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

Hormones play a major role in the aetiology of several of the commonest cancers worldwide, including cancers of the endometrium, breast and ovary in women and cancer of the prostate in men. It is likely that the main mechanisms by which hormones affect cancer risk are by controlling the rate of cell division, the differentiation of cells and the number of susceptible cells. Hormones have very marked effects on cell division in the endometrium; oestrogens stimulate mitosis whereas progestins oppose this effect. The risk for endometrial cancer increases with late menopause, oestrogen replacement therapy and obesity, and decreases with parity and oral contraceptive use; thus risk increases in proportion to the duration of exposure to oestrogens unopposed by progestins, probably because unopposed oestrogens stimulate endometrial cell division. The effects of hormones on breast epithelial cell division in non-pregnant women are much less clear-cut than their effects on the endometrium, but both oestrogens and progestins appear to stimulate mitosis. Breast cancer risk increases with early menarche, late menopause and oestrogen replacement therapy, probably due to increased exposure of the breasts to oestrogen and/or progesterone. Early first pregnancy and multiparity reduce the risk for breast cancer, probably due to the hormonally-induced differentiation of breast cells and the corresponding reduction in the number of susceptible cells. Hormones do not have marked direct effects on the epithelial cells covering the ovaries, but hormones stimulate ovulation which is followed by cell division during repair of the epithelium. Risk for ovarian cancer increases with late menopause and decreases with parity and oral contraceptive use, suggesting that the lifetime number of ovulations may be a determinant of risk. For all three of these cancers risk changes within a few years of changes in exposure to sex hormones and some of the changes in risk persist for many years, indicating that hormones can affect both early and late stages of carcinogenesis. Understanding of the role of sex hormones in the aetiology of prostate cancer and of some rarer cancers is less complete.
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PMID:Hormones and cancer in humans. 853 37

The association between dietary fat consumption and risk of cancer, especially colon, breast, prostate, and ovary cancer, has been debated for many years. Ecologic studies over the past 30 years have demonstrated the correlation of greater dietary fat intake with higher mortality due to various cancers. Migrant studies also have shown that increased fat consumption may be associated with increased risk of cancer. Specific saturated fatty acids raise blood cholesterol levels and, thereby, increase the risk of atherosclerosis. Greater fat, intake is a major cause of obesity and hypertension, diabetes, and gallbladder disease. Higher fat intake may heighten the risk of breast cancer directly through increased blood estrogen levels and/or secondarily through increased obesity. The critical experimental studies to determine the effects of a low-fat diet on disease risk have not been completed, but reducing fat in the US diet has the potential to decrease morbidity and mortality substantially.
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PMID:Dietary fat and chronic diseases: epidemiologic overview. 921 62

To investigate the role of selected medical conditions on the risk of ovarian cancer, we analysed data from a case-control study. Cases were 971 women below the age of 75 years with histologically confirmed epithelial ovarian cancer, admitted to a network of hospitals including the major teaching and general hospitals in the greater Milan area. Controls were 2758 women admitted to the same network of hospitals for acute, non-gynaecological, non-hormone related, non-neoplastic conditions. Obesity/severe overweight were inversely associated with the risk of ovarian cancer (multivariate relative risk, RR, 0.66, 95% confidence interval, CI, 0.52-0.85). Hyperlipidaemia was also inversely related to ovarian cancer risk, (RR 0.64, 95% CI 0.45-0.89). No relationship emerged between ovarian cancer risk and diabetes (RR 0.80, 95% CI 0.54-1.19), hypertension (RR 0.85, 95% CI 0.68-1.06), thyroid diseases (RR 0.89, 95% CI 0.63-1.13) and cholelithiasis (RR 0.86, 95% CI 0.66-1.12). A decreased frequency of ovarian cancer was seen in women with a history of uterine leiomyomas (RR 0.66, 95% CI 0.47-0.92) and benign ovarian cysts (RR 0.69, 95% CI 0.41-1.13).
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PMID:Ovarian cancer risk and history of selected medical conditions linked with female hormones. 938 10

