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Type: Journal article
Title: Aberrant CBFA2T3B gene promoter methylation in breast tumors
Author: Bais, A.
Gardner, A.
McKenzie, O.
Callen, D.
Sutherland, G.
Kremmidiotis, G.
Citation: Molecular Cancer, 2004; 3(22):www1-www16
Publisher: BioMed Central Ltd.
Issue Date: 2004
ISSN: 1476-4598
Statement of
Anthony J Bais, Alison E Gardner, Olivia LD McKenzie, David F Callen, Grant R Sutherland, and Gabriel Kremmidiotis
Abstract: BACKGROUND: The CBFA2T3 locus located on the human chromosome region 16q24.3 is frequently deleted in breast tumors. CBFA2T3 gene expression levels are aberrant in breast tumor cell lines and the CBFA2T3B isoform is a potential tumor suppressor gene. In the absence of identified mutations to further support a role for this gene in tumorigenesis, we explored whether the CBFA2T3B promoter region is aberrantly methylated and whether this correlates with expression. RESULTS: Aberrant hypo and hypermethylation of the CBFA2T3B promoter was detected in breast tumor cell lines and primary breast tumor samples relative to methylation index interquartile ranges in normal breast counterpart and normal whole blood samples. A statistically significant inverse correlation between aberrant CBFA2T3B promoter methylation and gene expression was established. CONCLUSION: CBFA2T3B is a potential breast tumor suppressor gene affected by aberrant promoter methylation and gene expression. The methylation levels were quantitated using a second-round real-time methylation-specific PCR assay. The detection of both hypo and hypermethylation is a technicality regarding the methylation methodology.
Keywords: Cell Line, Tumor; Humans; Breast Neoplasms; Sulfites; Tumor Suppressor Proteins; Phosphoproteins; Protein Subunits; Repressor Proteins; DNA, Neoplasm; Sequence Analysis, DNA; Gene Expression Regulation; Gene Expression Regulation, Neoplastic; Methylation; Promoter Regions, Genetic
Rights: © 2004 Bais et al; licensee BioMed Central Ltd. This is an open-access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
RMID: 0020041509
DOI: 10.1186/1476-4598-3-22
Appears in Collections:Paediatrics publications

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