BRCA1 expression is potentially an important tool for use in cancer management and should be assessed for predicting differential chemosensitivity and tailoring chemotherapy in lung cancer.
BRCA1 is a large protein that interacts with many other proteins that have diverse functions, so it has been a challenge to determine how defects in its function could lead to cancer.
BRCA1 overexpression sensitizes cancer cells to lovastatin via regulation of cyclin D1-CDK4-p21WAF1/CIP1 pathway: analyses using a breast cancer cell line and tumoral xenograft model.
BRCA1 and BRCA2 account for the majority of the known familial breast cancer risk, however, the impact of other cancer susceptibility genes largely remains to be elucidated.
BRCA1 mutant cells hypersensitivity could be linked to higher expression of ERbeta gene, which suggests that genistein may be an efficient inhibitor of cancer development in BRCA1 mutant breast cancer cells.
BRCA1 and BRCA2 are the major genes for high-penetrance familial breast and ovarian cancer, whereas mutations in ATM or Chek2 confer more modest cancer risk.
BRCA1 carriers with a previous diagnosis of cancer had significantly higher levels of cancer-related distress at 1 month posttest than those without cancer.
BRCA1 has been shown to directly interact with IGF signaling such that variants in this pathway may modify risk of cancer in women carrying BRCA mutations.
BRCA1 carriers aged > or = 50 at diagnosis of first invasive breast cancer were more likely to have an ER+ cancer compared to those aged < 50 (57% vs 29%, P = 0.005).
BRCA1-positive tumors had substantially increased tumor proliferation index compared with negative tumors (47.0 Ki67-positive nuclei versus 10.3, P = 0.0016) and were more likely to develop lethal cancer compared with BRCA1-negative tumors (hazard ratio, 4.6; 95% confidence interval, 2.4-8.7).
BRCA1/2 carriers were highly satisfied with the MDOSC, which met their needs and helped them to make informed decisions regarding their cancer risk management.