- Author:
Su-Ping ZHANG
1
;
Yu-Na NIU
;
Na YUAN
;
Ai-Hong ZHANG
;
Dan CHAO
;
Qiu-Ping XU
;
Li-Jun WANG
;
Xue-Guang ZHANG
;
Wen-Li ZHAO
;
Yun ZHAO
;
Jian-Rong WANG
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents; therapeutic use; Apoptosis; Apoptosis Regulatory Proteins; metabolism; Autophagy; drug effects; Humans; Leukemia, Myeloid, Acute; drug therapy; metabolism; pathology; Leukemia, Promyelocytic, Acute; drug therapy; metabolism; pathology; Molecular Targeted Therapy; Oncogene Proteins, Fusion; metabolism; Tretinoin; therapeutic use
- From:Chinese Journal of Cancer 2013;32(3):130-135
- CountryChina
- Language:English
- Abstract: Despite its dual role in determining cell fate in a wide array of solid cancer cell lines, autophagy has been robustly shown to suppress or kill acute myeloid leukemia cells via degradation of the oncogenic fusion protein that drives leukemogenesis. However, autophagy also induces the demise of acute leukemia cells that do not express the known fusion protein, though the molecular mechanism remains elusive. Nevertheless, since it can induce cooperation with apoptosis and differentiation in response to autophagic signals, autophagy can be manipulated for a better therapy on acute myeloid leukemia.