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

The epidemiological patterns for pancreatic and biliary cancers reveal more differences than similarities. Pancreatic carcinoma is common in western countries, although 2 Polynesian groups (New Zealand Maoris and native Hawaiians) have the highest rates internationally. In the United States the disease is rising in frequency, predominating in males and in blacks. The rates are elevated in urban areas, but geographic analysis uncovered no clustering of contiguous counties except in southern Louisiana. The origin of pancreatic cancer is obsure, but a twofold increased risk has been documented for cigarette smokers and diabetic patients. Alcohol, occupational agents, and dietary fat have been suspected, but not proven to be risk factors. Except for the rare hereditary form of pancreatitis, there are few clues to genetic predisposition. In contrast, the reported incidence of biliary tract cancer is highest in Latin American populations and American Indians. The tumor predominates in females around the world, except for Chinese and Japanese who show a male excess. In the United States the rates are higher in whites than blacks, and clusters of high-risk counties have been found in the north central region, the southwest, and Appalachia. The distribution of biliary tumors parallels that of cholesterol gallstones, the major risk factor for biliary cancer. Insights into biliary carcinogenesis depend upon clarification of lithogenic influences, such as pregnancy, obesity, and hyperlipoproteinemia, exogenous estrogens, familial tendencies, and ethnic-geographic factors that may reflect dietary habits. Noncalculous risk factors for biliary cancer include ulcerative colitis, clonorchiasis, Gardner's syndrome, and probably certain industrial exposures. Within the biliary tract, tumors of the gallbladder and bile duct show epidemiological distinctions. In contrast to gallbladder cancer, bile duct neoplasms predominate in males; they are less often associated with stones and more often with other risk factors. In some respects, bile duct and pancreatic tumors are alike. The male predominance of both tumors, an association between cholecystectomy and pancreatic cancer, and other considerations have prompted the notion that the same biliary carcinogens may affect the bile duct, ampulla of Vater, or, by reflux, the pancreatic duct. Various epidemiological and interdisciplinary approaches are needed to further clarify the origins of biliary tract and pancreatic cancers, but nutritional studies hold special promise in laying the groundwork for prevention of these tumors.
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PMID:Cancers of the pancreas and biliary tract: epidemiological considerations. 110 53

New markers of increased risk to breast cancer are examined and related to established risk markers. The following new evidence is highlighted: (1) Increased testosterone secretion by the ovaries is currently the only major steroid abnormality shown to be associated with increased risk of both premenopausal and postmenopausal breast cancer. (2) Upper body-type obesity is a marker for both hyperandrogenaemia and hyperinsulinaemia and is associated with an increased risk of breast cancer. Upper body type obesity may already be recognised in early puberty in caucasian girls and is associated with a characteristic androgen/oestrogen profile. (3) Relative tallness in women is associated with an increased risk of breast cancer. A hypothesis is offered on the significance of these markers in the aetiology of mammary cancer in women, and also a means of testing the hypothesis. The hormonal promotion of mammary carcinogenesis is likely to be greatest between puberty and the first full term pregnancy. The presence of hyperinsulinaemia can increase the ovarian production of androgen, and the abnormal hormonal profile may stimulate proliferative activity in mammary epithelium. This may increase the risk of epithelial atypia and carcinogenesis.
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PMID:New hormone-related markers of high risk to breast cancer. 149 60