Because it has been suggested that an environmental factor may play a role in the etiology of ovarian cancer, a case-control study was conducted to assess some environmental and other risk factors for ovarian cancer from 1994 to 1996 in northern Kyushu, Japan. We analyzed the data of 89 cases with epithelial ovarian cancer and 323 controls without any cancer or ovarian disorder. After controlling for the effect of potential confounders, the odds ratios of ovarian cancer across increasing quartiles of the heaviest body weight were 1.00, 1.15, 1.71, 2.29 (P = 0.008, test for trend). Significantly increased risks were noted for a history of diabetes mellitus (P < 0.05), and for a family history of ovarian cancer (P < 0.05). Significantly decreased trends for risk were obtained for the number of pregnancies (P < 0.01) and the number of live births (P < 0.001). This study provides additional support for an association between obesity and the risk of ovarian cancer. This relationship may at least partly explain the recent increase in the incidence of ovarian cancer in Japan, although possible contributions of other factors can not be ruled out.
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PMID:Anthropometric and other risk factors for ovarian cancer in a case-control study. 960 Jan 17

The incidence of gynecologic malignancies shows considerable regional differences which suggest a decisive role of environmental and endocrine factors in tumor genesis. The risk of developing breast cancer increases with increasing age, a positive family history, prolonged exposure to estrogens (early menarche, late menopause), nulliparity, alcohol consumption, and obesity. A relationship between a long exposure to estrogens and an increased risk of cancer may also be assumed in the case of endometrial cancer. Whether estrogens or their metabolites promote the initiation of cancer remains to be clarified. Endocrine monotherapy with only an estrogen, obesity, nulliparity/infertility as well as a late natural menopause are well-known risk factors of developing endometrial cancer. Whereas estrogens induce a hyperplasia of the endometrial mucosa, gestagens exert a protective effect on the endometrium. Old age, a family history of breast, endometrial and ovarian cancer as well as persistent or treated infertility are the established risk factors of ovarian cancer. Each pregnancy, the intake of oral contraceptives, a hysterectomy or tubal ligation are associated with a decreased risk of developing ovarian cancer; hormonal replacement therapy has no influence on the risk of ovarian cancer.
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PMID:[Epidemiologic considerations on the significance of hormones in carcinogenesis]. 981 21

Polycystic ovary syndrome is a common problem affecting approximately 5% of women of reproductive age when defined by clinical features of anovulation and hyperandrogenism. Metabolic derangements associated with this condition may predispose to a range of diseases with attendant morbidity and mortality risks. In general, available data support significantly increased rates of type II diabetes mellitus, dyslipidemia, and endometrial cancer in PCOS that are not completely explained by obesity; data also suggest that rates of hypertension, gestational diabetes, and pregnancy-induced hypertension may likewise be increased, although the extent to which obesity mediates these risks is not clear. The increased prevalence of several cardiovascular risk factors in PCOS and limited cross-sectional data suggest that cardiovascular disease should be more likely in PCOS, but prospective data are lacking to confirm this supposition. Limited data have suggested an association between PCOS and ovarian cancer risk and require further study. The present data do not support an increased risk for breast cancer in this condition. Long-term prospective data are clearly needed to better delineate the nature and magnitude of disease risks associated with PCOS, with appropriate adjustment for associated obesity. Such information is a necessary background for understanding the role of established and emerging PCOS therapies, including oral contraceptives, intermittent progesterone, ovulation induction agents, and insulin sensitizers, in modifying such risks. In the meantime, close follow-up of women with PCOS and encouragement of lifestyle practices likely to reduce disease risks, such as regular exercise and weight control, should be standard practice.
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PMID:The epidemiology of polycystic ovary syndrome. Prevalence and associated disease risks. 1035 18

