Reduced expression of TGF beta1RII in agnogenic myeloid metaplasia is not due to mutation or methylation

Agnogenic myeloid metaplasia (AMM) is characterized by bone marrow fibrosis and enhanced proliferation of megakaryocytes and CD34+ cells. We have analyzed the factors that could lead to reduced expression of TGF beta1RII in CD34+ cells of AMM patients. Our results demonstrate absence of mutations in...

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Bibliographic Details
Published in:Leukemia research 2006-01, Vol.30 (1), p.47-53
Main Authors: Hemavathy, Kirugaval C, Chang, Tsong H, Zhang, Haowei, Charles, William, Goldberg, Amit, Aithal, Sramila, Novetsky, Allan D, Wang, Jen C
Format: Article
Language:English
Subjects:
Cell Proliferation
CpG Islands
DNA Methylation
Female
Gene Expression Regulation - genetics
Histone Deacetylases - metabolism
Humans
Male
Megakaryocytes - metabolism
Megakaryocytes - pathology
Mutation
Primary Myelofibrosis - genetics
Primary Myelofibrosis - metabolism
Primary Myelofibrosis - pathology
Promoter Regions, Genetic
Protein-Serine-Threonine Kinases
Receptors, Transforming Growth Factor beta - biosynthesis
Receptors, Transforming Growth Factor beta - genetics
Transcription Factors - metabolism
Transcription, Genetic
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Summary:Agnogenic myeloid metaplasia (AMM) is characterized by bone marrow fibrosis and enhanced proliferation of megakaryocytes and CD34+ cells. We have analyzed the factors that could lead to reduced expression of TGF beta1RII in CD34+ cells of AMM patients. Our results demonstrate absence of mutations in the coding region and the promoter of this gene and absence of CpG methylation of its promoter in AMM patients. Further studies on transcriptional regulation of TGF beta1RII involving its cis-regulatory elements, the interacting transcription factors and their association with HDAC will provide valuable information on the pathogenesis of AMM and are under current investigation.
ISSN:0145-2126