workplaces, bars, and restaurants. Regulation of indoor smoking reduces smoking cues and amounts, ultimately will change social norms, and therefore has become a pillar of tobacco control, along with aggressive counteradvertising and taxation, which are effective in decreasing smoking prevalence Gritz advanced our understanding of cigarette smoking behavior in women and other special populations, addressing, for example, smoking initiation and smoking cessation in the seminal U.

Important disparities in smoking behavior and health consequences among people with a lower versus a higher socioeconomic status have been studied since the mids First published in and updated most recently in , the clinical practice guideline Treating Tobacco Use and Dependence of the U. Department of Health and Human Services presents state-of-the-art evidence for and meta-analyses of treating tobacco use with behavioral or pharmacologic approaches or both , An important commentary of observed that the reversal in total U. The MSA imposes certain restrictions on practices by the companies and requires them to pay compensation to the states for health costs of patients with smoking-related illnesses.

On the other side, the states agreed to settle existing litigation against the companies, and the companies received general protection from future law suits over harm from tobacco use. This is the largest civil settlement in U. Most ALF funding ended after 5 years, however, because its continuance depended on the companies who signed the MSA maintaining at least a Screening utilization and genetic counseling measures.

An important early step in the development of behavioral science methods for prevention and screening interventions was the Yale Conference on Behavioral Medicine held in , Behavioral approaches involving individual-level factors such as age, education level, preferences, and broader environmental factors, e. Behavioral approaches among high-risk women to treat the anxiety caused by, and help in understanding the health and social impact of, genetic testing followed the identification of genetic markers of familial, heritable cancers especially of the breast and ovary Psychosocial research in the area of genetic testing for cancer risk is designed to improve cancer prevention through risk-reducing surgery or chemoprevention and early detection through targeted surveillance and screening in high inherited risk populations.

In , Kessler first defined a psychological model for genetic counseling in general , which addressed the needs of individuals undergoing cancer-related genetic counseling. Prior to the availability of clinical genetic testing, several important studies published in — established that women who had close relatives with breast cancer were themselves at risk for increased psychological distress — Therefore, when clinical genetic testing for hereditary cancer risk first became available, a primary concern was adverse psychological consequences due to counseling and testing.

Other notable advances include identifying the importance of informed consent for cancer genetic testing and the importance of addressing both the educational and psychosocial needs of individuals undergoing counseling The first studies shedding light on how genetic testing influences the adoption of risk management behaviors , found that notification of positive mutation carrier status can improve uptake of screening recommendations for breast and colorectal cancers. These collective early findings promise to inform future applications of genetic and genomic advances toward tangible clinical and public health benefits.

Overweight and obesity control. The first reported studies of energy restriction and its impact on transplanted, chemically induced, and spontaneous tumors in mice appeared in The first study in humans a quasi-experimental design to determine if energy restriction improves health was reported in The concept of diet-gene interactions was posited in A preclinical animal study reported in provided the proof of concept that diet alters the epigenome , and an early preclinical study of exercise and cancer was reported in This work is very important to cancer prevention because the prevalence of obesity has increased dramatically over the past 30 years, especially in children, and the study of the obesity-cancer link may lead to new preventive strategies.

Recent scientific study has focused on the specific molecular basis of energy balance effects including effects on the AMP-activated protein kinase and Akt pathways Preventing new cancers in cancer survivors. The emphasis on promoting healthy behaviors among cancer survivors is increasing , A major intent of interventions targeting cancer survivors is to prevent recurrence; this approach is gaining acceptance because of trends in better early detection, more effective therapies, and the increased risk of survivors not only for recurrence but second primaries as well, thus increasing the motivation of survivors to participate in behavioral research.

In the early s, Ganz began pioneering studies of quality-of-life assessments in cancer patients, studying cancer survivorship and late effects of cancer treatment, cancer in the elderly, and quality of care for cancer patients , The first report of an RCT to attempt energy restriction in humans explicitly to inhibit recurrence of cancer appeared in The first exercise RCT designed to prevent cancer recurrence in humans was reported in NCI established the Office of Cancer Survivorship in in recognition that many cancer patients survive for long periods of time after diagnosis and have unique and poorly understood needs.

