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.
Authors
Meyer, StefanWhite, Daniel J
Will, Andrew M
Eden, Tim O B
Sim, Alyson
Brown, Robert
Strathdee, Gordon
Affiliation
Department of Paediatric Haematology and Oncology, Central Manchester and Manchester Children's University Hospitals NHS Trust, Manchester, UK. stefan.meyer-2@manchester.ac.ukIssue Date
2006-07
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Show full item recordAbstract
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.Citation
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. 2006, 134 (1):61-3 Br. J. Haematol.Journal
British Journal of HaematologyDOI
10.1111/j.1365-2141.2006.06107.xPubMed ID
16803569Type
ArticleLanguage
enISSN
0007-1048ae974a485f413a2113503eed53cd6c53
10.1111/j.1365-2141.2006.06107.x
Scopus Count
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