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      Acquired C797S Mutation upon Treatment with a T790M-Specific Third-Generation EGFR Inhibitor (HM61713) in Non-Small Cell Lung Cancer.

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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 EGFR-mutant 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.

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          Author and article information

          Journal
          J Thorac Oncol
          Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
          Elsevier BV
          1556-1380
          1556-0864
          Apr 2016
          : 11
          : 4
          Affiliations
          [1 ] Division of Hematology and Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea; Department of Internal Medicine, Gyeongsang National University School of Medicine, Jinju, Republic of Korea.
          [2 ] Division of Hematology and Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
          [3 ] Department of Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
          [4 ] Samsung Genome Institute, Seoul, Republic of Korea; Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
          [5 ] Division of Hematology and Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. Electronic address: silkahn@skku.edu.
          Article
          S1556-0864(15)00209-9
          10.1016/j.jtho.2015.12.093
          26749488

          EGFR, C797S mutation, HM61713, T790M mutation

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