Abstract
Treating BCR-ABL-positive chronic myeloid leukemia remains impeded by the development of clinical resistance to imatinib. It has been demonstrated that berberine, a plant alkaloid, has activity against imatinib-resistant BCR-ABL mutants by inducing autophagic degradation of BCR-ABL, thereby preventing the acquisition of drug-resistant mutations.See related article by Yin et al., p. 4040.
©2020 American Association for Cancer Research.
Publication types
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
-
Comment
MeSH terms
-
Antineoplastic Agents* / pharmacology
-
Benzamides / therapeutic use
-
Berberine* / therapeutic use
-
Berberis* / drug effects
-
Drug Resistance, Neoplasm / drug effects
-
Drug Resistance, Neoplasm / genetics
-
Fusion Proteins, bcr-abl / genetics
-
Humans
-
Imatinib Mesylate / therapeutic use
-
Leukemia, Myelogenous, Chronic, BCR-ABL Positive* / drug therapy
-
Leukemia, Myelogenous, Chronic, BCR-ABL Positive* / genetics
-
Piperazines / therapeutic use
-
Pyrimidines / therapeutic use
-
Trees / drug effects
-
Ubiquitin-Protein Ligases / therapeutic use
Substances
-
Antineoplastic Agents
-
Benzamides
-
Piperazines
-
Pyrimidines
-
Berberine
-
Imatinib Mesylate
-
LRSAM1 protein, human
-
Ubiquitin-Protein Ligases
-
Fusion Proteins, bcr-abl