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

10.18632/oncotarget.5436

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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
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Online Access:https://scholarbank.nus.edu.sg/handle/10635/174113
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spelling sg-nus-scholar.10635-1741132023-09-20T08:41:34Z The BIM deletion polymorphism: A paradigm of a permissive interaction between germline and acquired TKI resistance factors in chronic myeloid leukemia 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. DUKE-NUS MEDICAL SCHOOL 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 BIM protein biphenyl derivative dasatinib imatinib 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 gene deletion genetic polymorphism 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 Leukemia, Myelogenous, Chronic, BCR-ABL Positive Membrane Proteins Nitrophenols Piperazines Polymorphism, Genetic Protein Kinase Inhibitors Proto-Oncogene Proteins Pyrimidines Sulfonamides 10.18632/oncotarget.5436 Oncotarget 7 3 2721-2733 2020-09-03T10:32:26Z 2020-09-03T10:32:26Z 2016 Article 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. (2016). The BIM deletion polymorphism: A paradigm of a permissive interaction between germline and acquired TKI resistance factors in chronic myeloid leukemia. Oncotarget 7 (3) : 2721-2733. ScholarBank@NUS Repository. https://doi.org/10.18632/oncotarget.5436 19492553 https://scholarbank.nus.edu.sg/handle/10635/174113 Unpaywall 20200831
institution National University of Singapore
building NUS Library
continent Asia
country Singapore
Singapore
content_provider NUS Library
collection ScholarBank@NUS
topic 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
BIM protein
biphenyl derivative
dasatinib
imatinib
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
gene deletion
genetic polymorphism
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
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Membrane Proteins
Nitrophenols
Piperazines
Polymorphism, Genetic
Protein Kinase Inhibitors
Proto-Oncogene Proteins
Pyrimidines
Sulfonamides
spellingShingle 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
BIM protein
biphenyl derivative
dasatinib
imatinib
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
gene deletion
genetic polymorphism
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
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Membrane Proteins
Nitrophenols
Piperazines
Polymorphism, Genetic
Protein Kinase Inhibitors
Proto-Oncogene Proteins
Pyrimidines
Sulfonamides
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.
The BIM deletion polymorphism: A paradigm of a permissive interaction between germline and acquired TKI resistance factors in chronic myeloid leukemia
description 10.18632/oncotarget.5436
author2 DUKE-NUS MEDICAL SCHOOL
author_facet DUKE-NUS MEDICAL SCHOOL
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.
format Article
author 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.
author_sort Ko T.K.
title The BIM deletion polymorphism: A paradigm of a permissive interaction between germline and acquired TKI resistance factors in chronic myeloid leukemia
title_short The BIM deletion polymorphism: A paradigm of a permissive interaction between germline and acquired TKI resistance factors in chronic myeloid leukemia
title_full The BIM deletion polymorphism: A paradigm of a permissive interaction between germline and acquired TKI resistance factors in chronic myeloid leukemia
title_fullStr The BIM deletion polymorphism: A paradigm of a permissive interaction between germline and acquired TKI resistance factors in chronic myeloid leukemia
title_full_unstemmed The BIM deletion polymorphism: A paradigm of a permissive interaction between germline and acquired TKI resistance factors in chronic myeloid leukemia
title_sort bim deletion polymorphism: a paradigm of a permissive interaction between germline and acquired tki resistance factors in chronic myeloid leukemia
publishDate 2020
url https://scholarbank.nus.edu.sg/handle/10635/174113
_version_ 1778169695466160128