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Chinese Journal of Cancer ; (12): 130-135, 2013.
Article in English | WPRIM | ID: wpr-295849

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.


Subject(s)
Humans , Antineoplastic Agents , Therapeutic Uses , Apoptosis , Apoptosis Regulatory Proteins , Metabolism , Autophagy , Leukemia, Myeloid, Acute , Drug Therapy , Metabolism , Pathology , Leukemia, Promyelocytic, Acute , Drug Therapy , Metabolism , Pathology , Molecular Targeted Therapy , Oncogene Proteins, Fusion , Metabolism , Tretinoin , Therapeutic Uses
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