EGFR C797S as a Resistance Mechanism of Lazertinib in Non-small Cell Lung Cancer with EGFR T790M Mutation

被引：18

作者：

Park, Sehhoon ^{[1
]}

Ku, Bo Mi ^{[2
]}

Jung, Hyun Ae ^{[1
]}

Sun, Jong-Mu ^{[1
]}

Ahn, Jin Seok ^{[1
]}

Lee, Se-Hoon ^{[1
]}

Park, Keunchil ^{[1
]}

Ahn, Myung-Ju ^{[1
]}

机构：

[1] Sungkyunkwan Univ, Samsung Med Ctr, Dept Med, Div Hematol Oncol,Sch Med, 81 Irwon Ro, Seoul 06351, South Korea

[2] Sungkyunkwan Univ, Samsung Med Ctr, Samsung Biomed Res Inst, Sch Med, Seoul, South Korea

来源：

CANCER RESEARCH AND TREATMENT | 2020年 / 52卷 / 04期

关键词：

Non-small cell lung cancer; Lazertinib; Third-generation EGFR tyrosine kinase inhibitor; ErbB receptors;

D O I：

10.4143/crt.2020.278

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The non-small cell lung cancer with activating epidermal growth factor receptor (EGFR) mutation eventually acquires resistant to either first or second-generation EGFR tyrosine kinase inhibitor (TKI). As the following option, targeting EGFR T790M with third-generation EGFR TKI is now established as a standard treatment option. In this study, we are reporting the first case of resistance mechanism to the novel third-generation EGFR TKI, lazertinib, which showed promising clinical efficacy in phase 1-2 study. The patients showed resistance to the treatment by acquiring the additional EGFR C797S mutation in cis which is also confirmed from the patient-derived cell lines.

引用

页码：1288 / 1290

页数：3

共 4 条

[1] Lazertinib in patients with EGFR mutation-positive advanced non-small-cell lung cancer: results from the dose escalation and dose expansion parts of a first-in-human, open-label, multicentre, phase 1-2 study [J].

Ahn, Myung-Ju ;

Han, Ji-Youn ;

Lee, Ki Hyeong ;

Kim, Sang-We ;

Kim, Dong-Wan ;

Lee, Yun-Gyoo ;

Cho, Eun Kyung ;

Kim, Joo-Hang ;

Lee, Gyeong-Won ;

Lee, Jong-Seok ;

Min, Young Joo ;

Kim, Jin-Soo ;

Lee, Sung Sook ;

Kim, Hye Ryun ;

Hong, Min Hee ;

Ahn, Jin Seok ;

Sun, Jong-Mu ;

Kim, Heung Tae ;

Lee, Dae Ho ;

Kim, Sohee ;

Cho, Byoung Chul .

LANCET ONCOLOGY, 2019, 20 (12) :1681-1690

[2] Assessment of Resistance Mechanisms and Clinical Implications in Patients With EGFR T79OM-Positive Lung Cancer and Acquired Resistance to Osimertinib [J].

Oxnard, Geoffrey R. ;

Hu, Yuebi ;

Mileham, Kathryn F. ;

Husain, Hatim ;

Costa, Daniel B. ;

Tracy, Philip ;

Feeney, Nora ;

Sholl, Lynette M. ;

Dahlberg, Suzanne E. ;

Redig, Amanda J. ;

Kwiatkowski, David J. ;

Rabin, Michael S. ;

Paweletz, Cloud P. ;

Thress, Kenneth S. ;

Janne, Pasi A. .

JAMA ONCOLOGY, 2018, 4 (11) :1527-1534

[3] Genotypic and Histological Evolution of Lung Cancers Acquiring Resistance to EGFR Inhibitors [J].

Sequist, Lecia V. ;

Waltman, Belinda A. ;

Dias-Santagata, Dora ;

Digumarthy, Subba ;

Turke, Alexa B. ;

Fidias, Panos ;

Bergethon, Kristin ;

Shaw, Alice T. ;

Gettinger, Scott ;

Cosper, Arjola K. ;

Akhavanfard, Sara ;

Heist, Rebecca S. ;

Temel, Jennifer ;

Christensen, James G. ;

Wain, John C. ;

Lynch, Thomas J. ;

Vernovsky, Kathy ;

Mark, Eugene J. ;

Lanuti, Michael ;

Iafrate, A. John ;

Mino-Kenudson, Mari ;

Engelman, Jeffrey A. .

SCIENCE TRANSLATIONAL MEDICINE, 2011, 3 (75)

[4] CRISPR/Cas9 targeting events cause complex deletions and insertions at 17 sites in the mouse genome [J].

Shin, Ha Youn ;

Wang, Chaochen ;

Lee, Hye Kyung ;

Yoo, Kyung Hyun ;

Zeng, Xianke ;

Kuhns, Tyler ;

Yang, Chul Min ;

Mohr, Teresa ;

Liu, Chengyu ;

Hennighausen, Lothar .

NATURE COMMUNICATIONS, 2017, 8

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