Document Detail


Down-regulation of DLX3 expression in MLL-AF4 childhood lymphoblastic leukemias is mediated by promoter region hypermethylation.
MedLine Citation:
PMID:  17611665     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hypermethylation of CpG islands is the most well defined epigenetic change in neoplasia and plays an important role in the inactivation or silencing of cancer related genes. DLX genes (1-7), with large CpG islands in their 5' region, are implicated in a number of processes among which haematopoiesis. They are characterized by highly dynamic spatio-temporal expression and supposed to be involved in resistance to apoptosis of several tumor cell lines. In acute lymphoblastic leukemia (ALL) hypermethylation is a common phenomenon frequently associated with poor prognosis in specific genetic childhood leukemia subgroups. These data together with the presence of large CpG islands in the up-stream regions of the DLX genes make them attractive candidates for methylation regulated gene expression and leukemia related aberrancies. To validate the role of DLX genes in paediatric B-ALL cells, we studied two cell lines and two groups of patients with paediatric chromosomal rearrangements: MLL-AF4 and TEL-AML1, respectively. Analysis of methylation and gene expression patterns of DLX3 in 64 specimens of B-lineage ALL revealed that DLX3 presents aberrant methylation in paediatric B-ALL patients. In vitro experiments with 5-Aza-2'dC on leukemia cell lines, confirmed by Western blot analysis, indicated that the methylation of DLX3 CpG islands has a functional role and interferes with the DLX3 gene and DLX3 protein expression in B-ALL cells. Importantly, hypermethylation of DLX3 significantly reduces its expression in MLL-AF4 rearranged leukemias while methylation is almost absent in TEL-AML1 positive ALL specimens. These results show that differential DLX3 methylation could be a new epigenetic marker for genotypic B-cell leukemia subgroup with high-risk features.
Authors:
Marta Campo Dell'Orto; Barbara Banelli; Emanuela Giarin; Benedetta Accordi; Luca Trentin; Massimo Romani; Geertruy te Kronnie; Giuseppe Basso
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Oncology reports     Volume:  18     ISSN:  1021-335X     ISO Abbreviation:  Oncol. Rep.     Publication Date:  2007 Aug 
Date Detail:
Created Date:  2007-07-05     Completed Date:  2007-09-11     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9422756     Medline TA:  Oncol Rep     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  417-23     Citation Subset:  IM    
Affiliation:
Department of Paediatrics, University of Padova, I-35128 Padova, Italy.
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MeSH Terms
Descriptor/Qualifier:
Blotting, Western
Burkitt Lymphoma / genetics,  metabolism,  pathology*
Cell Line, Tumor
Child
DNA Methylation*
Down-Regulation
Gene Expression Regulation, Neoplastic
HL-60 Cells
Homeodomain Proteins / genetics*,  metabolism
Humans
Myeloid-Lymphoid Leukemia Protein / genetics*
Oncogene Proteins, Fusion / genetics*
Promoter Regions, Genetic / genetics*
Reverse Transcriptase Polymerase Chain Reaction / methods
Transcription Factors / genetics*,  metabolism
U937 Cells
Chemical
Reg. No./Substance:
0/Distal-less homeobox proteins; 0/Homeodomain Proteins; 0/MLL-AF4 fusion protein, human; 0/Oncogene Proteins, Fusion; 0/Transcription Factors; 149025-06-9/Myeloid-Lymphoid Leukemia Protein

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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