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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endogenous hormones may play a role in ovarian carcinogenesis. Postmenopausal obesity, although associated with higher circulating levels of estrogen and androgens, has not been linked consistently to ovarian cancer. The present study examined the relationship between body mass index (BMI), height, and ovarian cancer mortality among postmenopausal women in a large prospective mortality study of 300,537 women who were cancer free at enrollment in 1982 and had no history of hysterectomy or ovarian surgery. During 16 years of follow-up, 1,511 deaths occurred from ovarian cancer. Cox proportional hazard modeling was used to compute rate ratios (RRs) and to adjust for confounders. Ovarian cancer mortality rates were higher among overweight [BMI >/=25;RR, 1.16; 95% confidence interval (CI), 1.04-1.30] and obese women (BMI >/=30; RR, 1.26; 95% CI, 1.07-1.48) compared with women with BMI <25. Use of postmenopausal estrogens modified the association between BMI and ovarian cancer mortality (P = 0.05). The increased risk associated with obesity (BMI >/=30) was limited to women who never used postmenopausal estrogens (RR, 1.36; 95% CI, 1.12-1.66) and was not seen among ever users (RR, 0.93; 95% CI, 0.62-1.41). Height was positively associated with ovarian cancer mortality. Compared with women 152-156 cm tall, ovarian cancer mortality rates were lowest for the shortest women (RR, 0.72; 95% CI, 0.47-1.10 for women <152 cm) and highest for the tallest (RR, 1.41; 95% CI, 0.95-2.09 for women >/=177 cm). In this study, obesity and height appear to be independently associated with ovarian cancer mortality. The 36% increase in risk associated with obesity among women who had never used postmenopausal estrogens may have important public health implications because obesity is a growing problem in the United States.
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PMID:Body mass index, height, and the risk of ovarian cancer mortality in a prospective cohort of postmenopausal women. 1222 25

Prevention of cancer through interventions based on sound scientific research remains an important strategy of oncology research at the National Cancer Institute (NCI). Reducing the burden of cancer in the United States is focused on clinical investigations in medical settings and public health intervention research on cancer risk factors regarding lifestyle and diet. Chemoprevention research at the NCI has progressed systematically to identify potential agents that reduce cancer risk and to develop public health strategies that take advantage of basic research results. In addition, advances in our understanding of molecular targets and pathways and our use of new and emerging technologies have become important tools for oncology research. Priority areas for chemoprevention research, identified from experimental and clinical research, are investigated in clinical trials to determine their ability to reduce cancer risk in selected populations or in the general population. Priority areas discussed in this review are the relationship of the arachidonic acid pathway to carcinogenesis, lung cancer prevention in former smokers, breast cancer prevention, and prostate cancer prevention. In addition, two lifestyle factors that have potential to influence cancer risk-obesity and functionally enhanced foods-are discussed in the context of their link between clinical and public health-related research.
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PMID:Cancer prevention clinical trials. 1472 55

Scientific evidence is accumulating on physical activity as a means for the primary prevention of cancer. Nearly 170 observational epidemiologic studies of physical activity and cancer risk at a number of specific cancer sites have been conducted. The evidence for decreased risk with increased physical activity is classified as convincing for breast and colon cancers, probable for prostate cancer, possible for lung and endometrial cancers and insufficient for cancers at all other sites. Despite the large number of studies conducted on physical activity and cancer, most have been hampered by incomplete assessment of physical activity and a lack of full examination of effect modification and confounding. Several plausible hypothesized biological mechanisms exist for the association between physical activity and cancer, including changes in endogenous sexual and metabolic hormone levels and growth factors, decreased obesity and central adiposity and possibly changes in immune function. Weight control may play a particularly important role because links between excess weight and increased cancer risk have been established for several sites, and central adiposity has been particularly implicated in promoting metabolic conditions amenable to carcinogenesis. Based on existing evidence, some public health organizations have issued physical activity guidelines for cancer prevention, generally recommending at least 30 min of moderate-to-vigorous intensity physical activity on > or =5 d/wk. Although most research has focused on the efficacy of physical activity in cancer prevention, evidence is increasing that exercise also influences other aspects of the cancer experience, including cancer detection, coping, rehabilitation and survival after diagnosis.
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PMID:Physical activity and cancer prevention: etiologic evidence and biological mechanisms. 1242 70

