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Query: UMLS:C0006142 (breast cancer)
 160,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Breast cancer is a major health problem in America, accounting for almost one-third of cancer-related deaths in women. The prevention of breast cancer through dietary modification is an active area of clinical and epidemiologic research. It has been proposed that the dietary supplementation of vitamin E, a lipid-soluble antioxidant, may reduce a woman's risk of developing breast cancer. In animal models, vitamin E has decreased the incidence of carcinogen-induced mammary tumors. Intake and serum levels of vitamin E and their relation to breast cancer have been evaluated in epidemiologic studies. Results of epidemiologic studies, however, have been conflicting. In this review, we examine the evidence that is available pertaining to the relationship between vitamin E and breast cancer. Although epidemiologic study results have been inconsistent, further study of this nontoxic vitamin is warranted. Particular attention should be paid to the interactions of other antioxidants with vitamin E and to the duration and timing (pre- vs. postmenopausal) of vitamin E use in determining its preventive utility in breast cancer.
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PMID:Vitamin E and breast cancer: a review. 912 36

The purpose of this study was to document induction of apoptosis by vitamin E succinate (VES; RRR-alpha-tocopheryl succinate) in human breast cancer cells in culture and to characterize potential c-jun involvement. VES at 18.8 microM (10 micrograms/mL) induced DNA synthesis arrest, reduced total cell numbers, and induced apoptosis in estrogen receptor-positive and estrogen-responsive MCF-7 human breast cancer cells. VES at 10 micrograms/mL induced apoptosis in greater than 60% of cells within 3 d of treatment. Apoptosis was documented by detection of fragmented or condensed nuclei in 4',6-diamindino-2-phenylindole-stained cells, detection of terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeled DNA, and DNA laddering. Analyses of mRNA and protein levels of candidate molecules involved in apoptosis showed that MCF-7 cells treated with VES exhibited elevated and persistent expression of c-jun. MCF-7 cells stably transfected with a dominant-negative interfering mutant c-jun, TAM-67, and expressing high levels of mutant jun exhibited approximately 50% blockage of VES-mediated apoptosis. In addition to increased c-jun expression after VES treatment, VES-treated MCF-7 cells exhibited elevated activator protein-1 (AP-1) binding activity. Comparisons of AP-1 binding factors by super-shift analyses with jun-specific antibodies in cells sensitive to VES-induced apoptosis (empty-vector control 7-1 cells) and cells resistant to VES-induced apoptosis (TAM-67-containing TAM-9 cells) showed that the sensitive cells expressed c-jun and jun D and the resistant cells TAM-67 AP-1 binding proteins after VES treatment. These studies suggested that c-jun may be involved in the apoptotic process initiated by VES treatment of human MCF-7 breast cancer cells.
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PMID:Involvement of activator protein-1 (AP-1) in induction of apoptosis by vitamin E succinate in human breast cancer cells. 925 85

The relationship between diet and breast cancer has been analyzed by animal, ecologic, migrant, and epidemiologic studies. The 14 cohort and 33 case-control studies that have been published to date are reviewed in this article. Factors considered in these studies include caloric intake, as well as fat, protein, fiber, beta-carotene, and vitamin E and C consumption. The results of the published studies are summarized, and the point estimates of the risks corresponding to the highest category of consumption as compared to the lowest are presented in figures. Some of the disagreements among studies could be explained by the methodologic difficulties inherent in dietary investigations, such as the establishment of an accurate dietary history, or insufficient diversity in exposure. Further studies taking these points into account and minimizing biases inherent to a case-control design might help to elucidate the relationship between diet and breast cancer, and to define dietary recommendations. Only large long-term cohort studies such as are now in progress can help to resolve the still unanswered questions concerning the contribution of these dietary factors to the risk of breast cancer. We suggest the establishment of new dietary cohorts and the continued follow-up of the existing cohorts.
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PMID:Diet and breast cancer: review of the epidemiologic literature. 930 46