In Western and Northern Europe, as well as in the United States, ovarian cancer represents the third most frequent cancer of the female genital tract with an estimated 191,000 newly diagnosed cases per year worldwide. Due to its insidious onset, the disease is diagnosed in 70% of cases in an advanced stage. Consequently, ovarian cancer is the fifth leading cause of cancer-related deaths in women. Epidemiological and molecular studies reviewed here have identified demographic, geographic, molecular, genetic, endocrine, dietary, and environmental factors, which affect the risk of developing ovarian cancer: ethnic background, tumor suppressor gene mutations in the germline, positive family history, number of full-term pregnancies [odds ratio (OR): 0.17; 95% confidence interval (CI): 0.05-0.54], time spent breast feeding, oral contraceptive use [OR: 0.23; 95% CI: 0.1-0.50], unexplained infertility (OR: 2.64; 95% CI: 1.10-6.35), tubal ligation and prior hysterectomy (OR: 0.5; 95% CI: 0.2-0.9), dietary factors and obesity (OR: 1.7; 95% CI: 1.1-2.8). This knowledge provides the objective basis for an individual risk assessment for women, which should lead to sophisticated counseling and prevention. It should also help to individualize the therapeutic approach in the event that disease is diagnosed.
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PMID:Epidemiological and molecular aspects of ovarian cancer risk. 1121 17

Age-adjusted ovarian cancer deaths and mortality rates have increased annually in Japan from 1968 to 1995, with the absolute number of deaths increasing 4-fold during these years. Internationally, the mortality rates are high in North America or northern Europe, but their incidences have gradually decreased. However, the incidences of ovarian cancer have increased in France, Spain, and Japan. Risk factors for epithelial ovarian cancer include older age, being northern European or North American, family history of ovarian cancer, nulliparity, infertility, and obesity, and preventive factors include oral contraceptive use, gravidity, lactation, tubal ligation, and hysterectomy.
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PMID:[Ovarian cancer]. 1124 43

Energy balance can affect the risk for hormone-related cancers by altering sex hormone levels. Energy intake and expenditure are difficult to measure in epidemiological studies, but a chronic excess of intake relative to expenditure leads to a high BMI, which can be accurately measured. In premenopausal women obesity has little effect on the serum concentration of oestradiol, but causes an increase in the frequency of anovular menstrual cycles and thus a reduction in progesterone levels; these changes lead to a large increase in the risk for endometrial cancer. but little change, or a small decrease, in the risk for breast cancer. In post-menopausal women oestradiol levels are not regulated by negative feedback, and obesity causes an increase in the serum concentration of bioavailable oestradiol; this factor causes increases in the risk for both endometrial cancer and breast cancer. The development of ovarian cancer appears to be related more strongly to the frequency of ovulation than to direct effects of circulating levels of sex hormones, and BMI is not clearly associated with the risk for ovarian cancer. In men, increasing BMI has little effect on bioavailable androgen levels, and any effect of obesity on prostate cancer risk is small.
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PMID:Energy balance and cancer: the role of sex hormones. 1131 Apr 27

Breast cancer is among the most common world cancers. In Mexico this neoplasm has been progressively increasing since 1990 and is expected to continue. The risk factors for this disease are age, some reproductive factors, ionizing radiation, contraceptives, obesity and high fat diets, among other factors. The main risk factor for BC is a positive family history. Several families, in which clustering but no mendelian inheritance exists, the BC is due probably to mutations in low penetrance genes and/or environmental factors. In families with autosomal dominant trait, the BRCA1 and BRCA2 genes are frequently mutated. These genes are the two main BC susceptibility genes. BRCA1 predispose to BC and ovarian cancer, while BRCA2 mutations predispose to BC in men and women. Both are long genes, tumor suppressors, functioning in a cell cycle dependent manner, and it is believed that both switch on the transcription of several genes, and participate in DNA repair. The mutations profile of these genes is known in developed countries, while in Latin America their search has just began. A multidisciplinary group most be responsible of the clinical management of patients with mutations in BRCA1 and BRCA2, and the risk assignment and Genetic counseling most be done carefully.
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PMID:[Breast cancer genetics. BRCA1 and BRCA2: the main genes for disease predisposition]. 1133 51


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