In a deviation from the norm of less detailed descriptions in this review, this section will provide greater detail on the highly complex Women's Health Initiative WHI to clarify its design and outcomes, which heretofore have baffled many experts in the field, including us. With more than , women ages 50 to 79 years, the historical WHI is one of the most definitive, far-reaching research efforts ever undertaken for women's health in the United States.

While the Minority Populations trial was under way, Healy was named the first woman director of the U. She rolled hormone and low-fat diet trials into one program and added a calcium and vitamin D trial and an observational study, and the scope and budget of WHI were presented to and approved by Congress in the early s.

The RCT program randomized more than 68, postmenopausal women between and , and the observational study of chronic disease epidemiology in women involved 93, women. The complex RCT , tested three interventions to reduce the incidence of cardiovascular disease, cancer, and osteoporotic fractures.

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For the hormone therapy component, two parallel randomized, double-blind, placebo-controlled trials were conducted, one comparing estrogen alone with placebo 10, women with prior hysterectomy and the other comparing combined estrogen plus progestin with placebo 16, women with an intact uterus. The primary outcome for both trials was incident coronary heart disease, with invasive breast cancer incidence as the primary safety outcome.

The primary outcomes for the low-fat diet component were invasive breast and colorectal cancer, and colorectal cancer was a secondary outcome of the calcium and vitamin D trial. Regardless of the primary RCT end point s , total and site-specific cancer incidences were documented for all WHI participants. Both WHI hormone trials were stopped early because of adverse effects.

The estrogen plus progestin trial was stopped in because of adverse effects on breast cancer incidence , , leading to decreased hormone use and breast cancer rates in the general population , , coronary heart disease , , stroke , and venous thromboembolisms The estrogen-alone trial was stopped in because of an increased risk of stroke , The low-fat diet trial produced a modest nonsignificant trend toward reduced breast cancer risk [hazard ratio HR , 0.

The calcium and vitamin D trial had no appreciable effect on the rates of colorectal cancer HR, 1. The past cannot exist without the future, however, and there are several exciting, promising new directions with historical antecedents, of course that cancer prevention will use to embroider its future history. Selected events that have influenced the history and progress of cancer prevention.

The recent historical trial of DFMO and sulindac in colorectal neoplasia illustrates the leading future direction of molecular-targeted combinations; another promising combination in preclinical studies is an epidermal growth factor receptor EGFR tyrosine kinase inhibitor plus an NSAID in intestinal carcinogenesis The DFMO-plus-sulindac RCT opened the door to using two or more drugs for cancer prevention, echoing great earlier advances of the s and early s in developing combination chemotherapy for childhood leukemia and Hodgkin's disease Combinations offer the possibility to develop safer, more-effective regimens for clinical trials and practice.

Their development, which deviates from the norm of clinical prevention, will require extensive preclinical support from animal studies, mechanistic in vitro studies, the clinical research community, and federal granting agencies. Barriers to combination chemoprevention development include formidable regulatory and intellectual property problems. Vaccinations against hepatitis B—related liver cancer and HPV-related cervical cancer highlight the importance of population-wide approaches for preventing infection-related cancers Major issues of this research are an increased understanding of microbial oncogenesis, identifying critical factors of the host-microbe interaction e.

This is an extremely complex area of prevention, however, as illustrated by the control of H. Preclinical directions include the potential of angiogenesis targeting for cancer prevention. Our historical narrative cited the seminal transgenic mouse-model research of Folkman and Hanahan in showing the angiogenic switch or shift of balance between angiogenic stimulators [e.

Later studies in clinical specimens supported the occurrence of angiogenesis during human premalignancy in the lung and other sites A recent groundbreaking manifestation of this line of investigation for prevention involved findings that the angiogenesis inhibitor sunitinib predominantly a VEGF receptor tyrosine kinase inhibitor affected primary lung tumor development and growth, but not metastasis, in genetically engineered mice , Surprising in light of the general belief that angiogenesis mainly mediates the processes of tumor invasion and metastasis, this recent finding supports a potentially practical approach for lung cancer prevention through angiogenesis inhibition in the lung and head and neck , The mTOR inhibitor rapamycin was shown to be active in preclinical oral cancer prevention The promising natural agent myoinositol regressed dysplastic bronchial lesions in heavy smokers via inhibition of active Akt New imaging approaches for IEN include optical spectroscopy e.

