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

This review presents current knowledge of diet and breast cancer. In the first part it reviews current knowledge of nutritional risk factors. Obesity, total energy intake, intake of saturated fatty acids and alcohol were considered as high risk factors for breast cancer in the past. In addition to these factors intake of n-6 and n-3 polyunsaturated fatty acids has been discussed. Possible differences between their carcinogenic activity are summarized. The mechanisms of promotion and inhibition are described in the present review. In the second part there protective nutritional factors are reviewed: fiber, antioxidant micronutrients (vitamin C, vitamin b-A, carotene and other carotenoids, vitamin E, antioxidant trace elements), n-3 polyunsaturated fatty acids, olive oil and oestrogen compounds of plant origin. Influence of several diet components can not be considered individually. Nutrition has to be taken into account as a whole complex of protective and risk components. It is necessary to increase the intake of probably protective nutrients and minimize all cancer risk factors including nutrition. (Tab. 2, Fig. 3, Ref. 181.)
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PMID:[Nutrition and female breast tumors]. 1064 42

To evaluate whether the protective effect associated with vegetables and fruits in breast cancer could be explained by nutrients and bioactive substances present in these plant foods, we carried out a case-control study in Uruguay including 400 cases and 405 controls. The intake of vegetables, fruits, and related nutrients was estimated with a food frequency questionnaire on 64 food items. This questionnaire allowed the calculation of total energy intake, and nutrients were calorie adjusted by the residuals method. Odds ratios for study variables were estimated by unconditional multiple logistic regression. Total vegetable, total fruit, dietary fiber, vitamin C, vitamin E, lycopene, folate, and total phytosterol intakes were inversely associated with breast cancer risk [4th quartile odds ratio for total vegetable intake = 0.41, 95% confidence interval = 0.26-0.65, p (for trend) = 0.004]. The association with total vegetable intake was not independent of lycopene intake. The results related to vegetable and nutrient intakes are consistent with antioxidant and antiestrogenic effects. This could be mediated, among other nutrients, by dietary fiber and lycopene intake. The role of other unmeasured phytochemicals, correlated with dietary fiber and lycopene intakes, cannot be ruled out.
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PMID:Vegetables, fruits, and related nutrients and risk of breast cancer: a case-control study in Uruguay. 1069 63

If one were to wait for the perfect set of experimental results before launching a multi-agent chemoprevention or large risk reduction study, the trial would never be launched. On the other hand, non-scientific considerations have led to the premature launching of at least three prominent studies (CARET, Carotene and Retinol Efficacy Trial; ATBC, Apha Tocopherol Beta Carotene; PCPT, Prostate Cancer Prevention Trial) and the much delayed start-up of another, BCPT, the Breast Cancer Prevention Trial. Strong epidemiologic data by itself should not be adequate to justify starting a large trial; experimental and/or clinical data should be developed. On the other hand fear of secondary adverse events that are of low incidence should not be enough to delay a trial if the overall health benefit could be high. The development of multiagent chemoprevention trials requires that each agent is active and additively or synergistically so in combination in preclinical models. Additionally, side effects of each agent should be non-overlapping and low to non-existent, preferably a feature determined in formal phase IIa and IIb trials. These principles will be discussed in the context of prior (CARET, ATBC) and ongoing (EUROSCAN, acetylcysteine/retinol), as well as proposed future trials (difluromethyl/sulindac).
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PMID:Criteria for implementation of large and multiagent clinical chemoprevention trials. 1076 23

Chemoprevention is a recently introduced and rapidly growing area of oncology that is identifying agents with a potentially preventive role in cancer. Several clinical trials have recently shown the feasibility of this approach in reducing the risk of major human cancers. In the USA, a large trial that demonstrated a reduction of approximately 50% in the risk of developing breast cancer led to Food and Drug Administration (FDA) approval of tamoxifen as a preventive agent in women at increased risk. Although the results could not be reproduced in two smaller European trials, further investigations into this agent are clearly warranted. Raloxifene, another selective oestrogen receptor modulator which has reduced the risk of breast cancer in a trial in women with osteoporosis, is being compared with tamoxifen in a large primary prevention trial in at-risk women. Retinoids are a group of compounds that have proved especially effective in reducing the occurrence of second primary tumours in subjects with skin, head and neck or liver cancer. Fenretinide, a synthetic retinoic acid derivative, has recently been shown to decrease the occurrence of a second breast malignancy in premenopausal women. Results with non-steroidal anti-inflammatory drugs (NSAIDs) have proved consistently encouraging in epidemiological studies in lowering the incidence of colorectal cancer. Clinical trials with selective cyclo-oxygenase inhibitors potentially devoid of gastrointestinal (GI) toxicity are currently underway in at-risk subjects. Calcium and selenium have also received much attention as chemopreventive agents. Originally investigated against skin cancer, selenium showed efficacy in reducing prostate, lung and colon cancer incidence. Similarly, vitamin E was effective in reducing prostate cancer incidence and mortality in a lung cancer prevention trial in heavy smokers. The challenges of conducting well-designed and unequivocal chemoprevention trials are considerable, but advances in techniques of identification of at-risk subjects and establishing surrogate endpoint biomarkers should contribute greatly to future studies. Current knowledge suggests that a pharmacological approach to preventing cancer, using natural or synthetic agents, could become an important way forward.
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PMID:Recent advances in cancer chemoprevention, with emphasis on breast and colorectal cancer. 1076 41

