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Marissa Balak
Researcher at Memorial Sloan Kettering Cancer Center
Publications - 12
Citations - 3113
Marissa Balak is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: Epidermal growth factor receptor & Tyrosine kinase. The author has an hindex of 7, co-authored 12 publications receiving 2943 citations. Previous affiliations of Marissa Balak include Cornell University & University of Texas Southwestern Medical Center.
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Journal ArticleDOI
MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib
Jonathan F. Bean,Cameron Brennan,Jin-Yuan Shih,Gregory J. Riely,Gregory J. Riely,Agnes Viale,Lu Wang,Dhananjay Chitale,Noriko Motoi,Noriko Motoi,Janos Szoke,Stephen Broderick,Marissa Balak,Wen Cheng Chang,Chong-Jen Yu,Adi F. Gazdar,Harvey I. Pass,Valerie W. Rusch,William L. Gerald,Shiu Feng Huang,Pan-Chyr Yang,Vincent Miller,Vincent Miller,Marc Ladanyi,Chih-Hsin Yang,William Pao,William Pao +26 more
TL;DR: Analysis of tumor samples from multiple independent patient cohorts and array-based comparative genomic hybridization suggest that MET amplification occurs independently of EGFRT790M mutations and that MET may be a clinically relevant therapeutic target for some patients with acquired resistance to gefitinib or erlotinib.
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Novel D761Y and Common Secondary T790M Mutations in Epidermal Growth Factor Receptor–Mutant Lung Adenocarcinomas with Acquired Resistance to Kinase Inhibitors
Marissa Balak,Yixuan Gong,Gregory J. Riely,Romel Somwar,Allan R. Li,Maureen F. Zakowski,Anne C. Chiang,Guangli Yang,Ouathek Ouerfelli,Mark G. Kris,Marc Ladanyi,Vincent A. Miller,William Pao +12 more
TL;DR: The data suggest that the type and nature of kinase inhibitor resistance mutations may be influenced by both anatomic site and mode of binding to the kinase target.
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Induction of BIM Is Essential for Apoptosis Triggered by EGFR Kinase Inhibitors in Mutant EGFR-Dependent Lung Adenocarcinomas
Yixuan Gong,Romel Somwar,Katerina Politi,Marissa Balak,Juliann Chmielecki,Xuejun Jiang,William Pao +6 more
TL;DR: In drug-sensitive EGFR mutant lung cancer cells, induction of BIM is essential for apoptosis triggered by EGFR kinase inhibitors, which implies that the intrinsic pathway of caspase activation may influence sensitivity and/or resistance of EG FR mutant lung tumor cells to EGFR Kinase inhibition.
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Acquired resistance to epidermal growth factor receptor kinase inhibitors associated with a novel T854A mutation in a patient with EGFR-mutant lung adenocarcinoma.
Jonathan F. Bean,Gregory J. Riely,Marissa Balak,Jenifer L. Marks,Marc Ladanyi,Vincent A. Miller,William Pao +6 more
TL;DR: The T854A mutation is the second reported second-site acquired resistance mutation that is within contact distance of gefitinib and erlotinib, and suggests that acquired resistance to ATP-mimetic EGFR kinase inhibitors may often be associated with amino acid substitutions that alter drug contact residues in the EGFR ATP-binding pocket.
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Development of new mouse lung tumor models expressing EGFR T790M mutants associated with clinical resistance to kinase inhibitors.
Lucia Regales,Marissa Balak,Yixuan Gong,Katerina Politi,Ayana Sawai,Carl Le,Jason A. Koutcher,David B. Solit,Neal Rosen,Maureen F. Zakowski,William Pao,William Pao +11 more
TL;DR: These new mouse models of mutant EGFR-dependent lung adenocarcinomas provide insight into clinical observations and should be useful for developing improved therapies for patients with lung cancers harboring EGFRT790M alone or in conjunction with drug-sensitive EGFR kinase domain mutations.