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Encouragement to Submit Data of Clinical Response to EGFR-TKIs in Patients With Uncommon EGFRMutations

Encouragement to Submit Data of Clinical Response to EGFR-TKIs in Patients With Uncommon... EDIToRIAL Encouragement to Submit Data of Clinical Response to EGFR-TKIs in Patients With Uncommon EGFR Mutations Yasushi Yatabe, MD, PhD,* William Pao, MD, PhD,† and James R. Jett, MD‡ n the basis of the results of recent clinical phase III trials, epidermal growth factor Oreceptor (EGFR) mutations have emerged as the strongest predictor of response to EGFR-tyrosine kinase inhibitor (TKI) treatment. Most trials examined a limited number 1–6 of EGFR mutations, as summarized in Table 1. Association with drug-sensitivity is the strongest for the two major hotspots or classical mutation sites, including the point mutation at codon 858 in codon 21 (L858R) and the in-frame deletions in exon 19, which account for more than 90% of mutations. In contrast to data on these hotspot mutations, data on the remaining 10% of muta- tions is less clear. In-frame exon 20 insertions, constituting 4% to 9% of EGFR-TKI muta- tions, are reported to have baseline resistance to EGFR-TKI treatment. Exon 20 T790M mutations are associated with acquired resistance to treatment but can rarely be found in combination with classical mutations in primary lung cancers independent of EGFR-TKI treatment. G719X and L861Q substitutions seem to be associated with sensitivity, but these are http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Thoracic Oncology Wolters Kluwer Health

Encouragement to Submit Data of Clinical Response to EGFR-TKIs in Patients With Uncommon EGFRMutations

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Copyright
Copyright © 2012 by the International Association for the Study of Lung Cancer
ISSN
1556-0864
eISSN
1556-1380
DOI
10.1097/JTO.0b013e318251980b
pmid
22722783
Publisher site
See Article on Publisher Site

Abstract

EDIToRIAL Encouragement to Submit Data of Clinical Response to EGFR-TKIs in Patients With Uncommon EGFR Mutations Yasushi Yatabe, MD, PhD,* William Pao, MD, PhD,† and James R. Jett, MD‡ n the basis of the results of recent clinical phase III trials, epidermal growth factor Oreceptor (EGFR) mutations have emerged as the strongest predictor of response to EGFR-tyrosine kinase inhibitor (TKI) treatment. Most trials examined a limited number 1–6 of EGFR mutations, as summarized in Table 1. Association with drug-sensitivity is the strongest for the two major hotspots or classical mutation sites, including the point mutation at codon 858 in codon 21 (L858R) and the in-frame deletions in exon 19, which account for more than 90% of mutations. In contrast to data on these hotspot mutations, data on the remaining 10% of muta- tions is less clear. In-frame exon 20 insertions, constituting 4% to 9% of EGFR-TKI muta- tions, are reported to have baseline resistance to EGFR-TKI treatment. Exon 20 T790M mutations are associated with acquired resistance to treatment but can rarely be found in combination with classical mutations in primary lung cancers independent of EGFR-TKI treatment. G719X and L861Q substitutions seem to be associated with sensitivity, but these are

Journal

Journal of Thoracic OncologyWolters Kluwer Health

Published: May 1, 2012

References