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

A prospective, longitudinal study was performed to test the hypothesis that environmental factors (e.g., diet or cigarette smoking) modulate genetic damage caused by treatment for breast cancer and render these women more susceptible to developing second malignancies. A total of 107 women (49 with breast cancer, 52 with benign breast masses, and 6 normal women) were enrolled. This report describes initial studies at the time of enrollment and disease presentation. Mutant frequency at the hprt locus and cloning efficiency of peripheral blood lymphocytes did not differ significantly among the 3 groups. Mutant frequency increased with age, with a history of cigarette smoking, and with the number of years that current smokers used cigarettes. There was no correlation in women with benign masses between mutant frequency and the incidence of chromosome aberrations (28 women) or sister chromatid exchanges (23 women). A maternal history of breast cancer did not influence mutant frequency. There was no significant relationship between dietary intake of vitamins A, B12, C and E, folacin, selenium, calcium, caffeine, or multivitamin pills, and mutant frequency. Serum folate levels in the deficient range were associated (P = 0.02) with elevated mutant frequencies, whereas SCE rates inversely correlated with serum vitamin B12 levels. These results confirm the importance of age and, less so, cigarette smoking as factors that influence mutant frequency and suggest that a micronutrient, folic acid, may modify genetic damage at the hprt locus. To the extent that somatic mutation contributes to carcinogenesis, these environmental factors may enhance the risk of developing malignant transformation.
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PMID:Factors influencing mutation at the hprt locus in T-lymphocytes: studies in normal women and women with benign and malignant breast masses. 160 Sep 53

Pentoxifylline, a methylxanthine that is used to treat veno-occlusive disease, can increase perfusion in undervascularized tissues. Addition of high concentrations, like caffeine, causes progression through radiation or drug induced G2 phase blocks, thereby limiting time for repair of DNA breaks and crosslinks. We have examined the potential of pentoxifylline to augment the effects of antitumor alkylating agents in vitro and in vivo. In MCF-7 human breast cancer cells in vitro, pentoxifylline (2 mM) present for 24 h was only slightly cytotoxic (approximately 10% cell kill at 2 mM), but when present prior to and during AA it increased the cytotoxicity of CDDP by 2 logs at 250 microM. With L-PAM in vitro, pentoxifylline was much less effective and only at a concentration of 250 microM L-PAM did 2 mM pentoxifylline increase cytotoxicity (approximately 0.3 logs). In the FSaIIC murine fibrosarcoma system, 100 mg/kg of pentoxifylline i.p. immediately prior to the alkylating agent or 50 mg/kg x 5 of pentoxifylline over 24 h with the alkylating agent given immediately after the third dose increased the tumor cell kill achieved by CDDP, carboplatin, cyclophosphamide, and thiotepa. The increase in tumor cell killing was modest (2.9-fold). Pentoxifylline in the multiple dose regimen (50 mg/kg x 5 over 24 h) was more effective than in the single dose (100 mg/kg) protocol. In the EMT6 mouse mammary adenocarcinoma, pentoxifylline (100 mg/kg daily x 5) improved the tumor growth delay produced by CDDP (3.3 mg/kg alternate days x 3), carboplatin (25 mg/kg daily x 5), cyclophosphamide (100 mg/kg alternate days x 3) and thiotepa 5 mg/kg (daily x 5). Only with cyclophosphamide, however, did the interaction appear to be large, as a 2.4-fold increase was observed.
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PMID:Efficacy of pentoxifylline as a modulator of alkylating agent activity in vitro and in vivo. 174 13

