1,720,998 research outputs found
Nutrition and primary prevention of breast cancer: Foods, nutrients and breast cancer risk
No full textWorldwide, each year approximately one million women are newly diagnosed with breast cancer (BC), in Germany 65 new cases per 100,000 inhabitants are registered, yearly. The fact that incidence has been rising in parallel with economic development indicates that environmental factors might play a role in the causation of BC. Migrational data have pointed to nutrition as one of the more relevant external factors involved. Preventive dietary advice often includes a reduction of alcohol, red meat and animal fat and increasing the intake of vegetables, fruit and fibre and lately, phytoestrogens from various sources. Clearly, the scientific basis for these recommendations appears sparse. The available prospective data from epidemiological studies and interventional trials do not support the overall hypothesis that higher fat-intakes are a relevant risk factor for BC development, more important seems the relative distribution of various fatty acids. A non-vegetarian eating habit (consumption of animal products) per se does not elevate BC risk, while consumption of broiled or deep fried meats cannot be ruled out as a risk factor in genetically susceptible individuals. It appears prudent to abstain from regular and increased alcohol consumption. This should be particularly true for pubescent girls, in whom glandular breast tissue is particularly vulnerable. In general, if alcohol is consumed on a regular basis, a sufficient supply of fresh vegetables and fruit is essential. While there is no overall protective effect of a high fruit and vegetable consumption speculation remains over possible beneficial effects of certain subcategories, especially brassica vegetables like broccoli, cauliflower and cabbage. In essence, regional differences in BC incidence are probably partially attributable to life long dietary habits. There is no need to adopt a foreign dietary plan in order to protect oneself against BC. Traditional western diets also have their beneficial ingredients that should be regular constituents in our meals. Lignans from traditionally made sourdough rye bread, linseed/flaxseed and berries are local sources of potentially canceroprotective phyto-estrogens. Furthermore, indole-3-carbinol rich cabbage species might contribute to BC protection by diet. Nevertheless, clear cut recommendations for or against single nutrients or secondary plant metabolites are not yet possible, lacking sufficient data on individual bioavailability, safety and long term outcome. BC prevention by dietary means therefore relies on an individually tailored mixed diet, rich in basic foods and traditional manufacturing and cooking methods. (c) 2005 Elsevier Ireland Ltd. All rights reserved
Are estrogens carcinogens?
No full textUnopposed estrogens increase the risk of developing endometrial cancer. A relationship between estrogen exposure and the risk for breast cancer is very probable, an association of long-term estrogen substitution and ovarian cancer risk has been postulated recently. Estrogens have been considered as typical tumor promotors. Due to their estrogen-receptor-mediated mitogenic activity, these steroids were supposed to increase the statistical probability of spontaneous mutations. Recent experimental findings, however, suggest that estrogen metabolites, in particular 4-hydroxyes trogens are capable of inducing DNA-damage and transforming mutations.The clinical relevance of these genotoxic properties remains to be established. First molecular-epidemiologic studies suggest that some women might produce relevant amounts of mutagenic estrogen metabolites, increasing their risk for breast-, endometrial- or ovarian cancer. These findings might result in novel preventive strategies. The present data do not justify to abandon hormone replacement therapy. It seems to be wise, however, to restrict hormone replacement therapy to symptomatic women with a clear indication and according to the actual trend to limit it temporarily
Therapy-related hematologic neoplasias after breast cancer. Epidemiologic, etiologic and cytogenetic aspects and new risk factors according to published data and own results
No full textBackground: Breast cancer is the most frequent solid tumor in women. The incidence is increasing. In Germany, about 45,000 women are newly diagnosed each year. The general strategy aims for the best local control of the tumor by surgery and radiotherapy. This strategy is supplemented by systemic adjuvant chemotherapy and/or antihormonal therapy. The following substances have shown their efficacy in clinical trials: alkylating agents, antimetabolites, anthracyclines, topoisomerase inhibitors, platinum derivatives, and taxanes. Due to intensified treatment schedules remission rates and overall survival could be significantly improved. On the other hand, the long-term toxicity of this antineoplastic therapy is an increasing problem. Secondary Leukemias: Therapy-associated secondary leukemias frequently occur after treatment for malignant lymphomas and multiple myelomas. However, they can also be observed after antineoplastic therapy of solid tumors such as cancers of the breast, lung, testicles and ovaries and sarcomas. The highest risk for secondary leukemias has been attributed to concurrent radiochemotherapy. Therapy-associated hematologic neoplasias are a severe medical problem due to the high incidence of breast cancer and the dismal outcome of secondary leukemias, which occur in 0.3-5% of patients receiving antineoplastic therapy. Risk Factors: The delineation of new individual risk factors is urgently required to improve the safety of modern breast cancer treatment, which includes intensive combined radiochemotherapy. Candidate mechanisms could be polymorphisms in DNA repair and/or xenobiotic-metabolizing enzymes. Preliminary data suggest that the resulting deficiencies in xenobiotic-metabolizing enzymes such as glutathione S-transferases increase the risk for therapy-induced hematologic neoplasias in patients with breast cancer
