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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.

作者信息

Meyer Stefan, White Daniel J, Will A M, Eden Tim, Sim Alyson, Brown Robert, Strathdee Gordon

机构信息

Department of Paediatric Haematology and Oncology, Central Manchester and Manchester Children's University Hospitals NHS Trust, Manchester, UK.

出版信息

Br J Haematol. 2006 Jul;134(1):61-3. doi: 10.1111/j.1365-2141.2006.06107.x.

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.

摘要

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