The relationship between selected foods and nutrients and breast cancer risk was investigated in strata of age and menopausal status using data from a case-control study on breast cancer conducted between June 1991 and April 1994 in six Italian areas. Cases were 2,569 women with histologically confirmed incident breast cancer admitted to the major teaching and general hospitals of the study areas; controls were 2,588 women with no history of cancer admitted to hospitals in the same catchment area as cases for acute, nonneoplastic, nongynecological conditions unrelated to hormonal or digestive tract diseases or to long-term modifications of diet. Dietary habits were investigated using a validated food frequency questionnaire, including 78 foods or food groups. Among food groups, bread was directly and significantly related to breast cancer risk in older women and, consequently, in postmenopause, whereas the protection conferred by fish consumption was stronger in postmenopause and that exerted by raw vegetables was stronger in premenopause. Among nutrients, unsaturated fatty acids were inversely related to breast cancer risk, the association being stronger in postmenopausal and elderly women. The pattern was similar for total fats. For starch, available carbohydrates, and total proteins, no heterogeneity emerged across strata of age and menopausal status. Among micronutrients, protection diminished with increasing age for beta-carotene and calcium, whereas no heterogeneity emerged for vitamin E. Thus this age-specific analysis of the largest investigation to date on diet and breast cancer did not show any consistent pattern of breast cancer risk in relation to selected dietary factors across strata of age and menopausal status.
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PMID:Intake of selected foods and nutrients and breast cancer risk: an age- and menopause-specific analysis. 934 34

A large part of the epidemiological debate on diet and breast cancer has been dominated by the issue of whether fat, particularly animal fat, increases risk. Lately, the possible protective effect of various dietary constituents has received more attention. Vitamins C and E, and beta-carotene have antioxidant activity and may thus provide a cellular defence against reactive oxygen species that damage DNA. Dietary fibre may influence oestrogen metabolism. A large case-control study (2,569 breast cancer and 2,588 hospital controls) conducted in six Italian areas between 1991 and 1994 suggested that a diet rich in several micronutrients was associated with significantly lowered risk. After allowance for non-dietary risk correlates, energy intake and the mutual confounding effect of the various micronutrients, beta-carotene, vitamin E and calcium were associated with odds ratios in the highest intake quintile compared to the lowest one of 0.84, 0.75 and 0.81, respectively. Among different types of fibre, only cellulose intake showed a moderate inverse association. Evidence from other studies suggests that a favourable role of some micronutrients is possible, albeit probably less important than for cancers of the stomach and colon-rectum. Indeed, the relationship between fruit and vegetable intake is also less marked/consistent for breast cancer than for other sites. Among agents that have only recently been investigated, isoflavones, which are weak oestrogens, are of particular interest.
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PMID:Micronutrients and breast cancer. 949 55

The purpose of this study was to assess the validity and reproducibility of an interviewer-administered, semi-quantitative food frequency questionnaire (FFQ) among 132 volunteer New Mexico Hispanic (H) and non-Hispanic white (NHW) women, aged 35-74 years, with (n = 47) and without (n = 85) a breast cancer history, and to add to the limited data presently available on the performance of FFQs among different ethnic groups. Validity was measured at one month and six months from baseline against four-day food records, and reproducibility was tested by comparing FFQs. Unadjusted validity correlation coefficients were highest at one month, ranging from 0.38 (polyunsaturated and monounsaturated fat) to 0.57 (calcium); energy-adjusted correlation coefficients were highest at six months, ranging from 0.15 (polyunsaturated fat) to 0.68 (calcium). Energy-adjusted correlation coefficients were statistically significant by ethnicity for vitamins A and C, protein, carotene and calcium, and by case status for saturated fat, folate, fiber, and vitamins A and E. Reproducibility correlation coefficients (unadjusted) ranged from 0.40 (polyunsaturated fat) to 0.71 (carbohydrate, retinol); energy-adjusted correlation coefficients ranged from 0.42 (vitamin E) to 0.78 (fiber), and differed significantly by ethnicity for saturated fat and retinol, and by case status for carbohydrate. Overall, our FFQ has comparable characteristics to other FFQs and is suitable for use with New Mexico's H and NHW women.
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PMID:Validity and reproducibility of a food frequency questionnaire among Hispanic and non-Hispanic white women in New Mexico. 959 51