To investigate an association between colon cancer and obesity during early adulthood--a potentially important period in the etiology of this disease--the authors assembled, by computer linkage, a population-based historical cohort of 52,539 men born between 1913 and 1927 residing in Hawaii (USA), for whom weight and height had been recorded in 1942-43 and 1972. Linkage of this cohort to the Hawaii Tumor Registry resulted in the identification of 737 incident cases of colorectal cancer for 1972-86. An average of 3.8 cancer-free controls were matched to each case on month and year of birth and ethnicity of the parents. A case-control analysis in each anatomic subsite of the large bowel revealed that both early and middle-age body mass increased the risk of sigmoid cancer in men in a dose-dependent fashion. The odds ratios (OR) for sigmoid cancer for the highest compared with the lowest tertiles of Quetelet index were: 2.1 (95 percent confidence interval [CI] = 1.4-3.2) and 1.7 (CI = 1.1-2.5), at ages 15-29 and in prediagnostic years, respectively. These associations were additive and independent of socioeconomic status. Men who were above the median Quetelet index in 1942 and 1972 had an OR of 2.7 (CI = 1.8-4.0), compared with those who were below the median in both periods. This study provides further evidence for an association of obesity with colon cancer in men and suggests that this association is limited to the sigmoid colon and may be related to both early and late events of colon carcinogenesis.
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PMID:Obesity in youth and middle age and risk of colorectal cancer in men. 161 22

To further characterize the association of obesity and endometrial cancer, in particular with regard to the role of early-age obesity and adult weight gain, the authors assembled by computer linkage a population-based historical cohort of 30,266 women born between 1913 and 1932, for whom weight and height had been recorded in 1942-43 and 1972. Linkage of this cohort to the Hawaii Tumor Registry resulted in the identification of 214 (mainly post-menopausal) incident cases of endometrial cancer for 1972-1986. An average of 37 cancer-free controls were matched to each case on month and year of birth and ethnicity. A case-control analysis, conducted in each 5-year birth cohort, revealed no clear association of endometrial cancer with weight, height or body mass at ages 10 to 29 years. However, positive associations with adult body weight and gain in body mass since 1942 were observed for women diagnosed at age 60 or older. This association with obesity was strongest in women whose body mass was below the median in 1942 and equal to or above the median in 1972. No association with body size was detected in women diagnosed before age 60. Parity, age at first birth and socioeconomic indicators for 1942 and 1972 did not confound the analysis. These findings suggest that obesity affects the late stages of endometrial carcinogenesis, and the possibility that one or more determinants of weight gain may be independently associated with endometrial cancer risk.
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PMID:Early-age body size, adult weight gain and endometrial cancer risk. 186 Jul 27

Restriction of energy intake significantly reduces mammary tumorigenesis in normal rats exposed to carcinogens. Genetically obese LA/N-cp (corpulent) female rats were given 7,12-dimethylbenz[a]anthracene and fed purified diets ad libitum or restricted to 60% of the ad libitum caloric intake. Phenotypically lean littermates were also fed ad libitum. Obese animals developed large mammary tumors more rapidly than genetically normal rats so that 100% of the animals had tumors in less than 16 weeks. Only 21% of the lean animals developed tumors; the energy restricted obese animals had a tumor incidence of 27%. Although obese rats fed the restricted diet weighed significantly less than those fed ad libitum, percent body fat was not reduced, indicating that lean tissue was affected more. Obese animals were markedly hyperinsulinemic (1003 +/- 193 microunits/ml) and energy restriction reduced this to 328 +/- 41; the lean animals had insulin levels of 12 +/- 2. Tumor-bearing rats had higher insulin levels than rats without tumors. These data suggest that body fatness is not directly associated with risk of carcinogenesis. Lean body mass, adipose tissue mass, and their interaction with insulin in its capacity as a growth factor rather than body fatness per se may be determinants of tumor promotion.
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PMID:Reduction of enhanced mammary carcinogenesis in LA/N-cp (corpulent) rats by energy restriction. 190 Nov 69

