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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chemoprevention is a recently introduced and rapidly growing area of oncology that is identifying agents with a potentially preventive role in cancer. Several clinical trials have recently shown the feasibility of this approach in reducing the risk of major human cancers. In the USA, a large trial that demonstrated a reduction of approximately 50% in the risk of developing breast cancer led to Food and Drug Administration (FDA) approval of tamoxifen as a preventive agent in women at increased risk. Although the results could not be reproduced in two smaller European trials, further investigations into this agent are clearly warranted. Raloxifene, another selective oestrogen receptor modulator which has reduced the risk of breast cancer in a trial in women with osteoporosis, is being compared with tamoxifen in a large primary prevention trial in at-risk women. Retinoids are a group of compounds that have proved especially effective in reducing the occurrence of second primary tumours in subjects with skin, head and neck or liver cancer. Fenretinide, a synthetic retinoic acid derivative, has recently been shown to decrease the occurrence of a second breast malignancy in premenopausal women. Results with non-steroidal anti-inflammatory drugs (NSAIDs) have proved consistently encouraging in epidemiological studies in lowering the incidence of colorectal cancer. Clinical trials with selective cyclo-oxygenase inhibitors potentially devoid of gastrointestinal (GI) toxicity are currently underway in at-risk subjects. Calcium and selenium have also received much attention as chemopreventive agents. Originally investigated against skin cancer, selenium showed efficacy in reducing prostate, lung and colon cancer incidence. Similarly, vitamin E was effective in reducing prostate cancer incidence and mortality in a lung cancer prevention trial in heavy smokers. The challenges of conducting well-designed and unequivocal chemoprevention trials are considerable, but advances in techniques of identification of at-risk subjects and establishing surrogate endpoint biomarkers should contribute greatly to future studies. Current knowledge suggests that a pharmacological approach to preventing cancer, using natural or synthetic agents, could become an important way forward.
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PMID:Recent advances in cancer chemoprevention, with emphasis on breast and colorectal cancer. 1076 41

There is dramatic international variation in prostate cancer mortality rates. The variation suggests that the disease has an environmental cause and encourages the search for a way to prevent it. Androgenic stimulation over a period of time, perhaps due to a high fat diet, has been suggested as a cause of prostate cancer. The corollary to this hypothesis is that lowering androgenic stimulation over time will prevent prostate cancer. 5-Alpha-reductase inhibition through drugs like finasteride have been shown to decrease androgenic stimulation of the prostate. A clinical trial is underway using finasteride to assess this hypothesis. Epidemiological and laboratory studies also suggest that those with high selenium and vitamin E intake have a lower risk of prostate cancer. Recent serendipitous findings of two randomised clinical trials support this. A study to assess these compounds is currently being designed. Other promising but less developed interventions in the chemoprevention of prostate cancer include vitamin D supplementation and diet modification.
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PMID:Prostate cancer prevention trials in the USA. 1088 73

Chemoprevention of prostate cancer is the administration of agents to prevent, inhibit, or delay progression of prostate cancer. Asian men have a much lower incidence of prostate cancer than men in Europe or the USA. Asian food includes low-fat, high-fiber diets, which provide a rich supply of weak dietary estrogens. These estrogens have been proposed as chemopreventive agents. In addition to their estrogenic activity, many of these plant compounds can interfere with steroid metabolism and bioavailability and can also inhibit enzymes, such as tyrosine kinase or topoisomerase, which are important for cellular proliferation. In addition, nutritional factors such as reduced fat intake, vitamin E, vitamin D, and selenium may have a protective effect against prostate cancer. The fact was proven in large epidemiological studies as well as experimental observations. In the animal model, the progression of established tumors can be inhibited by these agents. A number of studies to investigate the effect of possible chemopreventive agents for men at high risk of prostate cancer are established. End points for evaluation are mainly based on changes in PSA, changes of histological precursors, or time of onset of clinical disease. The concept of chemoprevention in prostate cancer might have a significant impact on the incidence and mortality of this disease.
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PMID:[Chemoprevention of prostatic carcinoma]. 1095 70

