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.
Meyer, Stefan White, Daniel J Will, Andrew M Eden, Tim O B Sim, Alyson Brown, Robert Strathdee, Gordon
Meyer, Stefan
White, Daniel J
Will, Andrew M
Eden, Tim O B
Sim, Alyson
Brown, Robert
Strathdee, Gordon
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Abstract
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.
Description
Date
2006-07
Publisher
Keywords
Cancer Genes
Leukaemia
Leukaemia, Myeloid
Leukaemia
Leukaemia, Myeloid
Type
Article
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.