The descriptive and analytical epidemiology of endometrial cancer is reviewed. Over the last few decades, age-standardized incidence rates have been rising in several countries. The rise has been even greater in terms of absolute numbers of cases, and hence public health implications, due to the aging of the population. Although endometrial cancer rates were found to be higher in richer countries and urban populations, there is now evidence of some changes in the socioeconomic determinants of the disease in developed countries. In etiological terms, any factor that increases exposure to unopposed estrogens (such as menopausal replacement treatment, obesity, and irregular menstrual cycles) tends to increase the risk of the disease, while factors that decrease exposure to estrogens or increase progesterone levels (such as oral contraceptives or smoking) tend to be protective. Less well defined, or more difficult to explain in biological terms, is the role of other factors, such as births, miscarriages, or diabetes and hypertension, and only suggestive evidence is available on diet from analytical epidemiology. The data reviewed herein are discussed in terms of models of carcinogenesis, as well as attributable risks and public health implications.
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PMID:The epidemiology of endometrial cancer. 202 52

The presence of the viable yellow Avy and lethal yellow Ay genes has been demonstrated to accelerate the process of tumorigenesis in mice bearing genetically, chemically or virally initiated cells. This promoting effect has been reported in the liver, lung, breast, bladder and skin. Although it has been demonstrated that the accelerated process is associated with systemic, pathophysiologic alterations such as an alteration in the lipogenic pathway, which in turn leads to obesity, alteration in glucose metabolism and/or random immunologic alterations, no examination of the in vitro 'tumorigenic' susceptibility of the cells of animals bearing the yellow genes has yet been reported. In the current study, spontaneous and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced transformation was determined in skin-derived fibroblasts from C57BL/6N-Avy/a mice (Hy) and their black a/a litter mates (B1-). The growth rate of untreated fibroblasts was greater for those from the yellow mice than from the black, while susceptibility to MNNG toxicity was equivalent. However, the rate of spontaneous and chemically induced transformation was consistently and significantly higher in the cells obtained from the black a/a mice than in those from yellow, Avy/a litter mates. These findings, with others from the literature, suggest that the Avy gene may suppress transformation and carcinogenic susceptibility in specific cells, such as fibroblasts, while the systemic effects of the gene are promotional in other cells.
Carcinogenesis 1991 Jul
PMID:Suppression of in vitro chemical transformation by the carcinogenesis-promoting, viable yellow gene Avy. 207 Apr 79

Females in western societies have higher plasma levels of high-density lipoprotein cholesterol (HDL-C) than males. The difference in plasma lipids between the sexes is believed to contribute to differences in risk of heart disease. The evidence reviewed here demonstrates that plasma levels of HDL-C are also associated with factors influencing risk of breast cancer, a leading cause of death in women in western societies. Both breast cancer risk and HDL-C levels are higher in women who live in northern European countries than in those who live in Asia, in women who have never been pregnant compared with those who have, and in women of higher socioeconomic status. HDL-C levels are also affected by several other known or suspected factors in breast cancer risk; these include dietary fat intake, alcohol consumption, endogenous hormones, and premenopausal leanness. Increases in any of these factors are known to increase the level of HDL-C. Preliminary work has also shown HDL-C levels to be higher in subjects with mammographic dysplasia and a family history of breast cancer. Further, in serum-free culture systems, HDL-C appears to possess biologic properties that may be relevant to carcinogenesis. In other areas, evidence of a relationship between increased HDL-C levels and increased breast cancer risk is either incomplete or contradictory. These areas include obesity (in the risk of postmenopausal breast cancer), use of exogenous hormones (oral contraceptives or postmenopausal estrogens), and physical exercise. In addition, both elevated and depressed levels of HDL-C have been reported in women with breast cancer. Our findings suggest an association between high HDL-C levels and the epidemiology of breast cancer risk. We recommend additional studies of plasma lipid level as a possible risk factor for this disease.
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PMID:Evidence of association between plasma high-density lipoprotein cholesterol and risk factors for breast cancer. 231 17

