The BIM deletion polymorphism: A paradigm of a permissive interaction between germline and acquired TKI resistance factors in chronic myeloid leukemia

• Main Authors: Ko T.K., Chin H.S., Chuah C.T.H., Huang J.W.J., Ng K.-P., Khaw S.L., Huang D.C.S., Ong S.T.
• Other Authors: DUKE-NUS MEDICAL SCHOOL
• Format: Article
• Published: 2020
• Subjects: 4 [4 (4' chloro 2 biphenylylmethyl) 1 piperazinyl] n [4 [3 dimethylamino 1 (phenylthiomethyl)propylamino] 3 nitrobenzenesulfonyl]benzamide; BIM protein; imatinib; 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; ABT-737; apoptosis regulatory protein; BCR ABL protein; BCR-ABL1 fusion protein, human; biphenyl derivative; dasatinib; membrane protein; nitrophenol; oncoprotein; piperazine derivative; protein kinase inhibitor; pyrimidine derivative; sulfonamide; antineoplastic activity; apoptosis; Article; BCR ABL1 gene; BIM gene; cancer resistance; cell growth; chronic myeloid leukemia; concentration response; controlled study; drug mechanism; gene; gene deletion; genetic polymorphism; human; human cell; myeloid leukemia cell line; drug effects; genetics; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; tumor cell line; Apoptosis; Apoptosis Regulatory Proteins; Bcl-2-Like Protein 11; Biphenyl Compounds; Cell Line, Tumor; Dasatinib; Fusion Proteins, bcr-abl; Gene Deletion; Humans; Imatinib Mesylate; Membrane Proteins; Nitrophenols; Piperazines; Polymorphism, Genetic; Protein Kinase Inhibitors; Proto-Oncogene Proteins; Pyrimidines; Sulfonamides
• Online Access: https://scholarbank.nus.edu.sg/handle/10635/174113
• Institution: National University of Singapore

10.18632/oncotarget.5436