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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a worldwide population of 6 billion, in the year 2000, approximately 10 million cancers were diagnosed, and there were an estimated 6.2 million cancer deaths. Whereas the universality of cancer incidence and mortality is established, the burden of cancer by type or organ site is distributed unequally between developing and industrialized nations. Populations in developing countries are disproportionately affected by cancers in which infectious agents are causal. Our review of advances in cancer epidemiology underscores the complexity of pathogenic mechanisms mediated by chronic inflammation, obesity, and gene-environment interactions as in tobacco and alcohol carcinogenesis. Ultimately, the implementation of effective cancer control interventions that will serve to alleviate the cancer burden must integrate basic and applied research in the behavioral, social, biomedical, and population sciences.
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PMID:Advances in cancer epidemiology: understanding causal mechanisms and the evidence for implementing interventions. 1576 Feb 80

Epidemiological studies have found obesity to be a risk factor for women's breast cancer. The present study was to investigate whether there is a relationship between serum levels of leptin, insulin, and lipids and breast cancer incidence, in order to find experimental evidence that would be helpful in the diagnosis and prevention of breast cancer. Blood samples were collected from 130 patients with mammary disease and 103 healthy control subjects. Serum leptin, insulin, and lipids were determined by radioimmunoassay (RIA), enzyme-linked immunosorbent assays (ELISA), and Biochemistry Auto-analyzer, respectively. The data analysis was performed by use of the SPSS10.0 computer software. We found that the serum levels of leptin, insulin, and triglyceride (TG) were clearly higher in patients with breast cancer than in patients with benign breast disease and healthy controls, while serum HDL-C levels were lower in breast cancer patients (p < 0.03). Moreover, serum leptin levels were significantly correlated with BMI (body mass index) among three groups, whereas serum insulin levels were unrelated to BMI among three groups. Furthermore, the serum levels of leptin and insulin were not associated with menopausal status in patients with mammary disease (p > 0.05); however, the serum levels of F-Chol, T-Chol, TG, LDL-C, and APOB were significant higher in postmenopausal cases than those in premenopausal cases (p < 0.025). Interestingly, logistic regression analysis showed that subjects with elevated serum levels of leptin, insulin, TG, APOA1, and reduced level of serum HDL-C displayed increased risk of developing breast cancer than those with the normal levels, respectively. In conclusion, the present study suggested that aberrant serum levels of leptin, insulin, and lipids might play an important role in carcinogenesis of breast cancer. The elevated serum levels of leptin, insulin, TG, APOA1, and reduced level of serum HDL-C may be correlated with increased risk of breast cancer, suggesting that one way of preventing breast cancer would be carried out by controlling the intake of food.
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PMID:Serum levels of leptin, insulin, and lipids in relation to breast cancer in china. 1580 81

The majority of modern hormone replacement therapy (HRT) regimens contain estrogen and progestogens, given either in a cyclical or continuous manner. About 15% of the endometrial biopsies taken from women on sequential HRT show proliferative activity including atypical endometrial hyperplasia in up to 1% of the cases. The majority of biopsies from women under continuous combined HRT show an endometrial atrophy. About 2-3% of these women will present proliferative activity, usually without atypical hyperplasia. Contrary to breast cancer, an increased risk of endometrial cancer has not been reported in the WHI- and HERS-studies. However, endogenous factors, such as obesity, diabetes mellitus, the distribution of estrogen receptors alpha and beta and genetic polymorphisms for receptors and enzymes might alter the endometrial stimulation under different types of HRT. There should be a liberal indication for endometrial biopsies in Hereditary Non-Polyposis Colorectal Cancer (HNPCC). HNPCC-patients under HRT as well as for ultrasonographic evaluation of the endometrium. The risk of atypical hyperplasias or carcinoma under unopposed estrogen-therapy varies from 2 to 10%. So, this kind of HRT should not be used in non-hysterectomised women. As far as the risk of endometrial cancer under any kind of HRT is concerned, the different molecular pathways of endometrial carcinogenesis (type 1 and 2 cancers) should be taken into account. The use of tibolone leaves the endometrium unaffected.
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PMID:Hormone replacement therapy (HRT) and endometrial morphology under consideration of the different molecular pathways in endometrial carcinogenesis. 1592 47

