Peer-Reviewed Publication
Proc Natl Acad Sci U S A2022;119(30):e2206588119.July 26, 2022Journal Article
Allele-specific activation, enzyme kinetics, and inhibitor sensitivities of EGFR exon 19 deletion mutations in lung cancer.
Benjamin P Brown1,2, Yun-Kai Zhang3, Soyeon Kim4, Patrick Finneran5, Yingjun Yan3, Zhenfang Du3, Jiyoon Kim4, Abigail Leigh Hartzler4, Michele L LeNoue-Newton6, Adam W Smith4, Jens Meiler2,7,8, Christine M Lovly3,6
1Chemical and Physical Biology Program, Vanderbilt University, Nashville, TN 37235.
2Center for Structural Biology, Vanderbilt University, Nashville, TN 37232.
3Department of Medicine, Division of Hematology and Oncology, Vanderbilt University Medical Center, Nashville, TN 37232.
4Department of Chemistry, University of Akron, Akron, OH 44325.
5Menten AI, San Francisco, CA 94111.
6Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37232.
7Department of Chemistry, Vanderbilt University, Nashville, TN 37232.
8Institute for Drug Discovery, Leipzig University Medical School, Leipzig, SAC 04103, Germany.
Abstract
Oncogenic mutations within the epidermal growth factor receptor (EGFR) are found in 15 to 30% of all non-small-cell lung carcinomas. The term exon 19 deletion (ex19del) is collectively used to refer to more than 20 distinct genomic alterations within exon 19 that comprise the most common EGFR mutation subtype in lung cancer. Despite this heterogeneity, clinical treatment decisions are made irrespe…
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