Author:
Wei Yunxiong,Cao Yaqing,Sun Rui,Cheng Lin,Xiong Xia,Jin Xin,He Xiaoyuan,Lu Wenyi,Zhao Mingfeng
Abstract
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.
Funder
National Institutes of Natural Sciences
Reference117 articles.
1. Epidemiology, and End Results Program;Cancer Stat Facts: Acute Myeloid Leukemia (AML)
2. Midostaurin, enasidenib, CPX-351, gemtuzumab ozogamicin, and venetoclax bring new hope to AML;Wei;Blood,2017
3. High expression of Bcl-2 protein in acute myeloid leukemia cells is associated with poor response to chemotherapy;Tothova;Neoplasma,2002
4. Elevated expression of the apoptotic regulator Mcl-1 at the time of leukemic relapse;Kaufmann;Blood,1998
5. In vivo suppression of Bcl-XL expression facilitates chemotherapy-induced leukaemia cell death in a SCID/NOD-Hu model;Fennell;Br J Haematol,2001
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