Christine L.H. Snozek, Dennis J. O'Kane, Alicia Algeciras-Schimnich

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Presentation transcript:

Pharmacogenetics of Solid Tumors: Directed Therapy in Breast, Lung, and Colorectal Cancer Christine L.H. Snozek, Dennis J. O'Kane, Alicia Algeciras-Schimnich The Journal of Molecular Diagnostics Volume 11, Issue 5, Pages 381-389 (September 2009) DOI: 10.2353/jmoldx.2009.090003 Copyright © 2009 American Society for Investigative Pathology and Association for Molecular Pathology Terms and Conditions

Figure 1 Tamoxifen metabolism. CYP3A4/5 and CYP2D6 are the main enzymes involved in tamoxifen metabolism. CYP3A4/5 produces N-desmethyl-tamoxifen, the major metabolite, whereas several enzymes including CYP2D6 generate the minor metabolite 4-hydroxy-tamoxifen. N-desmethyl-tamoxifen and 4-hydroxy-tamoxifen are further transformed to the active metabolite endoxifen. In patients with CYP2D6 null alleles or potent inhibition, the metabolism of tamoxifen to 4-hydroxy-tamoxifen or endoxifen is blocked. The Journal of Molecular Diagnostics 2009 11, 381-389DOI: (10.2353/jmoldx.2009.090003) Copyright © 2009 American Society for Investigative Pathology and Association for Molecular Pathology Terms and Conditions

Figure 2 EGFR-dependent signaling. Dimerization of EGFR stimulates phosphorylation (P) of its cytoplasmic domain and enhances signaling (arrows) via several pathways. Ras proteins including K-Ras activate Raf and phosphoinositol-3 kinase to stimulate the MAPK and PI3K pathways, respectively; PI3K can also be activated directly by EGFR. MAPK and PI3K signaling affects transcription of genes involved in regulating proliferation, apoptosis, and other cellular processes. EGFR-directed therapies such as monoclonal antibodies and kinase inhibitors inhibit (bars) discrete steps in these signaling networks. The Journal of Molecular Diagnostics 2009 11, 381-389DOI: (10.2353/jmoldx.2009.090003) Copyright © 2009 American Society for Investigative Pathology and Association for Molecular Pathology Terms and Conditions