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

Obesity is known to adversely affect breast cancer prognosis. Since obesity is associated with increased oestrogen levels, and oestrogens are growth stimulators of oestrogen receptor (ER)-positive breast carcinomas, we evaluated the relationship between the ER and progesterone receptor (PR) status of the neoplastic tissue and obesity in a series of 615 breast cancer patients. Both ER and PR concentrations were significantly and positively correlated with obesity by multiple regression analysis. Furthermore, the estimated probability of having an ER+/PR+carcinoma was significantly higher in obese patients (odds ratio 2.65, 95% confidence interval 1.56-4.48). This association between receptor-positive status and obesity was observed both in premenopausal and postmenopausal patients. Our data suggest, therefore, that obesity plays a role in determining the ER status of breast cancer and raise the possibility that ER presence in breast carcinomas occurring in obese patients is not indicative of a favourable prognosis.
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PMID:Relation between steroid receptor status and body weight in breast cancer patients. 156 60

An Australian study of 513 women evaluated associations between obesity and both benign and malignant breast disease, and in particular investigated the role of female sex hormones. Women who gained more than 10 kg from early womanhood had a two-fold increase in risk of developing breast cancer, whereas lean women had a greater risk of being treated for benign breast disease. Obese women with breast cancer were more likely to have Stage II tumors but there was no significant association between obesity and tumor size or estrogen and progesterone receptor status. Obesity was strongly associated with the proportions of nonprotein-bound and albumin-bound estradiol, and inversely associated with sex hormone binding globulin (SHBG) levels and the proportion of SHBG-bound estradiol. In addition, age at menarche was inversely associated, and age at menopause directly associated with recalled weight at those time periods. These data demonstrate weight gain as a risk factor for breast cancer, and suggest a possible mechanism supporting its development.
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PMID:Obesity and breast disease. The role of the female sex hormones. 275 82

The relationship between obesity and breast cancer has been investigated in 1281 Auckland breast cancer patients. Using a definition of obesity as a Body Mass Index (BMI) of greater than or equal to 28 kg/m2, 179 (14%) breast cancer patients were classified as obese. The heights, weights, and BMI of 822 breast cancer patients aged 35-64 compared to 518 randomly selected Auckland women of similar age showed no significant difference. Within the breast cancer patients, there was no variation in nodal status or estrogen and progesterone receptor status between obese and non-obese women. However, tumours greater than 5 cm occurred significantly more often in obese patients. Time to recurrence was reduced in obese women with tumours less than or equal to 5 cm, no tumour in the axillary nodes, positive estrogen or progesterone receptor, and without metastases at the time of presentation of the disease. Although obesity has not been shown to influence breast cancer incidence, an effect on tumour recurrence is seen in patients with less advanced disease. This is similar to other reports which suggest that obesity is a weak but positive risk factor for recurrence.
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PMID:Influence of height, weight, and obesity on breast cancer incidence and recurrence in Auckland, New Zealand. 362 Jul 16

An association between hormone receptors in primary breast cancer and obesity determined prior to mastectomy was investigated in 128 Japanese women. The following criteria for obesity were used: (1) weight greater than or equal to 60 kg (132 lbs), (2) weight kg/height cm-105 greater than or equal to 1.3, (3) weight lbs/height in greater than or equal to 2.30, (4) body surface area greater than or equal to 1.56 m2. In view of the 4 criteria, tumor estrogen receptor (ER) values greater than or equal to 4 fmol/mg were observed in obese patients more often than in nonobese patients, though the difference was not statistically significant. The same tendency was observed in the postmenopausal subgroup, 62 patients, especially in the 36 patients more than 5 years beyond menopause. However, there was still no statistical difference between obese and nonobese patients because the number of subjects was small. The same tendency was observed in the case of progesterone receptor (PgR) (greater than or equal to 6 fmol/mg) as observed in the case of ER.
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PMID:Hormone receptors and obesity in Japanese women with breast cancer. 734 70

Epidemiologic studies suggest that ovarian hormones contribute to the development of breast cancer at all stages. Early menopause and premenopausal obesity reduces the risk while postmenopausal obesity and menopausal estrogen replacement therapy increases the risk. Combined oral contraceptives and Depo-Provera do not reduce the risk. It appears that estrogens and progestogens act through and with proto-oncogenes and growth factors to affect breast cell proliferation and breast cancer etiology. Animal studies suggest that estrogen causes interlobular ductal cell division and progesterone causes increased terminal duct lobular unit cell division in the luteal phase. Most breast carcinomas originate from terminal duct lobular unit cells. During pregnancy, these cells fully multiply. Their reproduction is also increased during the luteal phase. Yet, there is considerable interpersonal variation. No studies examining breast cell division have compared cell division rates with serum hormone concentrations, however. The peak of mitosis occurs about 3 days before breast cell death in the late luteal and very early follicular phases. Other research suggests that breast stem cell proliferation is linked to breast cancer development. Endocrine therapy reduces mitotic activity, indicating the estrogen and progesterone receptor content of breast cancers. Hormone-dependent breast cancer cell lines are all estrogen-dependent. Progesterone can block the estrogen-dependent cell lines which act like endometrial cells. The results of the various breast cell proliferation studies in relation to breast cancer are unclear and research identifying a molecular explanation would help in understanding the different findings.
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PMID:Estrogens, progestogens, normal breast cell proliferation, and breast cancer risk. 840 1

