<b>Conclusions:</b> Patients with breast cancer meeting >1 criterion constitute a population significantly enriched for <i>BRCA1/2</i> mutations, whereas those meeting only 1 criterion test positive at a rate similar to unselected patients with breast cancer.
<b>Methods:</b> Patients with Breast Cancer (BC) and/or Ovarian Cancer (OC) fulfilling established criteria were offered genetic counseling and BRCA1/2 testing; VUSs identified in index cases were checked in other relatives affected by BC/OC whenever possible.
<b>Purpose:</b> We aimed to characterize and target drug-tolerant BRCA1-deficient tumor cells that cause residual disease and subsequent tumor relapse.<b>Experimental Design:</b> We studied responses to various mono- and bifunctional alkylating agents in a genetically engineered mouse model for <i>BRCA1/p53</i>-mutant breast cancer.
<b>Results:</b> Forty-three women were studied, divided into 4 groups: 11 patients with BRCA1/2 gene mutation (M group), 12 patients with familiar positive history for BC (F group), 10 patients with sporadic BC (S group), and 10 healthy controls (C group).
<i>BRCA1</i> and <i>BRCA2</i> (<i>BRCA1/2</i>) variants classified ambiguously as variants of uncertain significance (VUS) are a major challenge for clinical genetic testing in breast cancer; their relevance to the cancer risk is unclear and the association with the response to specific <i>BRCA1/2</i>-targeted agents is uncertain.
<i>In vivo</i> therapeutic targeting of EF2K by CoFe-siRNA-nanoparticles leads to sustained <i>EF2K</i> gene knockdown and suppressed tumor growth in orthotopic xenograft models of BRCA1-mutated breast cancer.
<i>Method:</i> The mRNA level expression of the related genes of breast cancer was detected by FQ-PCR technique and the ratio of BRCA-1, Myc, C-erbB2 and β2 micro-globulin was used to express levels of BRCA-1, Myc and C-erbB2; the related proteins of breast cancer were detected through ELISA.
(5) The ratio of the risk of radiation-induced cancer in relatives to that in unrelated individuals in the population increases with the biological relatedness of the relative, being higher for close than for distant relatives; however, even when the mutant BRCA1 gene frequency and the proportion of breast cancers due to these mutations are high, as in Ashkenazi Jewish women, for values of predisposition strength and radiosensitivity differential < 10, the increase in breast cancer risks is only marginal, even for first-degree relatives.
107 BRCA1/2 negative women with a personal or family history of breast cancer consented to receive genetic research results and 82% completed survey items about their experience.
141 breast cancer (BC) patients, who demonstrated evident clinical features of hereditary BC but turned out to be negative for founder BRCA1/2 mutations, were subjected to the LGR analysis.
17 double heterozygous (DH) breast cancer (BC) patients were identified upon the analysis of 5,391 affected women for recurrent Slavic mutations in BRCA1, CHEK2, NBN/NBS1, ATM, and BLM genes.
19 out of 37 (51%) of BRCA1-positive ovarian cancer patients and 21 out of 55 (39%) BRCA1-positive breast cancer had negative family history of breast and/or ovarian cancer among first- and second-degree relatives.
364 familial breast cancers from the Ontario Familial Breast Cancer Registry (58 BRCA1-associated, 64 BRCA2-associated, and 242 familial non-BRCA1/2 cancers) were studied.
655 women with BRCA1/2 mutations diagnosed with breast cancer and treated with BCT (n = 302) or M (n = 353) were identified and underwent follow-up to assess local, regional, and systemic recurrence.
Breast cancer susceptibility gene BRCA1 has been implicated in the control of gene regulation and such regulated genes are thought to mediate the biological role of BRCA1.