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).
Original language | English |
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Pages (from-to) | 1697-9 |
Number of pages | 3 |
Journal | Haematologica |
Volume | 90 |
Issue number | 12 |
Publication status | Published - Dec 2005 |
Externally published | Yes |
Keywords
- Antibiotics, Antineoplastic/pharmacology
- Antigens, Differentiation, B-Lymphocyte/analysis
- Antineoplastic Agents/pharmacology
- Asparaginase/pharmacology
- B-Lymphocytes/drug effects
- Bone Marrow Cells/drug effects
- 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 Cell Lymphoblastic Leukemia-Lymphoma/enzymology
- Tumor Cells, Cultured/drug effects