The molecular evolution of acquired resistance to targeted EGFR blockade in colorectal cancers

Luis A. Diaz (), Richard T. Williams, Jian Wu, Isaac Kinde, J. Randolph Hecht, Jordan Berlin, Benjamin Allen, Ivana Bozic, Johannes G. Reiter, Martin A. Nowak, Kenneth W. Kinzler, Kelly S. Oliner () and Bert Vogelstein
Additional contact information
Luis A. Diaz: Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center
Richard T. Williams: Amgen Inc.
Jian Wu: Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center
Isaac Kinde: Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center
J. Randolph Hecht: David Geffen School of Medicine, University of California
Jordan Berlin: Vanderbilt University Medical Center
Benjamin Allen: Program for Evolutionary Dynamics, Harvard University
Ivana Bozic: Program for Evolutionary Dynamics, Harvard University
Johannes G. Reiter: Program for Evolutionary Dynamics, Harvard University
Martin A. Nowak: Program for Evolutionary Dynamics, Harvard University
Kenneth W. Kinzler: Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center
Kelly S. Oliner: Amgen Inc.
Bert Vogelstein: Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center

Nature, 2012, vol. 486, issue 7404, 537-540

Abstract: This work on colorectal cancer shows that secondary mutations in KRAS that confer resistance to panitumumab, an anti-EGFR monoclonal antibody, are already present when antibody treatment begins; the apparent inevitability of resistance suggests that combinations of drugs targeting at least two different oncogenic pathway will be needed for treatment.

Date: 2012
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DOI: 10.1038/nature11219

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