Differing risk factors between men and women for a number of vascular and metabolic diseases have been linked to regional obesity. The differences in the distribution of adipose tissues between men (abdominal or upper-body obesity) and women (gluteal/femoral or lower body obesity) suggest a role for sex steroids in the regional distribution of fat. Previous work from this laboratory has shown the presence of oestrogen receptor (ER) in gluteal, perirenal and omental adipose tissues of ewes with similar physical characteristics to the ER in uterine tissue. The concentration profile for adipose ER was gluteal > perirenal > omental. In this report, we determined the physiological significance of adipose ERs by showing an up-regulation of the progesterone receptor (PR) in adipose tissues after oestrogen treatment in a fashion similar to that seen in a major responsive tissue such as uterus. Using PR antibodies (PR-6 and C-262), Western blot analysis of PR from oestrogen-treated sheep indicated that PR was induced in uterus >>> gluteal adipose > perirenal adipose consistent with the concentration of ER contained in these tissues. PR could not be detected by Western blotting in omental adipose tissue from oestrogen-treated animals or in gluteal, perirenal and omental adipose tissues from untreated animals. Sucrose gradient profiles of progestin (R-5020) binding from uterus and gluteal adipose tissues of oestrogen-treated ewes showed specific binding in both the 5S and 9S regions of the gradient, while perirenal and omental adipose tissue had only the 5S peak. The amount of specific binding was increased with oestrogen treatment in all the tissues. When gluteal adipose tissue cytosol was preincubated with PR antibody (C-262) to prevent binding of ligand and subjected to sucrose gradient analysis, both the 5S and 9S regions were diminished, suggesting that both peaks contained PR. Dilution of uterine cytosol resulted in an increase in the ratio of the 5S to the 9S peak, indicating that the 9S PR complex dissociates at low concentrations; this may be the reason why only the 5S peak was observed in perirenal and omental adipose tissues. These data offer further support for a direct role of sex steroids in regional adipose accretion and metabolism.
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PMID:Regional differences and up-regulation of progesterone receptors in adipose tissues from oestrogen-treated sheep. 856 67

The present study consists of 1,238 women with unilateral breast cancer treated with modified radical mastectomy living in the geographic area of Haukeland Hospital. Their weight and height had been measured years before presentation of the disease. Age-adjusted Quetelet's index (weight/height2) showed that obese women had a 49% higher risk of dying from breast cancer than lean ones. The relative risk decreased slightly when adjusted for tumour diameter, lymph node status, and mean nuclear area of the tumour cells. The prognostic effect of Quetelet's index was examined according to the estrogen and/or progesterone receptor status of the tumour. In patients with a hormone receptor positive tumour, obese women had a risk that was more than three times higher than lean ones. In patients with hormone receptor negative tumour, the effect of obesity was reversed, lean patients having a risk that was more than six times higher than obese ones, even after adjustment for lymph node status, tumour diameter, and mean nuclear area. Quetelet's index, while being a prognostic variable in its own right, thus acts differently in patients with hormone receptor positive and negative tumours.
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PMID:Pre-morbid body-mass-index in breast cancer: reversed effect on survival in hormone receptor negative patients. 894 30

Blood-glucose and insulin were assayed by administering 40 g/sq.m glucose (per os) and 0.08 unit/kg body weight in 113 patients with early-stage breast tumors (glucose-tolerance test) and in 62 patients (insulin-sensitivity test). Sensitivity to insulin was assessed versus age, reproductive status, body size and smoker/non-smoker status. A direct correlation between high level of reactive insulinemia and obesity and an inverse one--between sensitivity to insulin and age were established on the basis of insulin test data and the insulin resistance factor. Smokers showed, on the average, lowered basal insulin levels and increased sensitivity to insulin (depending on age and number of cigarettes consumed). Smoking was found to influence prolactin reaction to hypoglycemia and to upset the correlation between age and progesterone receptor concentration in tumor which may account for certain peculiarities of the course of the disease in smokers with breast tumors.
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PMID:[Blood insulin and insulin sensitivity in breast cancer patients of various ages: the effect of smoking]. 957 30

A historical-prospective study is being conducted to determine whether there is a relationship between obesity and breast cancer recurrence and survival in African-American women. The primary data sources for the study are the medical record and cancer registry abstract. It has been found that data items such as occupation, menopausal status, height, weight, estrogen receptor and progesterone receptor values, stage, tumor size, number of positive nodes, family history of cancer, and tumor status are not always documented. Suggestions for improving documentation of the primary data sources are provided.
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PMID:Obstacles encountered in the use of the medical record and cancer registry abstract in breast cancer research. 1015 40

The purpose of this study was to determine prognostic significance of age and race as independent variables and to see role of age at the onset of breast carcinoma. A retrospective study was conducted of African American and white women with breast cancer treated at SUNY-Health Science Center Brooklyn and Kings County Hospital Center from 1983 to 1993. The objective was to analyze the differences in patterns of disease onset, as related to age and prognostic factors. A total of 738 patients were analyzed for race-adjusted comparison of stage, grade, disease-free survival, and median survival. Age at the time of diagnosis was analyzed to conduct age-specific comparisons of African American (AA) and white patients. The multivariate analysis indicated that AA women develop breast cancer 10 years earlier than white women (p = 0.00001). Corrected by stage and grade, i.e., chi2 test for stage-by-stage and grade-by-grade analysis has revealed that the AA women present with higher stage (p = 0.009), increased number of positive nodes (p = 0.00007), and more estrogen receptor/ progesterone receptor-negative tumors (p = 0.005). Further studies are required to probe into the etiologic possibilities of this significant difference. The important contributing factors could be hormonal, genetic, environmental, and socioeconomic. Obesity and dietary factors also need to be evaluated. Further studies to explore genetic susceptibility by ploidy is recommended to explain this significant difference. We conclude that the onset of breast cancer among AA women occurs at a significantly younger age than in white women, and their prognostic factors are poorer.
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PMID:Early onset of breast carcinoma in African American women with poor prognostic factors. 1052 Oct 53


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