作者: Christine L.H. Snozek , Dennis J. O'Kane , Alicia Algeciras-Schimnich
DOI: 10.2353/JMOLDX.2009.090003
关键词: Colorectal cancer 、 Tamoxifen 、 Oncology 、 Irinotecan 、 Pharmacogenetics 、 Breast cancer 、 Epidermal growth factor receptor 、 Endocrinology 、 Cancer 、 Lung cancer 、 Internal medicine 、 Medicine 、 Pathology and Forensic Medicine 、 Molecular medicine
摘要: Genetic variability in drug-metabolizing enzymes and signaling pathways affects chemotherapy-related toxicity treatment outcome cancer. In breast colorectal cancer, polymorphisms metabolic involved tamoxifen irinotecan therapies has led the U.S. Food Drug Administration to address genetic factors relevant patient consideration of with these compounds. Tamoxifen therapeutic failure cancer been associated reduced CYP2D6 activity due inefficient activation tamoxifen. Irinotecan is more common patients reduced-activity UGT1A alleles, resulting excessive exposure potent SN-38 metabolite. lung cancers, somatic mutations epidermal growth factor receptor downstream molecules have receptor-directed therapies. This review discusses current knowledge regarding utility single gene—UGT1A1, CYP2D6, EGFR, KRAS—or multigene analysis, for optimizing breast, colorectal, therapy. Current advances areas highlight how pharmacogenetics help personalized decision-making management.