The purpose of this study was to assess the influence of caffeine on the incidence of benign mammary tumors in carcinogen (DMBA) treated female Sprague-Dawley rats. Four different animal models were used in these studies, i.e., the administration of DMBA to: [1] 55 day old virgin rats; [2] 53 day old ovariectomized, estrogen treated virgin rats; [3] 135 day old virgin rats and [4] 135 day old parous rats. A high incidence of benign mammary fibroadenomas was observed in each of the four animal models. In addition, in the estrogen treated ovariectomized animals, a high incidence of secretory mammary gland cysts was observed. Caffeine (500 mg/L drinking water) was administered daily throughout the study commencing 3-31 days after carcinogen treatment. Caffeine treatment significantly (P less than 0.05 to P less than 0.001) reduced the incidence of benign mammary fibroadenomas in the 55 day old virgin rat model (P less than 0.01), in the 53 day old estrogen treated ovariectomized virgin rat model (P less than 0.05 to P less than 0.001) and in the 135 day old virgin rat model (P less than 0.05). The number of benign mammary fibroadenomas was reduced by caffeine in the 135 day old parous rat model but this reduction was not significant (P less than 0.10). In addition, in the estrogen treated ovariectomized virgin rat model, caffeine significantly (P less than 0.05 to P less than 0.001) reduced the incidence of mammary gland cysts. Caffeine treatment either increased or had no significant effect on body weight gains, depending upon the animal model.(ABSTRACT TRUNCATED AT 250 WORDS)
Breast Cancer Res Treat 1991 Nov
PMID:Caffeine inhibits development of benign mammary gland tumors in carcinogen-treated female Sprague-Dawley rats. 177 46

204 pts with breast cancer were compared to 208 pts of similar age, with pathologies other than cancer, to assess the frequency of biological and social factors related to breast cancer, in Chilean females. The pts with breast cancer were in the 40 to 65 year old group, had a higher frequency of AB blood group, lower pregnancy and delivery rates and later pregnancies. Age of menarche and menopause, prolonged breast feeding, oral contraceptives and nutritional state were not related to a higher frequency of breast cancer. Further studies that include the analysis of previous breast pathology, diabetes, psychosomatic factors, alcohol and caffeine consumption, tobacco and others are suggested.
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PMID:[Breast cancer epidemiology]. 184 1

The idea that caffeine might be involved in the etiology of breast disease was first proposed by Minton et al. in 1979. Since that time, numerous experimental and epidemiologic studies evaluating the relationship between methylxanthines and breast disease have been conducted. Results from studies on benign breast disease have been inconsistent, with some investigators observing a positive association and others no association. However, all but one of the studies which have examined methylxanthine intake and malignant breast disease have concluded that methylxanthines do not play a role in the development of this cancer. Although various methodologies were employed and different populations were evaluated, results were consistently negative. Thus, there appears to be no evidence of an association between coffee and other methylxanthine-containing beverages and breast cancer.
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PMID:Consumption of methylxanthine-containing beverages and the risk of breast cancer. 220 82

Despite the numerous risk factors for the development of breast cancer that have been investigated, only a few demonstrate a clear association with breast cancer development. Female gender and increasing age are the most important factors, followed by factors involving a woman's menstrual, reproductive, and family history. The risks related to menstruation and reproduction are probably related to the duration of estrogenic breast stimulation. The relationship of family history and breast cancer risk is unclear, but there may be a true genetic basis. The previous occurrence of breast cancer (invasive or in situ), the presence of proliferative pathological changes, especially with atypia, and the presence of other malignancies (e.g., primary ovarian and endometrial cancer) are histological risk factors for the development of new or recurrent breast cancer. Radiation exposure, the use of exogenous estrogens (both estrogen replacement therapy and oral contraceptives), diet (especially fat consumption), and alcohol intake may all play a role in cancer risk. Certain medications as well as patient demographics may also have a weak association. Cigarette smoking, caffeine consumption, and stress presently have little support for an association with breast cancer risk. It should be noted that in only one in four patients can breast cancer be accounted for by the known risk factors. This demonstrates that although presently known risk factors may help in screening for the early detection of breast carcinoma, in its possible prevention by modulation of influenceable factors, and in advising patients about their risks, these factors are merely strong associations with breast cancer incidence and not actual causations. The mechanisms of the development of breast cancer are as yet unknown.
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PMID:Risk factors for breast cancer. 226 13

