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dc.contributor.authorMeyer, Stefan
dc.contributor.authorWhite, Daniel J
dc.contributor.authorWill, Andrew M
dc.contributor.authorEden, Tim O B
dc.contributor.authorSim, Alyson
dc.contributor.authorBrown, Robert
dc.contributor.authorStrathdee, Gordon
dc.date.accessioned2009-07-07T15:47:38Z
dc.date.available2009-07-07T15:47:38Z
dc.date.issued2006-07
dc.identifier.citationNo 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.issn0007-1048
dc.identifier.pmid16803569
dc.identifier.doi10.1111/j.1365-2141.2006.06107.x
dc.identifier.urihttp://hdl.handle.net/10541/72864
dc.description.abstractFanconi 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.isoenen
dc.subjectCancer Genesen
dc.subjectLeukaemiaen
dc.subjectLeukaemia, Myeloiden
dc.subject.meshAcute Disease
dc.subject.meshAdolescent
dc.subject.meshCell Cycle Proteins
dc.subject.meshChild
dc.subject.meshChild, Preschool
dc.subject.meshChromosomal Instability
dc.subject.meshCpG Islands
dc.subject.meshDNA Methylation
dc.subject.meshFanconi Anemia Complementation Group F Protein
dc.subject.meshFanconi Anemia Complementation Group Proteins
dc.subject.meshGenes, Neoplasm
dc.subject.meshHumans
dc.subject.meshInfant
dc.subject.meshLeukemia
dc.subject.meshLeukemia, Myeloid
dc.subject.meshNuclear Proteins
dc.subject.meshPrecursor Cell Lymphoblastic Leukemia-Lymphoma
dc.titleNo 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.typeArticleen
dc.contributor.departmentDepartment of Paediatric Haematology and Oncology, Central Manchester and Manchester Children's University Hospitals NHS Trust, Manchester, UK. stefan.meyer-2@manchester.ac.uken
dc.identifier.journalBritish Journal of Haematologyen
html.description.abstractFanconi 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.


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