Autophagic degradation determines the fate of T315I-mutated BCR-ABL protein

Haematologica. 2019 May;104(5):e191-e194. doi: 10.3324/haematol.2018.194431. Epub 2018 Nov 22.

Authors

Haruka Shinohara¹, Yosuke Minami^{2

3}, Tomoki Naoe⁴, Yukihiro Akao⁵

Affiliations

¹ United Graduate School of Drug Discovery and Medical Information Sciences, Gifu University, 1-1 Yanagido harukashinohara313@gmail.com.
² Department of Hematology, National Cancer Center Hospital East, Chiba.
³ Department of Transfusion Medicine and Cell Therapy, Kobe University Hospital.
⁴ National Hospital Organization Nagoya Medical Center, Naka-ku, Japan.
⁵ United Graduate School of Drug Discovery and Medical Information Sciences, Gifu University, 1-1 Yanagido.

No abstract available

Publication types

Letter
Research Support, Non-U.S. Gov't

MeSH terms

Animals
Antineoplastic Agents / pharmacology
Autophagy*
Cells, Cultured
Drug Resistance, Neoplasm / drug effects*
Fusion Proteins, bcr-abl / genetics
Fusion Proteins, bcr-abl / metabolism*
Heterocyclic Compounds, 1-Ring / pharmacology
Humans
Ketones / pharmacology
Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism*
Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
Mice
Mutation
Precursor Cells, B-Lymphoid / drug effects
Precursor Cells, B-Lymphoid / metabolism
Precursor Cells, B-Lymphoid / pathology
Protein Kinase Inhibitors / pharmacology*
Proteolysis*

Substances

1-(azocan-1-yl)dec-3-en-1one
Antineoplastic Agents
Heterocyclic Compounds, 1-Ring
Ketones
Protein Kinase Inhibitors
Fusion Proteins, bcr-abl