作者: Alexandros Pintzas , Eftychia Oikonomou
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摘要: Novel activating mutations in sporadic colorectal cancer (CRC) have recently been identified on major kinase encoding genes such as BRAF and PI3KCA. The presence of these point mutations, including the well characterized KRAS oncogene represent up to 75% cases CRC. These genes, that implicated adenoma-carcinoma transition, cause deregulation constitutive activation MAP AKT/kinase pathways, rendering growth advantages colon tumor cells. This review focuses key genetic alterations underlying cumulative effect multiple within cell. Moreover, currently available alternative treatment approaches may target different are discussed, novel inhibitor. Identification differential gene expression analyzed by microarray reveal potential targets for combined therapeutic protocols which will result personalized treatments near future.