Endometrial cancer
No full textRadical surgery including complete pelvic and para-arortic lymph node dissection (LND) is both the main therapeutic effort and the decisive staging procedure in patients with invasive endometrial cancer (EC) and should be performed in specialized institutions. Vaginal cuff brachytherapy holds little serious side effects and may be beneficial in preventing vaginal recurrences. External irradiation treatment no longer has a routine indication in primary therapy. The omission of retroperitoneal staging (LND) at primary surgery does not indicate adjuvant radiotherapy but rather second-effort surgery removing pelvic and para-aortic lymph-nodes. External radiotherapy should be reserved for fully staged patients with residual non-resectable tumor manifestation and/or nodal involvement in relation to the extent of tumor involvement and surgical intervention. Hormonal and cytotoxic therapy is experimental in the adjuvant setting. The first step in palliative systemic treatment should be the administration of endocrine therapy when the tumor expresses progesterone receptors and tumor manifestations are not acutely life-threatening. In other cases or when endocrine treatment fails chemotherapy may be considered, which is often limited due to its toxicity. Preferably, palliative hormonal and/or chemotherapy should be administered in controlled clinical trials
Signal Transduction of the Melatonin Receptor MT1 Is Disrupted in Breast Cancer Cells by Electromagnetic Fields
No full textThe growth of estrogen-receptor positive breast cancer cells is inhibited by the pineal gland hormone, melatonin. Concern has been raised that power-line frequency and microwave electromagnetic fields (EMEs) could reduce the efficiency of melatonin on breast cancer cells. In this study we investigated the impact of EMIT's on the signal transduction of the high-affinity receptor MT1 M parental MCF-7 cells and MCF-7 cells transfected with the MT1 gene. The binding of the cAMP-responsive element binding (CREB) protein to a promoter sequence of BRCA-1 after stimulation with melatonin was analyzed by a gel-shift assay and the expression of four estrogen-responsive genes was measured in sham-exposed breast cancer cells and cells exposed to a sinusoidal 50Hz EMF of 1.2 mu T for 48 h. In sham-exposed cells, binding of CREB to the promoter of BRCA-1 was increased by estradiol and subsequently diminished by treatment with melatonin. In cells exposed to 1.2 mu T, 50Hz. EMF. binding of CREB was almost completely omitted. Expression of BRCA-1, p53, p21(WAF), and c-myc was increased by estradiol stimulation and subsequently decreased by melatonin treatment in both cell lines, except for p53 expression in the transfected cell line, thereby proving the antiestrogenic effect of melatonin at molecular level. In contrast, in breast cancer cells transfected with MT1 exposed to 1.2 mu T of the 50Hz EMF, the expression of p53 and c-myc increased significantly after melatonin treatment but for p21(WAF). the increase was not significant. These results convincingly prove the negative effect of EMF on the antiestrogenic effect of melatonin in breast cancer cells. Bioelectromagnetics 31:237-245, 2010. (C) 2009 Wiley-Liss, Inc
Antiproliferative activity of tamoxifen on MCF-7 breast cancer cells is modulated by weak electromagnetic field exposure
No full textEndocrine therapy of endometrial cancer and endometrial hyperplasia
No full textEndometrial cancer is, apart from breast cancer, the most common gynecologic malignancy in western industrialized countries with a mortality. rate of ca 20-25%. Estrogen-associated endometrial cancer (type 1) has a favourable prognosis; but the non-estrogen-related type 2 tends to have a poor outcome. Endometrial hyperplasias without atypia can be safely treated with endocrine interventions. Conservative treatment of atypical endometrial hyperplasias should be reserved for women who wish to preserve their fertility, provided a thorough histological follow-up is possible. The cornerstone of the treatment of invasive endometrial cancer is radical surgery including complete pelvic and para-aortic lymphonodectomy in tumors larger than stage 1a or with other risk factors. The routine use of adjuvant teletherapy is not indicated when correct surgical staging as been performed. There are no evidence based recommendations for adjuvant hormonal or chemotherapy. In patients with disseminated endometrial cancer, endo-crine therapy is a reasonable initial approach. Palliative chemotherapy is indicated after the failure of an endocrine treatment, in patients. with receptor-negative tumors, or when life threatening tumor manifestations require a fast response
GnRH agonist Triptorelin reverts increased expression of the cofactors A1B1 and SRC-1 in breast cancer cells
No full textInduction of tamoxifen resistance in breast cancer cells by ELF electromagnetic fields
No full textThe incidence of breast cancer in western societies has been rising ever since the Second World War. Besides the exposure to a multitude of new chemical compounds, electromagnetic field exposure has been linked to breast cancer through a radiation-mediated anti-melatonin pathway. We investigated, whether low-frequency electromagnetic field exposure interferes with the anti-estrogenic activity of tamoxifen. Two different clones of the breast cancer cell line MCF-7 were exposed to highly homogeneous 50 Hz electromagnetic fields and IC50 values were calculated from dose-response curves of tamoxifen at various field intensities. An intensity-dependent shift of tamoxifen dose-response curves to higher concentrations with a maximal response at 1.2 mu T was observed. Hypothetically, electromagnetic field exposure could contribute to tamoxifen resistance observed in breast cancer after long-term treatment. (c) 2005 Elsevier Inc. All rights reserved
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