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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cigarette smoking is an established risk factor for cancer and cardiovascular disease, and is the leading cause of avoidable disease in most industrialized countries. Less well-known are possible beneficial effects, which are briefly considered in this survey. Preliminary data suggest that there may be inverse associations of smoking with uterine fibroids and endometriosis, and protective effects on hypertensive disorders and vomiting of pregnancy are likely. Smoking has consistently been found to be inversely related to the risk of endometrial cancer, but cancers of the breast and colon seem unrelated to smoking. Inverse associations with venous thrombosis and fatality after myocardial infarction are probably not causal, but indications of benefits with regard to recurrent aphthous ulcers, ulcerative colitis, and control of body weight may well reflect a genuine benefit. Evidence is growing that cigarette smoking and nicotine may prevent or ameliorate Parkinson's disease, and could do so in Alzheimer's dementia. A variety of mechanisms for potentially beneficial effects of smoking have been proposed, but three predominate: the 'anti-estrogenic effect' of smoking; alterations in prostaglandin production; and stimulation of nicotinic cholinergic receptors in the central nervous system. Even established inverse associations cannot be used as a rationale for cigarette smoking. These data can be used, however, to clarify mechanisms of disease, and point to productive treatment or preventive options with more narrowly-acting interventions.
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PMID:Beneficial effects of nicotine and cigarette smoking: the real, the possible and the spurious. 874 97

The benefits of oestrogen replacement therapy (ERT) in preventing vasomotor symptoms, cardiovascular disease, osteoporosis, and colon cancer are well documented. Other potential benefits i.e. dementia and macular degeneration are being investigated. Although oestrogen is said to be contraindicated in women previously treated for breast and endometrial cancer, there is no data to support this admonition. Preliminary data would suggest ERT can be used safely in women who have had these cancers. Prospective randomised studies are currently on going in the United States and Europe addressing ERT in previously treated breast and endometrial cancer. Informed consent, patients' desires, and benefit-risk considerations are all part of information the woman needs to make a decision concerning ERT.
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PMID:HRT and women who have had breast or endometrial cancer. 1069 60

Use of hormone replacement therapy alleviates menopausal symptoms effectively, prevents osteoporosis and may even reduce the risk of cardiovascular disease and dementia. However, little is known about the risk of breast cancer and endometrial cancer after long-term use of different estrogen-progestin combinations. A large epidemiological study in Sweden, in which combined estrogen-progestin treatment was predominantly used, is reported.
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PMID:[Hormone therapy in climacteric. Different effects of estrogen and gestagen on the risk of breast and endometrial cancer]. 1122 82

Selective oestrogen receptor modulators (SERMs) are compounds that act as oestrogen agonists on selected targets while being oestrogen antagonists on others. The main targets of SERMs are oestrogen agonist activity on bone metabolism and several functions of the cardiovascular system, as well as oestrogen antagonism in the breast and uterus. They are indicated for the treatment and/or prevention of breast and endometrial cancer, osteoporosis and coronary heart disease. The extensive documentation of the multiple oestrogen effects on the CNS, greater understanding of the mechanisms of action, and especially the discovery of a second oestrogen receptor with differentiated distribution and mechanisms, have all led the way to the possibility of specific CNS-targeted SERMs. The demonstration that oestrogen selectively improves cognition, delays the appearance of Alzheimer's dementia, improves the feeling of well-being, as well as the response to antidepressant medications, provides targeted CNS indications for SERMs. The CNS effects of the currently marketed SERMs are not sufficiently explored yet. However, in postmenopausal women, tamoxifen and raloxifene probably show the most oestrogen agonist CNS effects. In women of reproductive age, competition with oestrogen probably exists, resulting in antagonist effects. Activity in men is still mostly unknown. It is quite safe to predict that the recent accumulation of knowledge, combined with the large, thirsty anticipated market for these 'designer oestrogens', will lead to clinical trials of CNS-targeted SERMs in the very near future.
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PMID:Selective oestrogen receptor modulators--current and future brain and behaviour applications. 1124 72

This statement summarizes the U.S. Preventive Services Task Force (USPSTF) recommendations for use of hormone replacement therapy for the primary prevention of chronic conditions in postmenopausal women and updates the 1996 USPSTF recommendations on this topic. The complete information on which this statement is based, including evidence tables and references, is available through the USPSTF Web site (http://www.preventiveservices.ahrq.gov) and through the National Guideline Clearinghouse (http://www.guideline.gov) The USPSTF reviewed the evidence on the use of postmenopausal hormone replacement therapy and the following outcomes: cardiovascular disease, including CHD and stroke; osteoporosis and fractures; thromboembolism; dementia and cognitive function; breast, colon, ovarian, and endometrial cancer; and cholecystitis. The USPSTF also reviewed evidence of the effects of hormone replacement therapy on phytoestrogens and osteoporosis and cardiovascular disease. The use of hormone replacement therapy for relieving active symptoms of menopause, such as hot flashes, urogenital symptoms, and mood and sleep disturbances, among others, is outside the scope of these USPSTF recommendations, and literature on this topic was not reviewed. Sources for estimates of benefits and harms cited in this Recommendation statement are described in the summary of the evidence available from the Agency for Healthcare Research and Quality.
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PMID:Postmenopausal hormone replacement therapy for primary prevention of chronic conditions: recommendations and rationale. 1243 33

