Zobrazeno 1 - 4
of 4
pro vyhledávání: '"Catherine B. Meador"'
Autor:
Kimberly B. Dahlman, Junfeng Xia, Kadoaki Ohashi, Franziska Michor, Hailing Jin, Catherine B. Meador, Zhongming Zhao, Valentina Pirazzoli, William Pao, Peilin Jia, Lin Liu, Katerina Politi
Publikováno v:
Genome Research. 23:1434-1445
Somatic mutations in kinase genes are associated with sensitivity of solid tumors to kinase inhibitors, but patients with metastatic cancer eventually develop disease progression. In EGFR mutant lung cancer, modeling of acquired resistance (AR) with
Autor:
David Westover, Elisa de Stanchina, Pengcheng Lu, William Pao, Christine M. Lovly, Robert McEwen, Joshua A. Bauer, Yingjun Yan, Eiki Ichihara, Marc Ladanyi, Catherine B. Meador, Darren Cross, Amanda Kulick, Fei Ye
Publikováno v:
Cancer research. 77(11)
Mutant-selective EGFR tyrosine kinase inhibitors (TKI), such as osimertinib, are active agents for the treatment of EGFR-mutant lung cancer. Specifically, these agents can overcome the effects of the T790M mutation, which mediates resistance to first
Autor:
Daniel C. Colvin, Katherine R. Amato, Shan Wang, William Pao, Nathanael S. Gray, Andrew K. Hastings, Catherine B. Meador, Wenqiang Song, Justin M M Cates, Fei Ye, Justin M. Balko, Li Tan, Jin Chen, Pengcheng Lu, Christine M. Lovly
Publikováno v:
Cancer research. 76(2)
Despite the success of treating EGFR-mutant lung cancer patients with EGFR tyrosine kinase inhibitors (TKI), all patients eventually acquire resistance to these therapies. Although various resistance mechanisms have been described, there are currentl
Autor:
Peter D. Smith, Catherine B. Meador, Ross Stewart, Catherine Anne Eberlein, Alwin Schuller, P. Spitzler, Melanie M. Frigault, William Pao, Martine J. Mellor, Eiki Ichihara, Phil Jewsbury, Sue Ashton, D. Cross, Celina M. D'Cruz
Publikováno v:
Annals of Oncology. 25:iv155
Aim: First-generation EGFR-TKIs, such as gefitinib, are active in first-line, EGFR-TKI-sensitising-mutant (EGFRm+), advanced NSCLC, but the duration of clinical benefit is limited by acquired tumour resistance. A common resistance mechanism is gain o