Acquired C797S mutation upon treatment with a T790M-specific third-generation EGFR inhibitor (HM61713) in non-small cell lung cancer

Haa Na Song, Ki Sun Jung, Kwai Han Yoo, Jinhyun Cho, Ji Yun Lee, Sung Hee Lim, Hae Su Kim, Jong Mu Sun, Se Hoon Lee, Jin Seok Ahn, Keunchil Park, Yoon La Choi, Woongyang Park, Myung Ju Ahn

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Abstract

T790M mutation is most common resistant mechanism to epidermal growth factor receptor gene (EGFR) tyrosin kinase inhibitor (TKI). Several third-generation EGFRmutant selective TKI, such as AZD9291 (AstraZeneca), Rociletinib (Clovis), or HM61713 (Hanmi) have been developed. Acquired resistant C797S mutation was known to be one of the resistance mechanisms of AZD9291, which has not been reported for HM61713 yet. This is the first case report of C797S mutation as resistance mechanism of HM61713.

Original languageEnglish
Pages (from-to)e45-e47
JournalJournal of Thoracic Oncology
Volume11
Issue number4
DOIs
StatePublished - 1 Jan 2016

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Keywords

  • C797S mutation
  • EGFR
  • HM61713
  • T790M mutation

Cite this

Song, H. N., Jung, K. S., Yoo, K. H., Cho, J., Lee, J. Y., Lim, S. H., Kim, H. S., Sun, J. M., Lee, S. H., Ahn, J. S., Park, K., Choi, Y. L., Park, W., & Ahn, M. J. (2016). Acquired C797S mutation upon treatment with a T790M-specific third-generation EGFR inhibitor (HM61713) in non-small cell lung cancer. Journal of Thoracic Oncology, 11(4), e45-e47. https://doi.org/10.1016/j.jtho.2015.12.093