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No evidence of significant silencing of Fanconi genes FANCF and FANCB or Nijmegen breakage syndrome gene NBS1 by DNA hyper‐methylation in sporadic childhood leukaemia
Author(s) -
Meyer Stefan,
White Daniel J.,
Will A. M.,
Eden Tim,
Sim Alyson,
Brown Robert,
Strathdee Gordon
Publication year - 2006
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 - 10.1111/j.1365-2141.2006.06107.x
Subject(s) - nijmegen breakage syndrome , fanconi anemia , chromosome instability , dna methylation , methylation , cancer research , biology , cpg site , medicine , genetics , gene , dna repair , dna damage , dna , gene expression , ataxia telangiectasia , chromosome
Summary Fanconi anaemia (FA) and Nijmegen breakage syndrome (NBS) carry a high risk of haematological cancer. Affected cellular pathways may be modulated in sporadic malignancies and silencing of FANCF through methylation has been shown to cause somatic disruption of the FA pathway. Combined bisulphite restriction analysis for methylation of FANCF , FANCB and NBS1 was used to investigate 81 sporadic acute childhood leukaemias. No methylation was detected at any associated CpG sites analysed. This does not exclude very low levels of FANCF , FANCB or NBS1 methylation, but suggests other factors are responsible for chemo‐sensitivity and chromosomal instability in sporadic childhood leukaemia.