The HDAC inhibitor SB939 overcomes resistance to BCR-ABL kinase Inhibitors conferred by the BIM deletion polymorphism in chronic myeloid leukemia

10.1371/journal.pone.0174107

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Main Authors:	Rauzan M., Chuah C.T.H., Ko T.K., Tiong Ong S.
Other Authors:	DUKE-NUS MEDICAL SCHOOL
Format:	Article
Published:	Public Library of Science 2020
Subjects:	BCR ABL protein BIM protein imatinib pracinostat protein tyrosine kinase inhibitor antineoplastic agent benzimidazole derivative enzyme inhibitor histone deacetylase inhibitor SB939 compound apoptosis Article BIM gene cancer resistance cell viability chronic myeloid leukemia controlled study DNA polymorphism drug efficacy drug mechanism drug sensitivity gene gene deletion human human cell leukemia cell RNA splicing antagonists and inhibitors drug effects genetics K-562 cell line pathology Antineoplastic Agents Apoptosis Bcl-2-Like Protein 11 Benzimidazoles Enzyme Inhibitors Fusion Proteins, bcr-abl Gene Deletion Histone Deacetylase Inhibitors Humans K562 Cells Leukemia, Myelogenous, Chronic, BCR-ABL Positive RNA Splicing
Online Access:	https://scholarbank.nus.edu.sg/handle/10635/166015
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Institution:	National University of Singapore

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spelling	sg-nus-scholar.10635-1660152023-10-31T08:39:56Z The HDAC inhibitor SB939 overcomes resistance to BCR-ABL kinase Inhibitors conferred by the BIM deletion polymorphism in chronic myeloid leukemia Rauzan M. Chuah C.T.H. Ko T.K. Tiong Ong S. DUKE-NUS MEDICAL SCHOOL BCR ABL protein BIM protein imatinib pracinostat protein tyrosine kinase inhibitor antineoplastic agent BCR ABL protein benzimidazole derivative BIM protein enzyme inhibitor histone deacetylase inhibitor SB939 compound apoptosis Article BIM gene cancer resistance cell viability chronic myeloid leukemia controlled study DNA polymorphism drug efficacy drug mechanism drug sensitivity gene gene deletion human human cell leukemia cell RNA splicing antagonists and inhibitors chronic myeloid leukemia drug effects gene deletion genetics K-562 cell line pathology Antineoplastic Agents Apoptosis Bcl-2-Like Protein 11 Benzimidazoles Enzyme Inhibitors Fusion Proteins, bcr-abl Gene Deletion Histone Deacetylase Inhibitors Humans K562 Cells Leukemia, Myelogenous, Chronic, BCR-ABL Positive RNA Splicing 10.1371/journal.pone.0174107 PLoS ONE 12 3 e0174107 2020-03-27T06:26:59Z 2020-03-27T06:26:59Z 2017 Article Rauzan M., Chuah C.T.H., Ko T.K., Tiong Ong S. (2017). The HDAC inhibitor SB939 overcomes resistance to BCR-ABL kinase Inhibitors conferred by the BIM deletion polymorphism in chronic myeloid leukemia. PLoS ONE 12 (3) : e0174107. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0174107 19326203 https://scholarbank.nus.edu.sg/handle/10635/166015 Public Library of Science Unpaywall 20200320
institution	National University of Singapore
building	NUS Library
continent	Asia
country	Singapore Singapore
content_provider	NUS Library
collection	ScholarBank@NUS
topic	BCR ABL protein BIM protein imatinib pracinostat protein tyrosine kinase inhibitor antineoplastic agent BCR ABL protein benzimidazole derivative BIM protein enzyme inhibitor histone deacetylase inhibitor SB939 compound apoptosis Article BIM gene cancer resistance cell viability chronic myeloid leukemia controlled study DNA polymorphism drug efficacy drug mechanism drug sensitivity gene gene deletion human human cell leukemia cell RNA splicing antagonists and inhibitors chronic myeloid leukemia drug effects gene deletion genetics K-562 cell line pathology Antineoplastic Agents Apoptosis Bcl-2-Like Protein 11 Benzimidazoles Enzyme Inhibitors Fusion Proteins, bcr-abl Gene Deletion Histone Deacetylase Inhibitors Humans K562 Cells Leukemia, Myelogenous, Chronic, BCR-ABL Positive RNA Splicing
spellingShingle	BCR ABL protein BIM protein imatinib pracinostat protein tyrosine kinase inhibitor antineoplastic agent BCR ABL protein benzimidazole derivative BIM protein enzyme inhibitor histone deacetylase inhibitor SB939 compound apoptosis Article BIM gene cancer resistance cell viability chronic myeloid leukemia controlled study DNA polymorphism drug efficacy drug mechanism drug sensitivity gene gene deletion human human cell leukemia cell RNA splicing antagonists and inhibitors chronic myeloid leukemia drug effects gene deletion genetics K-562 cell line pathology Antineoplastic Agents Apoptosis Bcl-2-Like Protein 11 Benzimidazoles Enzyme Inhibitors Fusion Proteins, bcr-abl Gene Deletion Histone Deacetylase Inhibitors Humans K562 Cells Leukemia, Myelogenous, Chronic, BCR-ABL Positive RNA Splicing Rauzan M. Chuah C.T.H. Ko T.K. Tiong Ong S. The HDAC inhibitor SB939 overcomes resistance to BCR-ABL kinase Inhibitors conferred by the BIM deletion polymorphism in chronic myeloid leukemia
description	10.1371/journal.pone.0174107
author2	DUKE-NUS MEDICAL SCHOOL
author_facet	DUKE-NUS MEDICAL SCHOOL Rauzan M. Chuah C.T.H. Ko T.K. Tiong Ong S.
format	Article
author	Rauzan M. Chuah C.T.H. Ko T.K. Tiong Ong S.
author_sort	Rauzan M.
title	The HDAC inhibitor SB939 overcomes resistance to BCR-ABL kinase Inhibitors conferred by the BIM deletion polymorphism in chronic myeloid leukemia
title_short	The HDAC inhibitor SB939 overcomes resistance to BCR-ABL kinase Inhibitors conferred by the BIM deletion polymorphism in chronic myeloid leukemia
title_full	The HDAC inhibitor SB939 overcomes resistance to BCR-ABL kinase Inhibitors conferred by the BIM deletion polymorphism in chronic myeloid leukemia
title_fullStr	The HDAC inhibitor SB939 overcomes resistance to BCR-ABL kinase Inhibitors conferred by the BIM deletion polymorphism in chronic myeloid leukemia
title_full_unstemmed	The HDAC inhibitor SB939 overcomes resistance to BCR-ABL kinase Inhibitors conferred by the BIM deletion polymorphism in chronic myeloid leukemia
title_sort	hdac inhibitor sb939 overcomes resistance to bcr-abl kinase inhibitors conferred by the bim deletion polymorphism in chronic myeloid leukemia
publisher	Public Library of Science
publishDate	2020
url	https://scholarbank.nus.edu.sg/handle/10635/166015
_version_	1781791999910739968

The HDAC inhibitor SB939 overcomes resistance to BCR-ABL kinase Inhibitors conferred by the BIM deletion polymorphism in chronic myeloid leukemia

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