Pigment synthesis by hair follicle melanocytes is modulated by a large number of environmental and genetic factors, many of which are discussed in this review. Eumelanic (non-yellow) pigment is produced by hair follicle melanocytes following the binding of alpha-melanocyte stimulating hormone to melanocortin receptor 1. Binding of this hormone to the melanocyte membrane is blocked by agouti signaling protein (ASP) which is encoded by the agouti locus and results in the synthesis of yellow pigment, instead of non-yellow (black/brown) pigment. The cyclical release of ASP by hair follicle cells results in a black/brown hair with a subapical yellow band. This is the wild-type coat color pattern of many mammals and is called agouti. Several dominant mutations at the agouti locus in mice, induced by retrotransposon-like intracisternal A particles, result in ectopic over-expression of ASP and animals with much higher proportions of all-yellow hairs. This abnormal presence of ASP in essentially all body cells results in the 'yellow agouti obese mouse syndrome.' The obesity has been associated with binding of ASP to melanocortin receptor 4 inactivating the latter. The syndrome also includes hyperinsulinemia, increased somatic growth, and increased susceptibility to hyperplasia and carcinogenesis. The physiologic and molecular bases for these syndrome components have not yet been elucidated. This historically orientated review is subdivided, where applicable, into pre- and post-1992 subsections to emphasize the impact of the cloning of the agouti and extension loci and their protein products on the identification of the molecular and physiological pathways modulating the manifold aspects of pheomelanogenesis.
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PMID:Regulation of yellow pigment formation in mice: a historical perspective. 1251 20

Calorie restriction (CR) is the most effective and reproducible intervention for increasing lifespan in a variety of animal species, including mammals. CR is also the most potent, broadly acting cancer-prevention regimen in experimental carcinogenesis models. Translation of the knowledge gained from CR research to human chronic disease prevention and the promotion of healthy aging is critical, especially because obesity, which is an important risk factor for several chronic diseases, including many cancers, is alarmingly increasing in the Western world. This review synthesizes the key biological mechanisms underlying many of the beneficial effects of CR, with a particular focus on the insulin-like growth factor-1 pathway. We also describe some of the opportunities now available for investigations, including gene expression profiling studies, the development of pharmacological mimetics of CR, and the integration of CR regimens with targeted, mechanism-based interventions. These approaches will facilitate the translation of CR research into strategies for effective human chronic disease prevention.
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PMID:Calorie restriction, aging, and cancer prevention: mechanisms of action and applicability to humans. 1252 70

Obesity is associated with a chronic inflammatory state that predisposes to atherogenesis, thrombogenesis, and carcinogenesis and may increase susceptibility to infections. Critically ill, obese patients have higher mortality. MOF is the best predictor of ICU mortality for obese patients. Pulmonary hypertension and higher BMI are associated with higher surgical risk. Progress in surgical technique and anesthesia has substantially improved the safety of performing operations in severely obese patients.
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PMID:Critical care of the obese and bariatric surgical patient. 1268 75

Peroxisome proliferator activated receptors (PPAR) belong to a family of nuclear receptors broadly distributed in the organism. Their pleiotropic role has been recently proved as well as their pathogenic significance in diabetes, obesity, cell cycle controlling, carcinogenesis, inflammation and atherosclerosis. The three types of PPAR identified until today have different tissue localization. PPARgamma, primarily identified in macrophages and adipocytes, play an important role in the expression of proteins essential for lipid metabolism and adipogenesis. PPARalpha are localized predominantly in hepatocytes and have also an important role in lipid metabolism. PPAR are though to be lipid sensors in organism. Carbohydrate metabolism is also under the control of PPAR and their exogenous ligands, (ie: thiasolidinediones), are important antidiabetic drugs.
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PMID:[Peroxisome proliferator activated receptors PPARs: their role in carbohydrate and lipid metabolism]. 1280 6