To evaluate motivational factors for participation in a breast cancer screening program and concurrently to examine beliefs regarding carcinoma of the breast held by those participants, we interviewed 135 consecutive women who took part in an American Cancer Society-sponsored breast screening project in an affluent suburb of Philadelphia. Ages were equally distributed between 30 and 69. Interestingly, cost was the greatest priority for patients, regardless of income. Even 50% of those patients reporting incomes in excess of $100,000 were concerned about cost. Additional motivating factors included reassurance if normal, media advertising, physician referral, and family history of breast cancer. Concerns about actually having breast cancer was least important. Additional questions indicated a number of fallacies regarding breast cancer, including relationships to smoking, caffeine, and trauma. We conclude that even in affluent, upper-middle-class populations, problems with education regarding breast cancer exist, and cost remains a primary deterrent to screening. Efforts must be increased to lower the cost of mammography and, at the same time, to improve patient education, perhaps through the appropriate use of the media.
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PMID:Motivational factors for participation in breast cancer screening. 240 Jun 71

This article presents a review of the epidemiologic evidence on the relationship between breast cancer risk and nutritional factors. Particular attention is given to the relationship between breast cancer and dietary fats. Other factors discussed include intake of alcohol, micronutrients, and caffeine.
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PMID:Diet and the risk of breast cancer. 269 89

The various risk factors for breast cancer have been recognized for many years. A table lists these established breast cancer risk factors together with the approximate magnitude of the increase in risk associated with them. Breast cancer incidence rates increase with age throughout the life span in Western countries, although the rate of increase is greater up to age 50 years than after 50 years. Breast cancer is more common among women in upper rather than lower social classes, among women who never have been married, among women living in urban areas, among women living in the northern US than in the southern US, and among whites than blacks, at least among those over age 50. Women in North American and Northern European countries have the highest risk for breast cancer, women in Southern European and Latin American countries are at intermediate risk, and women in Africa and Asian countries have the lowest risk. Yet, rapid rates of increase in incident rates have been noted in recent years in many Asian, Central European, and some South American countries. The later the age at which a woman has her 1st full-term pregnancy, the higher her risk for breast cancer; the earlier the age at menarche and the later the age at menopause the higher the risk; and among women who have a premenopausal oophorectomy, the earlier the age at which this occurs the lower the risk. Among postmenopausal women, obesity is associated with an increase in risk. Lactation is negatively associated with subsequent breast cancer risk. Some current research is considering potential risk factors that have not been well studied in the past, including alcohol consumption, cigarette smoking, caffeine consumption, exposure to diethylstilbestrol (DES), emotional stress, exposure to electric power, and lack of physical activity. Other areas of current research reviewed here include radiation, mammographic parenchymal patterns, a high-fat diet, use of oral contraceptives (OCs), use of estrogen replacement therapy, and endogenous hormones. Cigarette smoking and caffeine consumption do not appear promising as potential etiologic agents. The studies of the DES-exposed women and of OC users suggest that the timing of exposure may be critical, since the possible effect of both these hormonal agents may be limited to specific time periods of rapid breast development. If such a critical period does not exist in postmenopausal women, then there may be little effect of hormones used at this time. Studies with long-term follow-up and that include long-term users are essential to studies of effects of hormones and other exposures.
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PMID:Breast cancer epidemiology. 304 46

We investigated the relationship between methylxanthine consumption and breast cancer using data from a case-control study which included 1,510 cases and 1,882 controls identified through a nation-wide breast cancer screening program. There was no evidence of a positive association between methylxanthine consumption and risk of breast cancer. In fact, there was some suggestion of a negative association, particularly in women diagnosed after age 50. In addition, there was no evidence of increased risk with past or recent methylxanthine consumption, or with the consumption of caffeine or specific beverages, most notably brewed or instant caffeinated coffee and tea.
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PMID:Methylxanthines and breast cancer. 311 9


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