Potential antiproliferative effects of tocotrienols, the major vitamin E component in palm oil, were investigated on the growth of both estrogen-responsive (ER+) MCF7 human breast cancer cells and estrogen-unresponsive (ER-) MDA-MB-231 human breast cancer cells, and effects were compared with those of alpha-tocopherol (alphaT). The tocotrienol-rich fraction (TRF) of palm oil inhibited growth of MCF7 cells in both the presence and absence of estradiol with a nonlinear dose-response but such that complete suppression of growth was achieved at 8 microg/mL. MDA-MB-231 cells were also inhibited by TRF but with a linear dose-response such that 20 microg/mL TRF was needed for complete growth suppression. Separation of the TRF into individual tocotrienols revealed that all fractions could inhibit growth of both ER+ and ER- cells and of ER+ cells in both the presence and absence of estradiol. However, the gamma- and delta-fractions were the most inhibitory. Complete inhibition of MCF7 cell growth was achieved at 6 microg/mL of gamma-tocotrienol/delta-tocotrienol (gammaT3/deltaT3) in the absence of estradiol and 10 microg/mL of deltaT3 in the presence of estradiol, whereas complete suppression of MDA-MB-231 cell growth was not achieved even at concentrations of 10 microg/mL of deltaT3. By contrast to these inhibitory effects of tocotrienols, alphaT had no inhibitory effect on MCF7 cell growth in either the presence or the absence of estradiol, nor on MDA-MB-231 cell growth. These results confirm studies using other sublines of human breast cancer cells and demonstrate that tocotrienols can exert direct inhibitory effects on the growth of breast cancer cells. In searching for the mechanism of inhibition, studies of the effects of TRF on estrogen-regulated pS2 gene expression in MCF7 cells showed that tocotrienols do not act via an estrogen receptor-mediated pathway and must therefore act differently from estrogen antagonists. Furthermore, tocotrienols did not increase levels of growth-inhibitory insulin-like growth factor binding proteins (IGFBP) in MCF7 cells, implying also a different mechanism from that proposed for retinoic acid inhibition of estrogen-responsive breast cancer cell growth. Inhibition of the growth of breast cancer cells by tocotrienols could have important clinical implications not only because tocotrienols are able to inhibit the growth of both ER+ and ER- phenotypes but also because ER+ cells could be growth-inhibited in the presence as well as in the absence of estradiol. Future clinical applications of TRF could come from potential growth suppression of ER+ breast cancer cells otherwise resistant to growth inhibition by antiestrogens and retinoic acid.
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PMID:Tocotrienols inhibit the growth of human breast cancer cells irrespective of estrogen receptor status. 962 93

We have demonstrated that RRR-alpha-tocopheryl succinate (10 microg/mL vitamin E succinate (VES) treatment of estrogen receptor-negative MDA-MB-435 human breast cancer cells induces 9, 19, 51, and 72% apoptotic cells on days 1-4, respectively, after treatment, which involves transforming growth factor-beta signaling. Here, we show that VES-triggered apoptosis of MDA-MB-435 cells induced prolonged elevated expression of c-jun mRNA and protein (neither of which was caused by major increases in stability) and also induced enhanced activator protein-1 (AP-1) binding to the consensus DNA oligomer. Furthermore, VES treatments resulted in increased AP-1 transactivation activity, as measured with an AP-1 promoter/luciferase reporter construct and by the measurement of increased mRNA expression of the AP-1-dependent endogenous gene collagenase. Evidence of VES-induced involvement of the c-jun amino-terminal kinase in these AP-1-dependent events was suggested by data showing prolonged activity of this kinase, as measured by a kinase assay using glutathione S-transferase-c-jun as the substrate. The c-jun-dependent transcriptional activity was verified by cotransfection of a chimeric transcription factor having a galactose 4 DNA-binding domain coupled with the transactivation domain of c-jun plus the reporter plasmid 5X GAL4-luciferase. MDA-MB-435 cells infected with an adenovirus expression vector containing the TAM-67 sequence for dominant/negative-acting mutant c-jun or transiently transfected with c-jun antisense exhibited a 50-77% reduction in VES-mediated apoptosis as compared with control adenovirus-infected or control sense oligomer-transfected cells.
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PMID:RRR-alpha-tocopheryl succinate induction of prolonged activation of c-jun amino-terminal kinase and c-jun during induction of apoptosis in human MDA-MB-435 breast cancer cells. 972 17

A large case-control study (2,569 women with breast cancer and 2,588 control women) carried out in Italy between 1991 and 1994 permits elucidation of breast cancer risk in relation to dietary patterns in a southern European population. Major findings include direct associations with the intake of bread and cereal dishes, sugar, and pork meat, and inverse associations with the intake of vegetable oils, raw vegetables, fish, beta-carotene, vitamin E, and calcium.
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PMID:Diet and risk of breast cancer: major findings from an Italian case-control study. 975 3

Menopause is an expected event in a woman's life. Treatment for breast cancer can impact the onset of menopause and precipitate symptoms such as hot flashes. Yet this sequelae of events is not well measured, defined or assimilated into quality of life assessments for cancer survivors. Though not life threatening, hot flashes can greatly impact a woman's quality of life or functional ability. It is important for health care professionals to more fully understand the nature of the experience of hot flashes so as not to underestimate their disruptive potential. As part of a larger clinical trial to look at the effectiveness of vitamin E for hot flashes, breast cancer survivors kept a log of both the frequency and intensity of their hot flashes. These women then wrote descriptions to define the severity of those hot flashes. The purpose of this paper is to provide insight into the experience of hot flashes in breast cancer survivors and to describe the severity of hot flashes with narratives given by the women experiencing them.
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PMID:Definitions of hot flashes in breast cancer survivors. 984 28


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