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Targeting Bcl-2 Proteins in Acute Myeloid Leukemia

B cell lymphoma 2 (BCL-2) family proteins play an important role in intrinsic apoptosis. Overexpression of BCL-2 proteins in acute myeloid leukemia can circumvent resistance to apoptosis and chemotherapy. Considering this effect, the exploration of anti-apoptotic BCL-2 inhibitors is considered to ha...

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Autores principales: Wei, Yunxiong, Cao, Yaqing, Sun, Rui, Cheng, Lin, Xiong, Xia, Jin, Xin, He, Xiaoyuan, Lu, Wenyi, Zhao, Mingfeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7674767/
https://www.ncbi.nlm.nih.gov/pubmed/33251145
http://dx.doi.org/10.3389/fonc.2020.584974
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author Wei, Yunxiong
Cao, Yaqing
Sun, Rui
Cheng, Lin
Xiong, Xia
Jin, Xin
He, Xiaoyuan
Lu, Wenyi
Zhao, Mingfeng
author_facet Wei, Yunxiong
Cao, Yaqing
Sun, Rui
Cheng, Lin
Xiong, Xia
Jin, Xin
He, Xiaoyuan
Lu, Wenyi
Zhao, Mingfeng
author_sort Wei, Yunxiong
collection PubMed
description B cell lymphoma 2 (BCL-2) family proteins play an important role in intrinsic apoptosis. Overexpression of BCL-2 proteins in acute myeloid leukemia can circumvent resistance to apoptosis and chemotherapy. Considering this effect, the exploration of anti-apoptotic BCL-2 inhibitors is considered to have tremendous potential for the discovery of novel pharmacological modulators in cancer. This review outlines the impact of BCL-2 family proteins on intrinsic apoptosis and the development of acute myeloid leukemia (AML). Furthermore, we will also review the new combination therapy with venetoclax that overcomes resistance to venetoclax and discuss biomarkers of treatment response identified in early-phase clinical trials.
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spelling pubmed-76747672020-11-26 Targeting Bcl-2 Proteins in Acute Myeloid Leukemia Wei, Yunxiong Cao, Yaqing Sun, Rui Cheng, Lin Xiong, Xia Jin, Xin He, Xiaoyuan Lu, Wenyi Zhao, Mingfeng Front Oncol Oncology B cell lymphoma 2 (BCL-2) family proteins play an important role in intrinsic apoptosis. Overexpression of BCL-2 proteins in acute myeloid leukemia can circumvent resistance to apoptosis and chemotherapy. Considering this effect, the exploration of anti-apoptotic BCL-2 inhibitors is considered to have tremendous potential for the discovery of novel pharmacological modulators in cancer. This review outlines the impact of BCL-2 family proteins on intrinsic apoptosis and the development of acute myeloid leukemia (AML). Furthermore, we will also review the new combination therapy with venetoclax that overcomes resistance to venetoclax and discuss biomarkers of treatment response identified in early-phase clinical trials. Frontiers Media S.A. 2020-11-05 /pmc/articles/PMC7674767/ /pubmed/33251145 http://dx.doi.org/10.3389/fonc.2020.584974 Text en Copyright © 2020 Wei, Cao, Sun, Cheng, Xiong, Jin, He, Lu and Zhao http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Oncology
Wei, Yunxiong
Cao, Yaqing
Sun, Rui
Cheng, Lin
Xiong, Xia
Jin, Xin
He, Xiaoyuan
Lu, Wenyi
Zhao, Mingfeng
Targeting Bcl-2 Proteins in Acute Myeloid Leukemia
title Targeting Bcl-2 Proteins in Acute Myeloid Leukemia
title_full Targeting Bcl-2 Proteins in Acute Myeloid Leukemia
title_fullStr Targeting Bcl-2 Proteins in Acute Myeloid Leukemia
title_full_unstemmed Targeting Bcl-2 Proteins in Acute Myeloid Leukemia
title_short Targeting Bcl-2 Proteins in Acute Myeloid Leukemia
title_sort targeting bcl-2 proteins in acute myeloid leukemia
topic Oncology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7674767/
https://www.ncbi.nlm.nih.gov/pubmed/33251145
http://dx.doi.org/10.3389/fonc.2020.584974
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