Male sex, advancing age, racial origin, affected first degree relatives and the ubiquitous 'Western lifestyle' have all been cited as significant risk factors for the development of prostate cancer. Numerous epidemiological studies have been undertaken and others are in place to try and identify specific risk factors but diet has not been conclusively implicated to date. Most of the current prostate research suggests that the roles of dietary fat, soy proteins, selenium and possibly vitamin E are greater in determining the progression or stimulation of established tumours rather than in the development of new tumours per se. Certainly the hypothesis casts some light on the geographic variations of the disease. What part diet and nutritional factors play in the overall jigsaw of prostate cancer development needs to be further established. It is an area that will undoubtedly attract much more research interest in future years.
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PMID:Prostate cancer. What part does diet play? 1114 Feb 14

Prostate cancer lends itself ideally to chemoprevention due to a number of specific features of the disease. These include a high prevalence, long latency time, hormone dependency, the availability of an ideal marker (prostate serum antigen) and, last but not least, the availability of a defined precursor lesion (prostatic intraepithelial neoplasia) among the pathways leading to clinical disease. The large variability in the incidence of the tumor in different geographical regions suggests the possibility of nutritional influences regarding the stimulation and/or inhibition of clinical cancer, as there is a similar prevalence worldwide of the precursor lesion. A great number of publications have dealt with a number of nutritional factors, including fat, phytoestrogens, vitamins (especially vitamin E) and minerals such as selenium and calcium. These are among the most reported substances with a possible influence on disease development; however, unfortunately there are no conclusive results or study outcomes at present which satisfy accepted standards of evidence. Ongoing studies on nutrition and prostate cancer may bring the required evidence to support what is still only an hypothesis at present.
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PMID:Prevention of prostate cancer. 1114 4

Randomized controlled trials are regarded as the most definitive of study designs. The randomized controlled trials that have tested nutritional factors for cancer prevention are reviewed. Trials that have tested the effects of nutrients given as high-dose supplements have been largely disappointing, typically showing either no or harmful effects. Possible benefits of vitamin E for prostate cancer prevention and selenium for prostate, colorectal, and lung cancer prevention have emerged only as secondary endpoints in trials conducted for other purposes; confirmatory new trials for these nutrients are now underway or are planned. The limitations of both past and current randomized controlled trials for studying diet-cancer relationships are discussed. The disappointing findings that have emerged from short-term studies of high-dose supplements cannot be interpreted as direct tests of the diet-cancer relationship because high-dose supplements cannot fully simulate the effects of whole foods on cancer risk. As we await findings from current and future trials, we should not forget that the ample evidence from observational epidemiologic research--suggesting that diets rich in fruits and vegetables can reduce the risk of many of the most common cancers--can provide a sound basis for nutritional recommendations aimed at reducing cancer risk.
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PMID:What can randomized controlled trials tell us about nutrition and cancer prevention? 1119 49

In this review, we consider the evidence from geographic and metabolic epidemiology and laboratory studies with human prostate cancer cell lines and animal models that emphasizes the need for the development and implementation of a dietary intervention trial in prostate cancer patients. It is concluded that such a trial should include a reduction in total fat consumption to 15% of total calories and supplementation of the diet with selenium, vitamin E, and a soya product. The low-fat intervention would provide an appropriate reduction in the intake of any specifically targeted dietary fatty acid, such as linoleic acid or alpha-linolenic acid.
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PMID:Nutrition and prostate cancer: a proposal for dietary intervention. 1130 6

