Disease relevance of Brca1

• Using this polymorphic marker, we also investigated the loss of heterozygosity (LOH) of the Brca1 microsatellite marker in carcinogen- or radiation-induced mammary carcinomas in (WF x F344)F1 female rats [1].
• Breast cancer poses a serious public health problem, and it is hoped that identification of genetic and environmental factors that contribute to the development of breast cancer will enhance prevention efforts [2].
• A bioinformatic analysis was conducted to evaluate 246 BRCT missense mutations from high-risk breast and/or ovarian cancer patients (reported in the NIH Breast Cancer Information Core database) [3].
• Obesity is associated with increased risk for postmenopausal, but not premenopausal breast cancer [4].
• Breast cancer was induced in 36-day-old virgin female Sprague-Dawley rats, by a single intravenous injection of MNU (50 mg/kg body weight) [5].

High impact information on Brca1

• We show here that the conversion of OPCs to NSLCs depends on the reactivation of the sox2 gene, which in turn depends on the recruitment of the tumor suppressor protein Brca1 and the chromatin-remodeling protein Brahma (Brm) to an enhancer in the sox2 promoter [6].
• Breast cancer and thyroid therapy. Statement by the American Thyroid Association [7].
• However, no variation in Brca1 or Brca2 protein expression was demonstrated, whatever the experimental conditions were [8].
• Breast cancer is the leading cause of cancer death in women in the industrialized world, and the rates of breast cancer incidence are rising [9].
• The latter is also associated with hyperglycaemia, insulin resistance and type-2 diabetes, each of which independently increases breast cancer risk [10].

Chemical compound and disease context of Brca1

• These results suggest that obesity in postmenopausal women may increase breast cancer risk due to increased breast tissue exposure to adipose tissue-derived estrogen [4].

Biological context of Brca1

• Our findings suggest that the conversion of OPCs to NSLCs depends on progressive chromatin remodeling, mediated in part by Brca1 and Brm [6].
• Phytoestrogen-rich diets modulate expression of Brca1 and Brca2 tumor suppressor genes in mammary glands of female Wistar rats [8].
• With this intragenic microsatellite marker, we were able to map precisely the rat Brca1 gene to chromosome 10 using a genetic linkage study of (WKY x WF)F1 x WF backcross rats [1].
• Sequence analysis of the rat Brca1 homolog and its promoter region [11].
• The normal function of Brca1 is associated with DNA damage-related responses and the maintenance of genome integrity [12].

Anatomical context of Brca1

• Rat Brca1 mRNA was expressed in most tissues studied with the highest level in testis, consistent with studies in human and mouse [1].
• Previous work reported the differential expression of annexin I mRNA among rat adenocarcinoma cell lines of various metastatic potential (MTLn3, MTLn2, MTC.4: highest to lowest, respectively) (Pencil et al. 1993, Breast Cancer Res Treat, 25, 165-74) [13].

Associations of Brca1 with chemical compounds

• Certain point mutations within the hydrophobic transmembrane domains of class I receptor tyrosine kinases have been associated with oncogenic transformation in vitro and in vivo [Gullick, J., and Srinivasan, R. (1998) Breast Cancer Res. Treat. 52, 43-53] [14].
• Breast cancer chemoprevention: risk-benefit effects of the antioestrogen tamoxifen [15].

Analytical, diagnostic and therapeutic context of Brca1

• Brca1 and Brca2 mRNAs were quantified by real-time quantitative reverse transcription-PCR, and their proteins by immunohistochemistry [8].
• Partial cDNA fragments of the rat Brca1 homologue were isolated by RT-PCR [1].
• In conclusion, we have developed an animal model to further investigate the role of obesity in breast cancer development in postmenopausal women [4].
• Breast cancer imaging with PET and SPECT agents: an in vivo comparison [16].
• BACKGROUND: Breast cancer chemotherapy aims at employing cytotoxic agents that swing the balance between tumor cell invasion and host immune cells in favor of the latter [17].

References