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Analysis of Tumor Specimens at the Time of Acquired Resistance to EGFR-TKI Therapy in 155 Patients with <i>EGFR</i> -Mutant Lung Cancers

Clinical Cancer Research · 2013 · Vol. 19(8) · pp. 2240–2247

Helena A. Yu(Vanderbilt University)Maria E. Arcila(Memorial Sloan Kettering Cancer Center)Natasha Rekhtman(Memorial Sloan Kettering Cancer Center)Camelia S. Sima(Cornell University)Maureen F. Zakowski(Cornell University)William Pao(Vanderbilt-Ingram Cancer Center)Mark G. Kris(Memorial Sloan Kettering Cancer Center)Vincent A. Miller(Vanderbilt University)Marc Ladanyi(Vanderbilt University)Gregory J. Riely✉(Cornell University)

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Abstract

This is the largest series reporting mechanisms of acquired resistance to EGFR-TKI therapy. We identified EGFR T790M as the most common mechanism of acquired resistance, whereas MET amplification, HER2 amplification, and small cell histologic transformation occur less frequently. More comprehensive methods to characterize molecular alterations in this setting are needed to improve our understanding of acquired resistance to EGFR-TKIs.

Lung Cancer Treatments and Mutations Lung Cancer Research Studies Cancer Genomics and DiagnosticsT790MKRASGefitinibNeuroblastoma RAS viral oncogene homologMedicineLung cancerOncologyInternal medicineErlotinibEpidermal growth factor receptor

MeSH terms

Erlotinib HydrochlorideGefitinibAdenocarcinomaAdultAgedAged, 80 and overBiopsyDNA Mutational AnalysisFemaleHumansImmunohistochemistryLungLung NeoplasmsMaleMiddle Aged

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