Recent advances in autofluorescence with probability mapping should provide a more reliable screen for detecting oral neoplasia For example, it is currently impossible to assess the histopathologic or prognostic significance of colorectal polyps accurately and reliably without removing them, yet we know that the majority of such lesions are of little direct clinical consequence.

This is particularly true of small polyps and flat neoplastic lesions, although a small fraction of them may harbor advanced neoplasia of clinical importance In vivo assessments of such lesions could help to identify patients at greatest risk and the efficacy of chemopreventive agents against the fraction of lesions that matter most, and do so in a more accurate, reliable, and repeatable manner The deep history of preventing smoking-related cancer involves major behavioral initiatives in smoking cessation and control.

Whereas policy-driven control has had the greatest impact thus far on population-wide smoking behavior, the development and testing of nicotine vaccines and nicotine control trials will come increasingly into play going forward. Another important behavioral direction is the growing study and removal of disparities in smoking behavior and health consequences among people with a lower socioeconomic status — New directions in genetic associations with smoking behavior and lung cancer development include three genome-wide association studies that identified an association between single-nucleotide polymorphism variation at 15q24—15q Better molecular understanding of diffuse tissue injury and drug interactions induced by cigarette smoking includes studies of diffuse gene expression and proteomic abnormalities , and diffuse epigenetic abnormalities New lung neoplasia risk modeling includes studies of methylated genes in sputum and clinical-genomic models that integrate classic demographic and other risk factors with genomic genetic and epigenetic and germ-line and somatic risk factors , The past century of cancer prevention research comprises the cutting-edge science of many Nobel laureates, members of the National Academy of Sciences, and AACR presidents going back to The efforts of these and countless other cancer prevention investigators have helped and continue to help stem the tide of cancer and save lives.

We deeply hope that this Centennial series review does honor to the remarkable century of AACR contributions to cancer research. It has been a rare honor and pleasure to compile the astonishing record of cancer prevention history that we uncovered for ourselves and possibly some of you in the course of writing this review. Of course, any review owes a tremendous debt to the generally contemporaneous investigators who came before with their contributions to this or that topic under consideration. In our case in this review, however, we have enjoyed the company of many and diverse angels, both present and departed, as we discovered the rich history that makes cancer prevention such an exciting field to work in.

A great joy of this project has been weaving together innumerable and disparate threads of history that, if you are like us, may seem familiar but never quite fit together before. A great pitfall, however, is that historical benchmarks and events often inspire many different points of view in the literature, not unlike varying eye-witness accounts of a crime committed in front of a large crowd. Therefore, this recitation of the historical record is based on our best estimate of the most reliable source and may differ in cases from other accounts of the same event.

At least, we hope that incorporating these events into one cohesive narrative may provide a starting point for interested readers to research any specific questions they may have about exactly what happened and when. The many distant and more recent events in this history have imbued us with a sense of the eternal presence of the past in our own current and future research and practice of cancer prevention.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U. Section solely to indicate this fact. We also thank Margaret Chervinko for locating the rare Fig. Selected pioneers of cancer prevention. The order of appearance is according to the date cited in the text for each persons contribution to the field. Health, United States, We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail.

We do not retain these email addresses. Skip to main content. Lippman and Ernest T. Anderson Cancer Center, Houston, Texas. Abstract The rich, multidisciplinary history of cancer prevention recounted here begins with surgical and workplace recommendations of the s and ends with results of the enormous 35, men Selenium and Vitamin E [prostate] Cancer Prevention Trial SELECT. Introduction Cancer prevention generally is considered to be a relatively young field of medicine.

