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De novo methylation of tumour suppressor genes CDKN2A and CDKN2B is a rare finding in B‐cell chronic lymphocytic leukaemia
Author(s) -
Martel Véronique,
Guerci Agnès,
Humbert JeanClaude,
Gregoire MarieJosé,
Chery Michèle,
Lederlin Pierre,
Jonveaux Philippe
Publication year - 1997
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1997.3953209.x
Subject(s) - cdkn2b , cdkn2a , methylation , cancer research , biology , gene silencing , cpg site , dna methylation , suppressor , gene , microbiology and biotechnology , genetics , gene expression
De novo methylation of the 5′CpG island has been recently reported as an alternative mechanism of inactivation for the tumour suppressor genes CDKN2A and CDKN2B. We examined CDKN2A methylation status at diagnosis in 42 B‐cell chronic lymphocytic leukaemia (CLL) patients, in 19 cases the CDKN2B methylation status was also analysed. No homozygous CDKN2A/2B deletion was detected, but four patients (9%) displayed an aberrant CDKN2A methylation status and only one had hypermethylated CDKN2B. De novo methylation was associated with silencing of gene expression. These results confirm that CDKN2A/2B inactivation by deletion is a rare event in CLL and suggest that aberrant methylation could be an alternative way of inactivation very rarely involved in the development of some CLL.