Tamoxifen, a non-steroidal antiestrogen, has been used in the hormonal treatment for breast cancer. The hepatic estrogenic effect of tamoxifen causes severe triglyceridemia. The combined effect of tamoxifen, vitamin C and vitamin E on plasma lipid and lipoprotein is important, since, vitamin C and vitamin E encumbered the lipid abnormalities instigated by tamoxifen. Therefore supplementation of vitamin C (Celin 500 mg) and vitamin E (Evion 400 mg) for 90 days along with tamoxifen (10 mg twice a day) to postmenopausal breast cancer patients was ventured. In tamoxifen-treated patients, total cholesterol (TC), free cholesterol (FC), phospholipids (PL), free fatty acids (FFA), low density lipoprotein cholesterol (LDL) levels were decreased and the triglycerides (TG), ester cholesterol (EC), high density lipoprotein cholesterol (HDL) and very low density lipoprotein cholesterol (VLDL) levels were increased. Combination therapy reduce all the cholesterol level and VLDL, LDL. TG levels were significantly decreased and HDL, EC levels were significantly increased. These results suggested that tamoxifen treatment is the most effective during co-administration of vitamin C and vitamin E in that they reduce the tamoxifen-induced hypertriglyceridemia.
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PMID:Salubrious effect of vitamin C and vitamin E on tamoxifen-treated women in breast cancer with reference to plasma lipid and lipoprotein levels. 1076 15

We have shown that peptide YY, an endogenous gut hormone, and vitamin E succinate (VES) inhibit pancreatic cancer cell growth in vitro. We hypothesized that PYY and VES would inhibit breast cancer cell viability regardless of the hormone receptor status. Human breast ZR-75 ductal carcinoma (estrogen receptor negative) and MCF-7 adenocarcinoma (estrogen receptor positive) cells were cultured and exposed to VES (10 pg/ml), PYY (500 pmol), or both agents together. MTT assay was performed at 24, 48, and 72 h to evaluate cell viability. At every time interval, PYY and VES significantly inhibited cell growth compared to control. The effects of PYY were similar in magnitude to those of VES. Combining the agents resulted in a significant additive inhibition of growth with the greatest effect seen at 72 h. We have shown that PYY and vitamin E inhibit in vitro growth of breast cancer cells with variable hormone receptor status. When used in combination, the agents have a significant increase in effect. Further studies are ongoing to define the mechanism of action of these agents and to translate the experiments to an in vivo model.
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PMID:Peptide YY and vitamin E inhibit hormone-sensitive and -insensitive breast cancer cells. 1081 43

Tamoxifen (TAM) is widely used in the treatment of breast cancer. The cytostatic effects of TAM have been attributed to the antagonism of estrogen receptor (ER) and inhibition of estrogen-dependent proliferative events. However, the mechanism by which TAM is also effective against certain ER-negative breast tumors remains to be elucidated. Here we report that TAM induced the activity of caspase-3-like proteases in ER-negative breast cancer cell lines MDA-MB-231 and BT-20, as evidenced by the cleavage of fluorogenic tetrapeptide substrate and of poly(ADP-ribose) polymerase. The activation of caspase-3-like proteases preceded TAM-induced chromatin condensation and nuclear fragmentation, the typical apoptotic morphologies. Pretreatment of cells with a specific inhibitor of caspase-3, acetyl-Asp-Glu-Val-Asp-aldehyde, or with a general inhibitor of caspases, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone, prevented TAM-induced apoptosis. TAM also stimulated c-Jun NH2-terminal kinase (JNK) 1 activity, and interfering with the JNK pathway by over-expressing a DN JNK1 mutant attenuated TAM-induced apoptosis. In addition, treatment of cells with a lipid-soluble antioxidant vitamin E blocked TAM-induced caspase-3 and JNK1 activation as well as apoptosis, whereas water-soluble antioxidants N-acetyl L-cysteine and glutathione had little effect. Thus, this study demonstrates that TAM induces apoptosis in ER-negative breast cancer cells through caspase-3 and JNK1 pathways, which are probably initiated at the cell membrane by an oxidative mechanism.
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PMID:Activation of caspase-3 and c-Jun NH2-terminal kinase-1 signaling pathways in tamoxifen-induced apoptosis of human breast cancer cells. 1108 19