Chemoprevention Nutrients and nutrient-related agents. Surgical Prevention Prophylactic surgery. Behavioral Prevention Smoking cessation and control. Women's Health Initiative In a deviation from the norm of less detailed descriptions in this review, this section will provide greater detail on the highly complex Women's Health Initiative WHI to clarify its design and outcomes, which heretofore have baffled many experts in the field, including us. Download figure Open in new tab Download powerpoint. Disclosure of Potential Conflicts of Interest No potential conflicts of interest were disclosed.

Acknowledgments The costs of publication of this article were defrayed in part by the payment of page charges. Walthos, Wilkin, Bonwicke and Ward; Chirurgical observations relative to the cataract, the polypus of the nose, cancer of the scrotum, different kinds of ruptures, and the mortification of the toes and feet. Hawes, Clarke, Collins; Prevention of work-related cancers chapter Colditz GA, Hunter D, editors. Kluwer Academic Publishers; Yamagiwa K, Ichikawa K. Experimental study of the pathgenesis of carcinoma. J Cancer Res ; 3: The isolation of a cancer-producing hydrocarbon from coal tar.

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Hypervitaminosis A and fractures. BMJ ; Vitamin A and retinoids: Lancet ; 1: N - 4-Hydroxyphenyl retinamide, a new retinoid for prevention of breast cancer in the rat. Enhancement of regression of cervical intraepithelial neoplasia II moderate dysplasia with topically applied all- trans -retinoic acid: J Natl Cancer Inst ; Prevention of skin cancer in xeroderma pigmentosum with the use of oral isotretinoin. Effect of retinol in preventing squamous cell skin cancer in moderate-risk subjects: Cancer Epidemiol Biomarkers Prev ; 6: Prevention of second primary tumors with isotretinoin in squamous-cell carcinoma of the head and neck.

Randomized phase III trial of low-dose isotretinoin for prevention of second primary tumors in stage I and II head and neck cancer patients. Randomized phase III intergroup trial of isotretinoin to prevent second primary tumors in stage I non-small-cell lung cancer. Cyclin D1 genotype, response to biochemoprevention, and progression rate to upper aerodigestive tract cancer. Predicting cancer development in oral leukoplakia: Clin Cancer Res ; 6: Phenotype and genotype of advanced premalignant head and neck lesions after chemopreventive therapy. Frequent microsatellite alterations at chromosomes 9p21 and 3p14 in oral premalignant lesions and their value in cancer risk assessment.

Nat Med ; 2: A human retinoic acid receptor which belongs to the family of nuclear receptors. Nature ; Identification of a receptor for the morphogen retinoic acid. Department of Health and Human Services. Calcium supplements for the prevention of colorectal adenomas. Calcium Polyp Prevention Study Group. Randomized trials of antioxidant supplementation for cancer prevention: JAMA ; Effect of selenium and vitamin E on risk of prostate cancer and other cancers: Nutritional prevention of cancer: Nutrition intervention trials in Linxian, China: Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin.

A randomized controlled trial. Nutritional Prevention of Cancer Study Group. Phytother Res ; 1: Inhibitory effect of curcumin, chlorogenic acid, caffeic acid, and ferulic acid on tumor promotion in mouse skin by O -tetradecanoylphorbolacetate. Cancer chemopreventive activity of resveratrol, a natural product derived from grapes. Chemopreventive effects of deguelin, a novel Akt inhibitor, on tobacco-induced lung tumorigenesis. Cancer Lett ; The chemopreventive agent myoinositol inhibits Akt and extracellular signal-regulated kinase in bronchial lesions from heavy smokers.

Cancer Prev Res Phila Pa ; 2: Ambrosone CB, Tang L. Cruciferous vegetable intake and cancer prevention: Selenium, genetic variation, and prostate cancer risk: On the treatment of inoperable cases ofcarcinoma of the mamma: Lancet ; Appearance of mammary cancers in male mice subjected to folliculin injections. Comptes Rendus de l'Academie des Sciences ; Influence d'un facteur familial dans la production par la folliculine, de cancers mamaires chez la souris male.

J Soc Biol ; Toft D, Gorski J. A receptor molecule for estrogens: J Steroid Biochem ; 5: Huggins C, Hodges CV. Studies on prostatic cancer.


