title: Resistance to EGFR blockade in colorectal cancer: liquid biopsies and latent subclones.
abstract: Two recent papers identify KRAS activation as a mechanism of acquired resistance to EGFR blockade in colorectal cancer. In doing so, they suggest that resistance to single-agent EGFR blockade will be unavoidable because these alterations exist as latent subclones within the tumor even prior to the initiation of therapy.
authors: Broad Institute of Harvard and the Massachusetts Institute of Technology, 7 Cambridge Center, Cambridge, MA 02142, USA.
authors: David J
authors: DJ
authors: Konieczkowski
authors: Levi A
authors: LA
authors: Garraway
mesh_terms: D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized / Q000494:pharmacology; D000970:Antineoplastic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D045744:Cell Line, Tumor; D000068818:Cetuximab; D015179:Colorectal Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D004273:DNA, Neoplasm / Q000097:blood; D019008:Drug Resistance, Neoplasm / Q000187:drug effects*; D066246:ErbB Receptors / Q000037:antagonists & inhibitors* / Q000378:metabolism; D006801:Humans; D009154:Mutation; D000077544:Panitumumab; D018631:ras Proteins / Q000235:genetics / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents; D004273:DNA, Neoplasm; D000077544:Panitumumab; D066246:ErbB Receptors; D018631:ras Proteins; D000068818:Cetuximab