Women with obesity or/and diabetes form an increasing part of the peri- and post-menopausal women cared for by general practicioners and gynaecologists. Menopausal obese/diabetic women have a different hormonal milieu than lean women, with increased exposure to androgens and oestrogens. In spite of this, obese women experience more menopause-related symptoms, particularly vasomotor symptoms and urinary incontinence. Obese and diabetic women also have a higher risk of breast and endometrial cancer, dementia, coronary heart disease (CHD) and venous and arterial thromboembolism. Bone mineral density loss is variable yet diabetic women show a uniformly higher rate of fractures, partly through a greater likelihood of falls. Although oestrogen-progestagen-type hormone therapy (HT) -improves glycaemic control and the lipoprotein profile in diabetic women, HT should be used very cautiously in obese and diabetic postmenopausal women because of accrued risks of thrombosis and CHD. Instead, the primary goal is to stimulate physical activity which improves general fitness and body weight control during the menopause transition, and which reduces the risk of breast cancer and osteoporosis. Also, vitamin D sufficiency should be ensured together with a healthy calcium intake, but anti-osteoporosis drugs which strongly suppress bone remodelling should be used with caution.
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PMID:Menopause care for obese and diabetic women. 2547 79

The present review aims to ascertain whether different infertility etiologies share particular genes and/or molecular pathways with other pathologies and are associated with distinct and particular risks of later-life morbidity and mortality. In order to reach this aim, we use two different sources of information: (1) a public web server named DiseaseConnect ( http://disease-connect.org ) focused on the analysis of common genes and molecular mechanisms shared by diseases by integrating comprehensive omics and literature data; and (2) a literature search directed to find clinical comorbid relationships of infertility etiologies with only those diseases appearing after infertility is manifested. This literature search is performed because DiseaseConnect web server does not discriminate between pathologies emerging before, concomitantly or after infertility is manifested. Data show that different infertility etiologies not only share particular genes and/or molecular pathways with other pathologies but they have distinct clinical relationships with other diseases appearing after infertility is manifested. In particular, (1) testicular and high-grade prostate cancer in male infertility; (2) non-fatal stroke and endometrial cancer, and likely non-fatal coronary heart disease and ovarian cancer in polycystic ovary syndrome; (3) osteoporosis, psychosexual dysfunction, mood disorders and dementia in premature ovarian failure; (4) breast and ovarian cancer in carriers of BRCA1/2 mutations in diminished ovarian reserve; (5) clear cell and endometrioid histologic subtypes of invasive ovarian cancer, and likely low-grade serous invasive ovarian cancer, melanoma and non-Hodgkin lymphoma in endometriosis; and (6) endometrial and ovarian cancer in idiopathic infertility. The present data endorse the principle that the occurrence of a disease (in our case infertility) is non-random in the population and suggest that different infertility etiologies are genetically and clinically linked with other diseases in single meta-diseases. This finding opens new insights for clinicians and reproductive biologists to treat infertility problems using a phenomic approach instead of considering infertility as an isolated and exclusive disease of the reproductive system/hypothalamic-pituitary-gonadal axis. In agreement with a previous validation analysis of the utility of DiseaseConnect web server, the present study does not show a univocal correspondence between common gene expression and clinical comorbid relationship. Further work is needed to untangle the potential genetic, epigenetic and phenotypic relationships that may be present among different infertility etiologies, morbid conditions and physical/cognitive traits.
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PMID:Infertility etiologies are genetically and clinically linked with other diseases in single meta-diseases. 2658 2

Heart disease and cancer are the leading causes of death in the United States. In women, the clinical appearance of both entities-coronary heart disease and cancer (breast, endometrium, and ovary)-escalate during the decades of the midlife transition encompassing the menopause. In addition to the impact of aging, during the interval between the age of 40 and 65 years, the pathophysiologic components of metabolic syndrome also emerge and accelerate. These include visceral adiposity (measured as waist circumference), hypertension, diabetes, and dyslipidemia. Osteoporosis, osteoarthritis, sarcopenia, depression, and even cognitive decline and dementia appear, and most, if not all, are considered functionally related. Two clinical reports confirm the interaction linking the emergence of disease: endometrial cancer and metabolic syndrome. One describes the discovery of unsuspected endometrial cancer in a large series of elective hysterectomies performed in aged and metabolically susceptible populations. The other is from the Women's Health Initiative Observational Study, which found a positive interaction between endometrial cancer and metabolic syndrome regardless of the presence or absence of visceral adiposity. Both provide additional statistical support for the long-suspected causal interaction among the parallel but variable occurrence of these common entities-visceral obesity, heart disease, diabetes, cancer, and the prevalence of metabolic syndrome. Therefore, 2 critical clinical questions require analysis and answers: 1: Why do chronic diseases of adulthood-metabolic, cardiovascular, endocrine-and, in women, cancers of the breast and endometrium (tissues and tumors replete with estrogen receptors) emerge and their incidence trajectories accelerate during the postmenopausal period when little or no endogenous estradiol is available, and yet the therapeutic application of estrogen stimulates their appearance? 2: To what extent should identification of these etiologic driving forces require modification of the gynecologist's responsibilities in the care of our patients in the postreproductive decades of the female life cycle? Part l of this 2-part set of "expert reviews" defines the dimensions, gravity, and interactive synergy of each clinical challenge gynecologists face while caring for their midlife (primarily postmenopausal) patients. It describes the clinically identifiable, potentially treatable, pathogenic mechanisms driving these threats to quality of life and longevity. Part 2 (accepted, American Journal of Obstetrics & Gynecology) identifies 7 objectives of successful clinical care, offers "triage" prioritization targets, and provides feasible opportunities for insertion of primary preventive care initiatives. To implement these goals, a reprogrammed, repurposed office visit is described.
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PMID:The midlife transition and the risk of cardiovascular disease and cancer Part I: magnitude and mechanisms. 3249 14