The development of effective cancer preventive interventions is being enhanced by the use of relevant animal models to confirm, refine, and extend potential leads from clinical and epidemiologic studies. In particular, genetically altered mice, with specific cancer-related genes modulated, are providing powerful tools for studying carcinogenesis, as well as important conduits for translating basic research findings from the laboratory bench to the bedside. This review explores the utility of genetically altered mice for developing cancer preventive strategies that can offset increased cancer susceptibility resulting from specific genetic lesions. Examples will focus on preventing cancer by dietary interventions, particularly obesity prevention/energy balance modulation, as well as chemoprevention, in mice with alterations in genes such as the p53 or Apc tumor suppressors, components of the ErbB pathway, and other pathways frequently altered in human cancer.
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PMID:The utility of genetically altered mouse models for nutrition and cancer chemoprevention research. 1599 Jan 22

The prevalence of obesity has markedly increased over the past two decades, especially in the industrialized countries. While the impact of excess body weight on the development of cardiac disease and diabetes has been well documented, the link between obesity and carcinogenesis is just being recognized. This review will focus on the link between leptin, a cytokine that is elevated in obese individuals, and cancer development. First, we briefly discuss the biological functions of leptin and its signaling pathways. Then, we summarize the effects of leptin on different cancer types in experimental cellular and animal models. Next, we analyze epidemiological data on the relationship between obesity and the presence of cancer or cancer risk in patients. Finally, leptin as a target for cancer treatment and prevention will be discussed.
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PMID:Leptin and cancer. 1611 Apr 83

The beta3-adrenergic receptor (beta3-AR) may play a key role in the regulation of lipid metabolism and glucose homeostasis. Adrenaline and noradrenaline beta3-AR stimulate lipolysis and thermogenesis in human fat cells and increase glucose uptake in skeletal muscle. Therefore, the beta3-AR gene may be associated with obesity and related diseases, such as type 2 diabetes, coronary heart disease and hypertension. Many studies in different ethnic groups showed an association of beta3-AR gene polymorphism with insulin resistance, obesity and its metabolic disorders such as type 2 diabetes, coronary heart disease and hypertension. A Trp64Arg mutation in the beta3-AR gene has been reported to be correlated with the occurrence of those disorders among obese. Several studies revealed also the influence of the Trp/Arg polymorphism on carcinogenesis and its contribution to the link between cancer and obesity. Since obesity is a serious problem as a civilization-related disease, it is very important to investigate genes suspected to be connected with it.
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PMID:[Beta3-adrenergic receptor]. 1620 45

The natural history of Non Alcoholic Fatty Liver Disease (NAFLD) is difficult to assess, but there is mounting evidence that patients with NAFLD may eventually develop cirrhosis and hepatocellular carcinoma (HCC). Retrospective, case-control studies have shown that features suggestive of Non Alcoholic SteatoHepatitis (NASH) are more frequent in HepatoCellular Carcinoma (HCC) complicating cryptogenic cirrhosis than in matched HCC patients with known etiology. In the only available prospective cohort study, there is the absence of HCC as a complication of NASH-associated cirrhosis after a mean follow up of 7 years (median 5 years). However prospective NASH studies are too short to exclude late complications. In fact the average lenght of cirrhosis before the diagnosis of HCC was 16 years. The prevalence of risk factors associated with NASH can account for the increasing incidence of cryptogenic cirrhosis and subsequent HCC. Obesity and diabetes per se are significantly associated with the development of HCC. In particular diabetes was found to be a risk factor for HCC independent of age, gender, and race. Chronic hyperinsulinaemia and insulin-like growth factor 1 (IGF-1) might be involved in hepato-carcinogenesis. Exposure to physiological insulin concentrations stimulate proliferation of human and rat hepatoma cell line. Changes in the expression pattern of IGF-system components has been observed in patients with HCC, in human hepatoma cell lines and in their conditioned culture medium.
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PMID:Steatosis and hepatocellular carcinoma risk. 1623 92

