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Overexpression of an isoform of AML1 in acute leukemia and its potential role in leukemogenesis
- Source :
- Nature Precedings
- Publication Year :
- 2008
-
Abstract
- AML1/RUNX1 is a critical transcription factor in hematopoietic cell differentiation and proliferation. From the AML1 gene, at least three isoforms, AML1a, AML1b and AML1c, are produced through alternative splicing. AML1a interferes with the function of AML1b/1c, which are often called AML1. In the current study, we found a higher expression level of AML1a in ALL patients in comparison to the controls. Additionally, AML1a represses transcription from promotor of macrophage-colony simulating factor receptor (M-CSFR) mediated by AML1b, indicating that AML1a antagonized the effect of AML1b. In order to investigate the role of AML1a in hematopoiesis and leukemogenesis in vivo, bone marrow mononuclear cells (BMMNCs) from mice were transduced with AML1a and transplanted into lethally irradiated mice, which develop lymphoblastic leukemia after transplantation. Taken together, these results indicate that overexpression of AML1a may be an important contributing factor to leukemogenesis.
- Subjects :
- Gene isoform
Cancer Research
Myeloid
Transcription, Genetic
Bone Marrow Cells
Receptor, Macrophage Colony-Stimulating Factor
Biology
Mice
chemistry.chemical_compound
Transactivation
Transduction, Genetic
hemic and lymphatic diseases
Molecular Cell Biology
medicine
Animals
Humans
Protein Isoforms
General Materials Science
Promoter Regions, Genetic
Transcription factor
Bone Marrow Transplantation
Cancer
Acute leukemia
Leukemia
Myeloid leukemia
Promoter
Hematology
Precursor Cell Lymphoblastic Leukemia-Lymphoma
medicine.disease
Molecular biology
Hematopoiesis
Gene Expression Regulation, Neoplastic
Transplantation
Leukemia, Myeloid, Acute
Haematopoiesis
medicine.anatomical_structure
Oncology
RUNX1
chemistry
Case-Control Studies
Acute Disease
Core Binding Factor Alpha 2 Subunit
Cancer research
Bone marrow
Subjects
Details
- Database :
- OpenAIRE
- Journal :
- Nature Precedings
- Accession number :
- edsair.doi.dedup.....8e3885939a279468c95439fb00ab5b60