Resistance to EGFR blockade in colorectal cancer: liquid biopsies and latent subclones.

Cell Res

Authors	David Konieczkowski Levi Garraway
Keywords	Humans Mutation Antineoplastic Agents ras Proteins Cell Line, Tumor Drug Resistance, Neoplasm Antibodies, Monoclonal DNA, Neoplasm Antibodies, Monoclonal, Humanized Cetuximab Colorectal Neoplasms Receptor, Epidermal Growth Factor
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.
Year of Publication	2013
Journal	Cell Res
Volume	23
Issue	1
Pages	13-4
Date Published	2013 Jan
ISSN	1748-7838
URL	http://dx.doi.org/10.1038/cr.2012.115
DOI	10.1038/cr.2012.115
PubMed ID	22847744
PubMed Central ID	PMC3541651
Links	PubMed DOI Google Scholar
Grant list	T32 GM007753 / GM / NIGMS NIH HHS / United States

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