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Monitoring EGFR

Monitoring EGFR EDITORIAL Monitoring EGFR-Mutant Lung Cancers By Means of the Blood William Pao, MD, PhD (J Thorac Oncol. 2006;1: 199–200) omatic activating mutations in the gene encoding the epidermal growth factor receptor S(EGFR) are found in a proportion of non–small-cell lung cancers (NSCLCs) and have been associated with sensitivity of lung tumors to the EGFR tyrosine kinase inhibitors (TKIs), gefitinib (Iressa; AstraZeneca, London, England) and erlotinib (Tarceva; Genen- 1–3 tech, Inc., South San Francisco, CA). Such mutations occur in the exons (18 –21) encoding the kinase domain of the protein; approximately 90% of such mutations occur as exon 19 deletions, which eliminate an LREA motif, or as exon 21 missense mutations, resulting in substitution of arginine for leucine at position 858 (L858R). These two types of mutations also appear to be the dominant mutations that predict sensitivity to treatment. Thus, testing tumors for drug-sensitive EGFR mutations can be relatively straightforward in the clinic, provided that adequate tissue specimen is available for analysis and that sensitive, reliable assays have been established. Up to now, most research has focused on analysis of DNA from tumor specimens for EGFR mutations. However, in this issue of the Journal of Thoracic Oncology, Kimura and colleagues http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Thoracic Oncology Wolters Kluwer Health

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ISSN
1556-0864

Abstract

EDITORIAL Monitoring EGFR-Mutant Lung Cancers By Means of the Blood William Pao, MD, PhD (J Thorac Oncol. 2006;1: 199–200) omatic activating mutations in the gene encoding the epidermal growth factor receptor S(EGFR) are found in a proportion of non–small-cell lung cancers (NSCLCs) and have been associated with sensitivity of lung tumors to the EGFR tyrosine kinase inhibitors (TKIs), gefitinib (Iressa; AstraZeneca, London, England) and erlotinib (Tarceva; Genen- 1–3 tech, Inc., South San Francisco, CA). Such mutations occur in the exons (18 –21) encoding the kinase domain of the protein; approximately 90% of such mutations occur as exon 19 deletions, which eliminate an LREA motif, or as exon 21 missense mutations, resulting in substitution of arginine for leucine at position 858 (L858R). These two types of mutations also appear to be the dominant mutations that predict sensitivity to treatment. Thus, testing tumors for drug-sensitive EGFR mutations can be relatively straightforward in the clinic, provided that adequate tissue specimen is available for analysis and that sensitive, reliable assays have been established. Up to now, most research has focused on analysis of DNA from tumor specimens for EGFR mutations. However, in this issue of the Journal of Thoracic Oncology, Kimura and colleagues

Journal

Journal of Thoracic OncologyWolters Kluwer Health

Published: Mar 1, 2006

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