Data from Investigating Novel Resistance Mechanisms to Third-Generation EGFR Tyrosine Kinase Inhibitor Osimertinib in Non–Small Cell Lung Cancer Patients Article Swipe

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Zhe Yang , Nong Yang , Qiuxiang Ou , Yi Xiang , Tao Jiang , Xue Wu , Hua Bao , Xiaoling Tong , Xiaonan Wang , Yang Shao , Yunpeng Liu , Yan Wang , Caicun Zhou ·

YOU? · · 2023 · Open Access · · DOI: https://doi.org/10.1158/1078-0432.c.6525738.v1

Purpose: The third-generation EGFR tyrosine kinase inhibitor osimertinib is approved to treat patients with EGFR T790M-positive non–small cell lung cancer (NSCLC) who have developed resistance to earlier-generation drugs. Acquired EGFR C797S mutation has been reported to mediate osimertinib resistance in some patients. However, the remaining resistance mechanisms are largely unknown.Experimental Design: We performed mutation profiling using targeted next-generation sequencing (NGS) for 416 cancer-relevant genes on 93 osimertinib-resistant lung cancer patients' samples, mainly cell-free DNAs (cfDNAs), and matched pretreatment samples of 12 patients. In vitro experiments were conducted to functionally study the secondary EGFR mutations identified.Results: EGFR G796/C797, L792, and L718/G719 mutations were identified in 24.7%, 10.8%, and 9.7% of the cases, respectively, with certain mutations coexisting in one patient with different prevalence. L792 and L718 mutants markedly increased the half inhibitory concentration (IC₅₀) of osimertinib in vitro, among which the L718Q mutation conferred the greatest resistance to osimertinib, as well as gefitinib resistance when not coexisting with T790M. Further analysis of the 12 matched pretreatment samples confirmed that these EGFR mutations were acquired during osimertinib treatment. Alterations in parallel or downstream oncogenes such as MET, KRAS, and PIK3CA were also discovered, potentially contributing to the osimertinib-resistance in patients without EGFR secondary mutations.Conclusions: We present comprehensive mutation profiles of a large cohort of osimertinib-resistance lung cancer patients using mainly cfDNA. Besides C797 mutations, novel secondary mutations of EGFR L718 and L792 residues confer osimertinib resistance, both in vitro and in vivo, and are of great clinical and pharmaceutical relevance. Clin Cancer Res; 24(13); 3097–107. ©2018 AACR.

Related Topics

Epidermal Growth Factor Receptor

Erlotinib

Concepts

Osimertinib T790M Gefitinib Lung cancer Cancer research Medicine Chemistry Cancer Internal medicine Epidermal growth factor receptor Erlotinib

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Type: preprint
Language: en
Landing Page: https://doi.org/10.1158/1078-0432.c.6525738.v1
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DOI: https://doi.org/10.1158/1078-0432.c.6525738.v1

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Title: Data from Investigating Novel Resistance Mechanisms to Third-Generation EGFR Tyrosine Kinase Inhibitor Osimertinib in Non–Small Cell Lung Cancer Patients

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Type: preprint

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Language: en

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Publication year: 2023

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Publication date: 2023-03-31

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Authors: Zhe Yang, Nong Yang, Qiuxiang Ou, Yi Xiang, Tao Jiang, Xue Wu, Hua Bao, Xiaoling Tong, Xiaonan Wang, Yang Shao, Yunpeng Liu, Yan Wang, Caicun Zhou

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Concepts: Osimertinib, T790M, Gefitinib, Lung cancer, Cancer research, Medicine, Chemistry, Cancer, Internal medicine, Epidermal growth factor receptor, Erlotinib

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abstract_inverted_index.<i>EGFR</i>	3, 14, 29, 92, 95, 169, 199, 226
abstract_inverted_index.<i>PIK3CA</i>	187
abstract_inverted_index.(IC<sub>50</sub>)	132
abstract_inverted_index.AACR</i>.</p></div>	254
abstract_inverted_index.unknown.</p><p><b>Experimental	49
abstract_inverted_index.<div>Abstract<p><b>Purpose:</b>	0
abstract_inverted_index.identified.</p><p><b>Results:</b>	94
abstract_inverted_index.mutations.</p><p><b>Conclusions:</b>	201
cited_by_percentile_year
countries_distinct_count	0
institutions_distinct_count	13
sustainable_development_goals[0].id	https://metadata.un.org/sdg/3
sustainable_development_goals[0].score	0.699999988079071
sustainable_development_goals[0].display_name	Good health and well-being
citation_normalized_percentile.value	0.1348608
citation_normalized_percentile.is_in_top_1_percent	False
citation_normalized_percentile.is_in_top_10_percent	False