The relation between 17 micronutrients and breast-cancer risk was analyzed in a case-control study conducted between 1993 and 1999 in the Swiss Canton of Vaud. Cases were 289 women with incident, histologically confirmed breast cancer, and controls were 442 women admitted to the same hospital for a wide spectrum of acute non-neoplastic conditions unrelated to long-term modifications of diet. Dietary habits were investigated using a validated food-frequency questionnaire. Odds ratios (ORs) were obtained after allowance for age, education, parity, menopausal status, body mass index, total energy intake and alcohol drinking. For several micronutrients, the ORs tended to decline with increasing tertile of intake, with significant inverse trends in risk for potassium (OR for the highest tertile = 0.21), total carotenoids (OR = 0.42), lycopene (OR = 0.43), folic acid (OR = 0.45), vitamin C (OR = 0.19), vitamin E (OR = 0.37) and vitamin B(6) (OR = 0.54). In a model including a continuous term for the 7 micronutrients significantly related to breast cancer, the only persisting significant inverse relations were for vitamin C (OR = 0.23) and lycopene (OR = 0.64).
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PMID:Dietary intake of selected micronutrients and breast-cancer risk. 1114 55

Case report of a 60 year-old patient with an ulcerated radiation-induced fibrosis after therapy for breast cancer. Treatment with oral administration of pentoxifylline 3 x 400 mg/day and vitamin E 2 x 200 mg/day was started. The ulcers were almost completely healed after 18 months. Sonographic examination showed a reduction in dermal thickness and in the laser Doppler fluxmetry, a regulation in the amplitude and increase in flux was found compared to the measurements made before the start of treatment. The therapy was very well tolerated without any side effects. The treatment of radiation-induced fibrosis with PTX and vitamin E is a practicable and cost-effective regimen, especially for inoperable patients. The efficacy of this treatment is probably due to a combination of blood flow stimulation and immune modulation which lead to a reduction in the fibrosis.
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PMID:Crux medicorum ulcerated radiation-induced fibrosis - successful therapy with pentoxifylline and vitamin E. 1117 36

Dietary antioxidant vitamins and retinol have been proposed to be protective against breast cancer on the basis of their ability to reduce oxidative DNA damage and their role in cell differentiation. Epidemiologic studies have not been convincing in supporting this hypothesis, but women with high exposure to free radicals and oxidative processes have not been specifically considered. We explored these issues in the Swedish Mammography Screening Cohort, a large population-based prospective cohort study in Sweden that comprised 59,036 women, 40-76 years of age, who were free of cancer at baseline and who had answered a validated 67-item food frequency questionnaire. During 508,267 person-years of follow-up, 1,271 cases of invasive breast cancer were diagnosed. Cox proportional hazards models were used to obtain hazard ratios (HRs) and 95% confidence intervals (CIs). There was no overall association between intake of ascorbic acid, beta-carotene, retinol or vitamin E and breast cancer incidence. High intake of ascorbic acid was inversely related to breast cancer incidence among overweight women (HR=0.61; 95% CI 0.45-0.82, for highest quintile of intake among women with body mass index>25 kg/m(2)) and women with high consumption of linoleic acid (HR=0.72; 95% CI 0.52-1.02, for highest quintile of ascorbic acid intake and average consumption of more than 6 grams of linoleic acid per day). Among women with a body mass index of 25 or below, the hazard ratio for breast cancer incidence was 1.27 (95% CI 0.99-1.63), comparing the highest to the lowest quintile of ascorbic acid intake. Consumption of foods high in ascorbic acid may convey protection from breast cancer among women who are overweight and/or have a high intake of linoleic acid.
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PMID:Dietary antioxidant vitamins, retinol, and breast cancer incidence in a cohort of Swedish women. 1125 82


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