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.
dc.contributor.author | Meyer, Stefan | |
dc.contributor.author | White, Daniel J | |
dc.contributor.author | Will, Andrew M | |
dc.contributor.author | Eden, Tim O B | |
dc.contributor.author | Sim, Alyson | |
dc.contributor.author | Brown, Robert | |
dc.contributor.author | Strathdee, Gordon | |
dc.date.accessioned | 2009-07-07T15:47:38Z | |
dc.date.available | 2009-07-07T15:47:38Z | |
dc.date.issued | 2006-07 | |
dc.identifier.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. | en |
dc.identifier.issn | 0007-1048 | |
dc.identifier.pmid | 16803569 | |
dc.identifier.doi | 10.1111/j.1365-2141.2006.06107.x | |
dc.identifier.uri | http://hdl.handle.net/10541/72864 | |
dc.description.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. | |
dc.language.iso | en | en |
dc.subject | Cancer Genes | en |
dc.subject | Leukaemia | en |
dc.subject | Leukaemia, Myeloid | en |
dc.subject.mesh | Acute Disease | |
dc.subject.mesh | Adolescent | |
dc.subject.mesh | Cell Cycle Proteins | |
dc.subject.mesh | Child | |
dc.subject.mesh | Child, Preschool | |
dc.subject.mesh | Chromosomal Instability | |
dc.subject.mesh | CpG Islands | |
dc.subject.mesh | DNA Methylation | |
dc.subject.mesh | Fanconi Anemia Complementation Group F Protein | |
dc.subject.mesh | Fanconi Anemia Complementation Group Proteins | |
dc.subject.mesh | Genes, Neoplasm | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Infant | |
dc.subject.mesh | Leukemia | |
dc.subject.mesh | Leukemia, Myeloid | |
dc.subject.mesh | Nuclear Proteins | |
dc.subject.mesh | Precursor Cell Lymphoblastic Leukemia-Lymphoma | |
dc.title | 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. | en |
dc.type | Article | en |
dc.contributor.department | Department of Paediatric Haematology and Oncology, Central Manchester and Manchester Children's University Hospitals NHS Trust, Manchester, UK. stefan.meyer-2@manchester.ac.uk | en |
dc.identifier.journal | British Journal of Haematology | en |
html.description.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. |