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RESEARCH PRODUCT
The dark side of the moon: The PI3K/PTEN/AKT pathway in colorectal carcinoma
Antonio RussoStefania TommasiDaniele SantiniNicola SilvestrisEttore FistolaGiuseppe ColucciGiuseppe ToniniDaniela PetriellaGianmauro NumicoEvaristo Maiellosubject
PTENCancer ResearchClass I Phosphatidylinositol 3-KinasesPrognosiSettore MED/06 - Oncologia MedicaColorectal cancerCetuximabColorectal NeoplasmPhosphoinositide 3-kinasemedicine.disease_causePhosphatidylinositol 3-KinasesAntineoplastic Combined Chemotherapy ProtocolsBiomarkers TumormedicineHumansPTENPanitumumabEpidermal growth factor receptorProtein kinase BPI3K/AKT/mTOR pathwayClass I Phosphatidylinositol 3-KinaseAntineoplastic Combined Chemotherapy ProtocolbiologyCetuximabAKTMTORPanitumumabPTEN PhosphohydrolaseAntibodies MonoclonalGeneral MedicinePrognosismedicine.diseaseErbB ReceptorsOncologyMutationbiology.proteinCancer researchReceptor Epidermal Growth FactorKRASPhosphatidylinositol 3-KinaseColorectal NeoplasmsProto-Oncogene Proteins c-aktHumanSignal Transductionmedicine.drugdescription
Wild-type KRAS status is required but not sufficient to confer sensitivity to anti-epidermal growth factor receptor (EGFR) monoclonal antibodies (mAbs) in colorectal cancer patients. As a consequence, one of the major challenges is to identify, in non-mutant KRAS patients, other markers that can predict lack of response to this therapy. Small series have investigated the clinical effect of PIK3CA mutations on resistance to anti-EGFR mAbs and discrepant results have been observed. Furthermore, PTEN loss in metastases may be predictive of resistance to anti-EGFR mAbs, even if PTEN determination is far from an immediate clinical application. The introduction of modulators of the PI3K/AKT/mTOR pathway as potential targeted anticancer drugs is encouraging, but this attractive therapy option is still at an early stage of development. Copyright © 2010 S. Karger AG.
year | journal | country | edition | language |
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2009-01-01 |