Molecular mechanisms of resistance to cetuximab and panitumumab in colorectal cancer.

By A. Bardelli, S. Siena. Journal of Clinical Oncology, 2010

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A molecularly annotated platform of patient-derived xenografts ("xenopatients") identifies HER2 as an effective therapeutic target in cetuximab-resistant colorectal cancer. (2011, background): “The population of potential responders has been recently enriched thanks to a biomarkerdevelopment strategy that is driven by the plausible biological rationale that constitutive activation of signaling pathways parallel to or downstream from EGFR, such as the RAS-RAF axis, should circumvent EGFR in”
ESMO consensus guidelines for the management of patients with metastatic colorectal cancer. (2016, methodology): “There is no clear evidence for HER3 overexpression and HER3 mutations, mesenchymal– epidermal transition (MET)/MET alterations (overexpression or gene amplification) or KRAS amplification, EGFR mutations [tyrosine kinase (TK) or ligand-binding domains] or amplification in the resistance to EGFR anti”
VarDict: a novel and versatile variant caller for next-generation sequencing in cancer research (2016, background): “On the other hand, failure to detect a KRAS mutation might direct a colon cancer patient into EGFR therapies, such as cetuximab or panitumumab, which has been proven to not be beneficial (28,29).”