Peroxisome proliferation is a cellular response to many chemical compounds affects including natural and modified fatty acids, phthalate and adipate ester plasticizers, leukotriene antagonists, acetylsalicylic acid and certain pathophysiological conditions including dramatic change of cellular morphology and enzymatic activity. Peroxisome proliferation phenomenon is seen primarily in liver and kidney. Hormones and nutritional factor can regulate peroxisome proliferation response. Sustained peroxisome proliferation can lead to hepatocarcinogenesis. The three types of peroxisome proliferator activated receptor, termed PPAR alpha, PPAR beta, and PPAR gamma, expressed in specific tissue, are consisted of a specific a nuclear receptor superfamily. After more than 10 years world wide research, the function of PPAR is clarified, as PPAR gamma, the master of thrifty genes, controls the expression of genes relative to adipogenesis, diabetes mellitus and obesity. The receptor is involved in transcriptional control of numerous cellular processes including cell cycle control, inflammation, immunoregulation and carcinogenesis.
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PMID:[PPAR gamma--the master of thrifty genes]. 1290 43

The levels of dehydroepiandrosterone (DHEA) and its sulfate (DHEA-S) peak in human in their twenties, then decrease gradually with age. The physiological importance of DHEA was not clear until recent research reports showing that DHEA has beneficial effects on preventing diabetes, malignancy, inflammation, osteoporosis, and collagen disease. We summarize our results concerning diabetes, hepatitis, and colon cancer. In 1982, Coleman et al. [Diabetes 31 (1982) 830] reported that DHEA decreased hyperglycemia in diabetic db/db mice, which become insulin resistant. We measured hepatic gluconeogenic enzymes in an attempt to elucidate the mechanical mechanism of DHEA action. The activity and gene expression of hepatic gluconeogenic enzyme such as glucose-6-phosphatase (G6Pase) was increased in db/db mice despite hyperinsulinemia compared to control db/+m mice. DHEA, like troglitazone, decreased these levels in db/db mice. We also showed that DHEA improved the insulin resistance caused by aging or obesity using the glucose clamp technique in another animal model. In humans, the serum DHEA concentration was shown to be associated with hyperinsulinemia in diabetes. It also became clear that DHEA increased insulin secretion in old-aged db/db mice. DHEA increases not only insulin sensitivity due to the effects in the liver and muscle, but also insulin secretion. As an effect of DHEA on T-cell mediated hepatitis induced by concanavalin A (ConA), DHEA reduced hepatic injury by inhibiting several inflammatory mediators and apoptosis. As an effect of DHEA on carcinogenesis, DHEA would be a potential chemopreventative agent against colon cancer because it decreases the number of azoxymethane (AOM) induced aberrant crypt foci, which is a possible precursor to adenoma and cancer in a murine model.Thus, since DHEA has many beneficial effects experimentally, we should consider administration of DHEA in the future, and common mechanisms among these actions of DHEA should be elucidated in further studies.
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PMID:Prevention of diabetes, hepatic injury, and colon cancer with dehydroepiandrosterone. 1294 37

The genetic and histopathological backgrounds of adrenocortical tumorigenesis remain poorly characterized. In other tissues, there is conclusive evidence that hyperplasia and adenomas precede cancer. In the adrenal, there are few clinical cases of either hyperplasia or adenoma associated with later development of cancer, and there are few biological studies that attempt to characterize this process molecularly. Current research focuses on the early lesions of the adrenal cortex because of their possible molecular link with carcinogenesis, and evidence of their frequent association with atypical forms of Cushing's and Conn's syndromes, obesity, hypertension and/or diabetes. These studies indicate a model for oncogenesis that is the same as that in other tissues. The rarity of adrenal cancer compared to benign lesions could be a clue to unique features of adrenocortical cells. It might also highlight the function of genes that are associated with endocrine tumors in the context of which the concept of gene 'conductors' is introduced here.
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PMID:Genetics of adrenocortical tumors: gatekeepers, landscapers and conductors in symphony. 1458 Jul 59


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