Shades of T790M: Intratumor Heterogeneity in EGFR-Mutant Lung Cancer.

Ichihara E, Lovly CM
Cancer Discov. 2015 5 (7): 694-6

PMID: 26152920 · PMCID: PMC4499857 · DOI:10.1158/2159-8290.CD-15-0616

In the setting of recent exciting clinical results and numerous ongoing trials, Piotrowska and colleagues explore mechanisms of acquired resistance to the mutant-specific EGFR inhibitor rociletinib, and demonstrate that loss of T790M, EGFR amplification, and small-cell transformation are all clinically relevant mechanisms of drug resistance. The authors provide a new paradigm for using quantitative assessment of the EGFR T790M:activation mutation allele frequency ratio to prognosticate responses to rociletinib and also demonstrate that plasma-based assessments of circulating tumor DNA can be used to monitor drug response and the emergence of drug resistance.

©2015 American Association for Cancer Research.

MeSH Terms (8)

Acrylamides Drug Resistance, Neoplasm ErbB Receptors Humans Lung Neoplasms Protein Kinase Inhibitors Pyrimidines Small Cell Lung Carcinoma

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