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Volumn 8, Issue 11, 2017, Pages 18609-18614

Transformation to small-cell carcinoma as an acquired resistance mechanism to AZD9291: A case report

Author keywords

Acquired resistance; AZD9291; EGFR TKI; NSCLC; Transformation

Indexed keywords

BEVACIZUMAB; CISPLATIN; DOCETAXEL; ERLOTINIB; GEMCITABINE; NEDAPLATIN; OSIMERTINIB; PEMETREXED; ACRYLAMIDE DERIVATIVE; ANILINE DERIVATIVE; PROTEIN KINASE INHIBITOR;

EID: 85015205318     PISSN: None     EISSN: 19492553     Source Type: Journal    
DOI: 10.18632/oncotarget.14506     Document Type: Article
Times cited : (52)

References (14)
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    • Yu HA, Tian SK, Drilon AE, Borsu L, Riely GJ, Arcila ME, Ladanyi M. Acquired Resistance of EGFR-Mutant Lung Cancer to a T790M-Specific EGFR Inhibitor: Emergence of a Third Mutation (C797S) in the EGFR Tyrosine Kinase Domain. JAMA Oncol. 2015; 1: 982-4.
    • (2015) JAMA Oncol , vol.1 , pp. 982-984
    • Yu, H.A.1    Tian, S.K.2    Drilon, A.E.3    Borsu, L.4    Riely, G.J.5    Arcila, M.E.6    Ladanyi, M.7
  • 6
    • 84938196408 scopus 로고    scopus 로고
    • The Allelic Context of the C797S Mutation Acquired upon Treatment with Third-Generation EGFR Inhibitors Impacts Sensitivity to Subsequent Treatment Strategies
    • Niederst MJ, Hu H, Mulvey HE, Lockerman EL, Garcia AR, Piotrowska Z, Sequist LV, Engelman JA. The Allelic Context of the C797S Mutation Acquired upon Treatment with Third-Generation EGFR Inhibitors Impacts Sensitivity to Subsequent Treatment Strategies. Clin Cancer Res. 2015; 21: 3924-33.
    • (2015) Clin Cancer Res , vol.21 , pp. 3924-3933
    • Niederst, M.J.1    Hu, H.2    Mulvey, H.E.3    Lockerman, E.L.4    Garcia, A.R.5    Piotrowska, Z.6    Sequist, L.V.7    Engelman, J.A.8
  • 7
    • 84973438966 scopus 로고    scopus 로고
    • High MET amplification level as a resistance mechanism to osimertinib (AZD9291) in a patient that symptomatically responded to crizotinib treatment post-osimertinib progression
    • Ou SH, Agarwal N, Ali SM. High MET amplification level as a resistance mechanism to osimertinib (AZD9291) in a patient that symptomatically responded to crizotinib treatment post-osimertinib progression. Lung Cancer. 2016; 98: 59-61.
    • (2016) Lung Cancer , vol.98 , pp. 59-61
    • Ou, S.H.1    Agarwal, N.2    Ali, S.M.3
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    • Transformation from non-small-cell lung cancer to smallcell lung cancer: molecular drivers and cells of origin
    • Oser MG, Niederst MJ, Sequist LV, Engelman JA. Transformation from non-small-cell lung cancer to smallcell lung cancer: molecular drivers and cells of origin. Lancet Oncol. 2015; 16: e165-72.
    • (2015) Lancet Oncol , vol.16 , pp. e165-e172
    • Oser, M.G.1    Niederst, M.J.2    Sequist, L.V.3    Engelman, J.A.4
  • 11
    • 84879880262 scopus 로고    scopus 로고
    • Rapid increase of serum neuron specific enolase level and tachyphylaxis of EGFRtyrosine kinase inhibitor indicate small cell lung cancer transformation from EGFR positive lung adenocarcinoma?
    • Zhang Y, Li XY, Tang Y, Xu Y, Guo WH, Li YC, Liu XK, Huang CY, Wang YS, Wei YQ. Rapid increase of serum neuron specific enolase level and tachyphylaxis of EGFRtyrosine kinase inhibitor indicate small cell lung cancer transformation from EGFR positive lung adenocarcinoma? Lung Cancer. 2013; 81: 302-5.
    • (2013) Lung Cancer , vol.81 , pp. 302-305
    • Zhang, Y.1    Li, X.Y.2    Tang, Y.3    Xu, Y.4    Guo, W.H.5    Li, Y.C.6    Liu, X.K.7    Huang, C.Y.8    Wang, Y.S.9    Wei, Y.Q.10


* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.