Nutrients included in commonly used dietary supplements, such as vitamins C and E, may affect cancer risk. To better understand how supplement use may affect the interpretation of cancer prevention trials, we examined dietary supplement use among participants in the Prostate Cancer Prevention Trial, a double-blind, placebo-controlled trial of the drug finasteride (Proscar) for the primary prevention of prostate cancer. Of 15,387 men who completed food frequency questionnaires and dietary supplement questionnaires, 44.3% used a multivitamin, 35% used single supplements of vitamin C or E, and 10-15% used antioxidant mixtures or single supplements of vitamins A and D, zinc, or beta-carotene at least three times per week. The strongest correlates of supplement use were higher education and lower body mass index (p < 0.001), and whites and Asians were more likely to use multivitamins and single supplements of vitamins C and E than were blacks and Hispanics. Supplement users obtained 87% of their total daily vitamin E intake, 61-64% of vitamins A, C, and D, and about half of beta-carotene, folate, and zinc from supplements. Because supplements, especially antioxidants, may confer independent cancer-preventive effects, analytic models of study findings should include exposure measurement of dietary supplements with appropriate tests for interaction. Our results can be generalized to similar chemoprevention trials.
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PMID:Dietary supplement use in the Prostate Cancer Prevention Trial: implications for prevention trials. 1264 Oct 91

gamma-tocopherol is the major form of vitamin E in many plant seeds and in the US diet, but has drawn little attention compared with alpha-tocopherol, the predominant form of vitamin E in tissues and the primary form in supplements. However, recent studies indicate that gamma-tocopherol may be important to human health and that it possesses unique features that distinguish it from alpha-tocopherol. gamma-Tocopherol appears to be a more effective trap for lipophilic electrophiles than is alpha-tocopherol. gamma-Tocopherol is well absorbed and accumulates to a significant degree in some human tissues; it is metabolized, however, largely to 2,7,8-trimethyl-2-(beta-carboxyethyl)-6-hydroxychroman (gamma-CEHC), which is mainly excreted in the urine. gamma-CEHC, but not the corresponding metabolite derived from alpha-tocopherol, has natriuretic activity that may be of physiologic importance. Both gamma-tocopherol and gamma-CEHC, but not alpha-tocopherol, inhibit cyclooxygenase activity and, thus, possess antiinflammatory properties. Some human and animal studies indicate that plasma concentrations of gamma-tocopherol are inversely associated with the incidence of cardiovascular disease and prostate cancer. These distinguishing features of gamma-tocopherol and its metabolite suggest that gamma-tocopherol may contribute significantly to human health in ways not recognized previously. This possibility should be further evaluated, especially considering that high doses of alpha-tocopherol deplete plasma and tissue gamma-tocopherol, in contrast with supplementation with gamma-tocopherol, which increases both. We review current information on the bioavailability, metabolism, chemistry, and nonantioxidant activities of gamma-tocopherol and epidemiologic data concerning the relation between gamma-tocopherol and cardiovascular disease and cancer.
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PMID:gamma-tocopherol, the major form of vitamin E in the US diet, deserves more attention. 1172 51

The dramatic international variation in prostate cancer mortality rates suggest an environmental influence. This combined with a building understanding of the genetic mechanisms of carcinogenesis encourages a search for ways to prevent it. Androgenic stimulation over a period of time has been suggested a cause of prostate cancer. The corollary to this hypothesis is that lowering androgenic stimulation over time will prevent prostate cancer. Decreasing androgenic stimulation of the prostate with 5-alpha-reductase inhibitors such as finasteride has been shown to decrease prostate size and may prevent prostate cancer. A large, long-term clinical trial is underway using finasteride to determine if it can prevent prostate cancer. Results are expected in 2004. Epidemiologic and laboratory studies also suggest that high selenium and vitamin E intake lowers risk of prostate cancer. Recent serendipitous findings of two randomized clinical trials support the hypothesis that selenium and vitamin administration will decrease prostate cancer risk. A study to assess these compounds is beginning. Other promising, but less developed, interventions in chemoprevention of prostate cancer include vitamin D supplementation and diet modification. All will need to be rigorously evaluated before they can be advocated for prostate cancer prevention.
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PMID:The future of prostate cancer prevention. 1179 34


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