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The effect of castration, of estrogen and of androgen injection on serum phosphatases in metastatic carcinoma of the prostate. Cancer Res ; 1: Up-regulation of cyclooxygenase 2 gene expression in human colorectal adenomas and adenocarcinomas. Gastroenterology ; Cell ; Induction of angiogenesis during the transition from hyperplasia to neoplasia.

Hanahan D, Folkman J. Patterns and emerging mechanisms of the angiogenic switch during tumorigenesis. Effects of angiogenesis inhibitors on multistage carcinogenesis in mice. Biochem Biophys Res Commun ; Feinberg AP, Vogelstein B. Hypomethylation distinguishes genes of some human cancers from their normal counterparts. Methylation of the oestrogen receptor CpG island links ageing and neoplasia in human colon.

Nat Genet ; 7: Suppression of intestinal neoplasia by DNA hypomethylation. Tamoxifen for prevention of breast cancer: Potential role of tamoxifen in prevention of breast cancer. The effect of celecoxib, a cyclooxygenase-2 inhibitor, in familial adenomatous polyposis. The influence of finasteride on the development of prostate cancer. Effects of tamoxifen vs raloxifene on the risk of developing invasive breast cancer and other disease outcomes: A randomized clinical trial evaluating tamoxifen in the treatment of patients with node-negative breast cancer who have estrogen-receptor-positive tumors.

Long-term results of tamoxifen prophylaxis for breast cancer—month follow-up of the randomized IBIS-I trial. Estimating rates of true high-grade disease in the prostate cancer prevention trial. Cancer Prev Res Phila Pa ; 1: High-grade prostate cancer and the Prostate Cancer Prevention Trial. Pathologic characteristics of cancers detected in the Prostate Cancer Prevention Trial: Finasteride and high-grade prostate cancer in the Prostate Cancer Prevention Trial.

Finasteride does not increase the risk of high-grade prostate cancer: Blinded 2-year results abstract Treatment of colonic and rectal adenomas with sulindac in familial adenomatous polyposis. A randomized trial of aspirin to prevent colorectal adenomas. A randomized trial of aspirin to prevent colorectal adenomas in patients with previous colorectal cancer.

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Celecoxib for the prevention of sporadic colorectal adenomas. Cardiovascular risk of celecoxib in 6 randomized placebo-controlled trials: Circulation ; Five-year efficacy and safety analysis of the Adenoma Prevention with Celecoxib Trial. Cytochrome P 2C9 variants influence response to celecoxib for prevention of colorectal adenoma. Difluoromethylornithine plus sulindac for the prevention of sporadic colorectal adenomas: Inhibition of intestinal carcinogenesis in rats: Clinical prevention of recurrence of colorectal adenomas by the combination of difluoromethylornithine and sulindac: Combination chemoprevention of cancer.

The treatment of malignant tumors by repeated inoculations of erysipelas: Amer J Med Sc ; BCG immunotherapy of bladder cancer: Am J Hyg ; 9: Intracavitary Bacillus Calmette-Guerin in the treatment of superficial bladder tumors. J Urol ; Treatment of carcinoma in situ of the bladder with BCG.


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A phase II trial. Cancer Immunol Immunother ; 9: A randomized trial of intravesical doxorubicin and immunotherapy with bacille Calmette-Guerin for transitional-cell carcinoma of the bladder. Initial report on intravesical administration of N -trifluoroacetyladriamycinvalerate AD 32 to patients with refractory superficial transitional cell carcinoma of the urinary bladder. Urology ; Universal hepatitis B vaccination in Taiwan and the incidence of hepatocellular carcinoma in children.

Taiwan Childhood Hepatoma Study Group. Hepatitis B virus infection. A serum antigen Australia antigen in Down's syndrome, leukemia, and hepatitis. Ann Intern Med ; The relation of infection with the hepatitis B agent to primary hepatic carcinoma. Am J Pathol ; Innesto positivo con filtrato di verruca volgari. Jiorn Ital Mal Venereol ; Attempts to detect virus-secific DNA in human tumors.

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Cancer Prevention and Treatment by Wholistic Nutrition

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