Development of predictive models for the prognosis of triple-negative breast cancer using multiple transcriptomic analyses. [PDF]
Hwangbo S, Choi Y, Ryu JY.
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Impaired glucose tolerance in women with BRCA1 versus BRCA2 pathogenic or likely pathogenic variants: Results from a prospective cohort study. [PDF]
Grandi G +20 more
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Decisional Conflict About Contralateral Prophylactic Mastectomy in Patients with Breast Cancer with and Without Pathogenic Variants in <i>BRCA</i> Genes. [PDF]
Sung JH, Katapodi MC, Park SY.
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Germline Pathogenic Variants in HER2-Positive Breast Cancer: Spectrum and Clinical Implications in a High-Risk Chinese Cohort. [PDF]
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Identification and Characterization of Cancer-Related Risk Metabolic Subpathways Reveal Their Functional Significance in Cancer. [PDF]
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To BRCA or Not to PALBTO THE EDITOR: Kaufman et al1 report interesting data from anonrandomized phase II multicenter study of an oral poly (ADPribose)polymerase (PARP) inhibitor, olaparib, monotherapy in aspectrum of germline BRCA1 and BRCA 2 (BRCA 1/2) –mutatedcancers (ovarian, breast, pancreatic, and prostate cancer).
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BRCA-1, BRCA-2, and Hereditary Breast Cancer
2002I. INTRODUCTION The etiology of breast cancer is multifactorial, involving environmental factors, hormones, genetic susceptibility, and genetic changes during progression. Mutations in a number of genes are known to cause susceptibility to breast cancer.
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Ovarian cancer (OC) is one of the most lethal gynecological cancers with a 5-year survival rate that ranges from 30% to 40%. Breast cancer genes (BRCA1 and BRCA2) play a key role in maintaining genomic stability. Mutations in BRCA1/2 genes lead to the accumulation of double-strand breaks, resulting in tumorigenesis.
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