Adipose tissue-produced hormones significantly affect the metabolism of lipids and carbohydrates as well as numerous other processes in human body. It is generally accepted that endocrine dysfunction of adipose tissue may represent one of the causal links between obesity and insulin resistance/diabetes. Epidemiological studies underlined that obesity represents a significant risk factor for the development of cancer, although the exact mechanism of this relationship remains to be determined. Multiple recent studies have indicated that some of adipose tissue-derived hormones may significantly influence the growth and proliferation of tumorous stroma and malignant cells within. Here we review current knowledge about possible relationship of leptin and adiponectin to the etiopathogenesis of different malignant tumors. Most of the studies indicated that while leptin may potentiate the growth of cancer cells in vitro, adiponectin appears to have an opposite effect. Further studies are necessary to decide whether obesity-induced endocrine dysfunction of adipose tissue can directly influence carcinogenesis in different tissues and organs.
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PMID:Adipocytokines and cancer. 1623 54

The metabolic syndrome, defined as a cluster of visceral obesity, insulin resistance, dyslipidemia and elevated blood pressure, is associated with pro-thrombotic, pro-atherogenic and inflammatory risk factors that predispose to cardiovascular disease. Although activators of the peroxisome proliferator-activated receptors (PPARalpha,gamma,delta) in various combinations are under development for treating the metabolic syndrome, they are hampered by adverse effects related to increased adipogenesis, weight gain, fluid overload and carcinogenesis. The recent discovery that telmisartan and irbesartan, antihypertensive angiotensin II type 1 receptor (AT1-R) blockers (ARBs), were uniquely capable of activating PPARgamma, has provided a novel approach to addressing the multifactorial components of the metabolic syndrome. Both drugs have established favorable safety profiles and can activate PPARgamma at concentrations potentially achievable at therapeutic doses. Emerging studies have revealed that both these drugs have beneficial metabolic profiles. This information provides a strategic rationale and pharmacological platform for the development of novel dual ARB/PPARgamma agonists to target the metabolic syndrome and its cardiovascular sequelae, for which therapy is presently insufficient or non-existent. Beneficial effects of these agents include increased energy expenditure, improved lipid profile, increased insulin sensitivity, blood pressure reduction, and amelioration of the associated pro-inflammatory and pro-atherogenic risk profiles. The potential benefit for treatment of the metabolic syndrome, cardiovascular protection, and prevention of related end-organ complications could be of immense clinical value.
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PMID:Treating the metabolic syndrome using angiotensin receptor antagonists that selectively modulate peroxisome proliferator-activated receptor-gamma. 1629 56

We have recently proposed a common mechanistic pathway by which obesity and hypertension lead to increased renal cell cancer risk. Our hypothesis posits lipid peroxidation, which is a principal mechanism in rodent renal carcinogenesis, as an intermediate step that leads to a final common pathway shared by numerous observed risks (including obesity, hypertension, smoking, oophorectomy/hysterectomy, parity, preeclampsia, diabetes, and analgesics) or protective factors (including oral contraceptive use and alcohol) for renal cell cancer [Cancer Causes Control 2002;13:287-93]. During this exercise, we have noticed how certain risk factors for renal cell carcinoma are protective for breast cancer and how certain protective factors for renal cell carcinoma increase risk for breast cancer. Parity and oophorectomy, for example, are positively associated with renal cell carcinoma but are negatively associated with breast cancer. Similarly, obesity and hypertension are positively associated with renal cell carcinoma, but obesity is negatively associated with breast cancer in premenopausal women and hypertension during pregnancy is negatively associated with breast cancer. Furthermore, alcohol intake, negatively associated with renal cell carcinoma, is also positively associated with breast cancer. We propose here the possibility that lipid peroxidation may represent a protective mechanism in breast cancer. Although this runs counter to the conventional view that lipid peroxidation is a process that is harmful and carcinogenic, we present here the chemical and biological rationale, based on epidemiologic and biochemical data, which may deserve further consideration and investigation.
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PMID:Role of lipid peroxidation in the epidemiology and prevention of breast cancer. 1636 97


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