Obese mottled yellow Avy/a, lean pseudoagouti Avy/a and lean black a/a (YS X VY) F-1 hybrid female mice were fed diet containing 160 p.p.m. lindane (gamma-hexachlorocyclohexane) for 6, 12, 18 or 24 months. Clara cell hyperplasia was present in a majority of the mice after six months of lindane ingestion; however, more yellow mice (77%) than pseudoagouti (50%) or black (56%) mice had developed this lesion. Continued ingestion of lindane increased the incidence of Clara cell hyperplasia and resulted in similar prevalences in the three phenotypes. Lung tumors associated with lindane ingestion for 24 months were found only in yellow (19%) and pseudoagouti (14%) mice but not in the black mice. Prevalences of hepatocellular adenomas and carcinomas were very low (less than 10%) in untreated pseudoagouti and black mice. Lindane ingestion for 24 months resulted in an hepatocellular adenoma prevalence of 12% in pseudoagouti mice and 3% in black mice; comparable hepatocellular carcinoma prevalences were 5% and 1%. Among yellow mice fed lindane diet for 24 months, adenoma prevalence was 35% (9% among untreated controls) but carcinoma prevalence was only 17% (13% among controls). The tumorigenic responses evoked by lindane feeding in the lean pseudoagouti Avy/a mice but not in the black a/a mice indicate, for the first time, that the Avy gene itself, in the absence of obesity, sensitizes cells to transformation. The greater prevalence of hepatocellular adenomas in obese yellow Avy/a than in lean pseudoagouti Avy/a mice implicates obesity-associated factors in tumor promotion. Similarly, the increased prevalence of hepatocellular carcinomas in untreated obese yellow Avy/a mice, as compared to lean pseudoagouti mice, implicates obesity-associated factor as favoring histiotypic progression of liver tumors. Thus, the Avy gene not only sensitizes cells to respond to tumorigenic stimuli but also, by the induction of obesity, enhances promotion and progression of transformed cells.
Carcinogenesis 1987 Dec
PMID:Tumorigenic responses to lindane in mice: potentiation by a dominant mutation. 244 99

Epidemiological evidence for prenatal carcinogenesis includes associations between cancer in young people and intrauterine exposure to X-rays, drugs and hormones and prezygotic events such as specific chromosomal aberrations associated with specific cancers. Recent findings suggest that the hormonal environment during early gestation can result not only in the development of clear-cell adenocarcinoma of the vagina but also in the development of germ cell tumours of the testes and ovary. Hormone-related risk factors for testicular germ cell neoplasms include maternal use of exogenous oestrogens during early gestation and, possibly, maternal nausea, maternal obesity and race as well. Ovarian germ cell tumours also appear to be related to maternal use of hormones and obesity. Several epidemiological studies of cancer in young people have been directed towards suggested associations with parental occupational exposures, parental cigarette smoking and household exposures to electric and magnetic fields (EMF). The findings of the many studies of parental occupational exposures are inconsistent and are often nonspecific with respect to the type of childhood cancer and the job exposure implicated. Parental cigarette smoking has been associated in some studies with an increased risk for cancer among children and young adults, and in other studies with an increased risk among mature adults, but the findings are not consistent across studies. Three studies of all types of childhood cancer found risk to be related to household exposures to EMF; in all three, the risk for central nervous system tumours was increased, and in two of the three leukaemia risk as well. A fourth study showed no association between childhood leukaemia and EMF. A hypothesis is proposed which suggests that prenatal and early childhood exposure to N-nitroso compounds (NOC) may be related to the development of primary tumours of the brain in children. Experimentalists have shown that various NOC are potent nervous system carcinogens, particularly when animals are exposed transplacentally. This experimental model and findings from a Los Angeles case-control study (209 pairs) of brain tumours in young people led to the proposed epidemiological hypothesis. Although this and other epidemiological studies of NOC have major limitations, findings from epidemiological studies of congenital defects and of other childhood cancers lend the hypothesis some support. A large international collaborative case-control study of childhood brain tumours was begun recently. This study has a major advantage over most case-control studies in adults because the exposure period of greatest interest (gestation) is clearly defined.
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PMID:Epidemiological studies of perinatal carcinogenesis. 268 Sep 50


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