The role of Fas-associated phosphatase 1 in leukemia stem cell persistence during tyrosine kinase inhibitor treatment of chronic myeloid leukemia

• Published in: Leukemia Vol. 30; no. 7; pp. 1502 - 1509
• Main Authors: Huang, W, Luan, C-H, Hjort, E E, Bei, L, Mishra, R, Sakamoto, K M, Platanias, L C, Eklund, E A
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.07.2016; Nature Publishing Group
• Subjects: 13; 13/106; 13/109; 13/2; 13/95; 14; 14/63; 38; 38/1; 38/77; 631/45/607/1164; 631/67/1059/2326; 631/67/1059/99; 631/67/1990/283/1896; 82; Analysis; Animal models; Animals; Antibodies; Apoptosis; Apoptosis - drug effects; BCR-ABL protein; Blast crisis; Blast Crisis - etiology; Blast Crisis - pathology; Bone marrow; Cancer Research; Care and treatment; CD34 antigen; Chronic myeloid leukemia; Critical Care Medicine; Cytokines; Development and progression; Drug metabolism; Drug resistance; Drug Resistance, Neoplasm - drug effects; Drug therapy; Enzyme inhibitors; fas Receptor - metabolism; Fusion protein; Genetic aspects; Glycogen; Glycogen synthase kinase 3; Glycogens; Health aspects; Hematology; Humans; Intensive; Internal Medicine; Kinases; Leukemia; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy; Medicine; Medicine & Public Health; Methods; Mice; Molecular targeted therapy; Myeloid leukemia; Neoplastic Stem Cells - pathology; Oncology; original-article; Patient outcomes; PDZ Domains; Phosphatase; Phosphatases; Protein Binding - drug effects; Protein Kinase Inhibitors - administration & dosage; Protein Kinase Inhibitors - pharmacology; Protein Kinase Inhibitors - therapeutic use; Protein Tyrosine Phosphatase, Non-Receptor Type 13 - antagonists & inhibitors; Protein Tyrosine Phosphatase, Non-Receptor Type 13 - metabolism; Protein Tyrosine Phosphatase, Non-Receptor Type 13 - physiology; Protein-tyrosine-phosphatase; Proteins; Recurrence; Remission; Remission (Medicine); Stem cell transplantation; Stem cells; Substrates; Tyrosine; Tyrosine kinase inhibitors; β-Catenin; United States; United States > US; Chicago Illinois

Chronic myeloid leukemia (CML) is characterized by expression of Bcr-abl, a tyrosine kinase oncogene. Clinical outcomes in CML were revolutionized by development of Bcr-abl-targeted tyrosine kinase inhibitors (TKIs), but CML is not cured by these agents. CML leukemia stem cells (LSCs) are relatively...