Hypermethylation of a 5′ CpG island of p16 is a frequent event in non-Hodgkin’s lymphoma

• DOI: 10.1038/sj.leu.2400579
• Publication Date: 2002-09-04T18:16:23Z
• Authors: B Martinez-Delgado; J Fernandez-Piqueras; MJ Garcia; E Arranz; J Gallego; C Rivas; M Robledo; J Benitez
• Keywords: 0301 basic medicine; Binding Sites; Lymphoma, B-Cell; Lymphoma, Non-Hodgkin; DNA, Neoplasm; Exons; Lymphoma, B-Cell, Marginal Zone; DNA Methylation; Lymphoma, T-Cell; Polymerase Chain Reaction; Gene Expression Regulation, Neoplastic; Blotting, Southern; 03 medical and health sciences; Humans; Genes, Tumor Suppressor; Carrier Proteins; Cyclin-Dependent Kinase Inhibitor p16

Hypermethylation of a 5' CpG island of p16 gene has been recently described as a possible way of inactivation of this tumor suppressor gene, alternative to deletions and mutations. We have investigated if hypermethylation of a 5' CpG island of p16 occurs in non-Hodgkin's lymphoma (NHL) and normal lymphoid tissue. A total of 82 NHLs were examined for p16 methylation by Southern blot and PCR analysis. Hypermethylation was detected in approximately 20% of B cell lymphomas of both low and high grade and in 15% of T cell NHL. The highest rate of p16 gene methylation in tumors was found among MALT (mucosa-associated lymphoid tissue) lymphomas in which the percentage of cases with p16 gene methylation reached 67%. However, normal lymphoid tissue was always unmethylated at p16 locus. These results indicate that p16 gene methylation is a frequent event in NHLs, mainly in MALT lymphomas, and suggest that it could be an important mechanism of inactivation of this gene.