Abstract
The fusion protein TEL-AML1 in t(12;21)+ acute lymphoblastic leukemia (ALL) recruits co-repressors and histone deacetylases (HDAC), which transrepress AML1 target genes. Normal bone marrow cells were more resistant to HDAC inhibitor FK228 induced cell killing than were cells from ALL patients with or without t(12;21). FK228 induced differentiation in ALL, irrespective of the presence of t(12;21).
Publication types
-
Comparative Study
-
Letter
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Antibiotics, Antineoplastic / pharmacology*
-
Antigens, Differentiation, B-Lymphocyte / analysis
-
Antineoplastic Agents / pharmacology
-
Asparaginase / pharmacology
-
B-Lymphocytes / drug effects*
-
B-Lymphocytes / pathology
-
Bone Marrow Cells / drug effects
-
Bone Marrow Cells / enzymology
-
Butyrates / pharmacology
-
Cell Differentiation / drug effects
-
Core Binding Factor Alpha 2 Subunit / analysis*
-
Depsipeptides / pharmacology*
-
Histone Deacetylase Inhibitors*
-
Humans
-
Myeloid Cells / drug effects
-
Oncogene Proteins, Fusion / analysis*
-
Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / enzymology
-
Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
-
Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology*
-
Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology
-
Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
-
Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology*
-
Tumor Cells, Cultured / drug effects
-
Tumor Cells, Cultured / enzymology
Substances
-
Antibiotics, Antineoplastic
-
Antigens, Differentiation, B-Lymphocyte
-
Antineoplastic Agents
-
Butyrates
-
Core Binding Factor Alpha 2 Subunit
-
Depsipeptides
-
Histone Deacetylase Inhibitors
-
Oncogene Proteins, Fusion
-
TEL-AML1 fusion protein
-
romidepsin
-
Asparaginase