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dc.contributor.authorBallabio, E-
dc.contributor.authorRegan, R-
dc.contributor.authorGarimberti, E-
dc.contributor.authorHarbott, J-
dc.contributor.authorBradtke, J-
dc.contributor.authorTeigler-Schlegel, A-
dc.contributor.authorBiondi, A-
dc.contributor.authorCazzaniga, G-
dc.contributor.authorGiudici, G-
dc.contributor.authorWainscoat, JS-
dc.contributor.authorBoultwood, J-
dc.contributor.authorBridger, JM-
dc.contributor.authorKnight, SJL-
dc.contributor.authorTosi, S-
dc.identifier.citationPLoS ONE, 6(6): e20607, Jun 2011en_US
dc.descriptionCopyright @ 2011 Ballabio et al.en_US
dc.description.abstractLeukaemia is often associated with genetic alterations such as translocations, amplifications and deletions, and recurrent chromosome abnormalities are used as markers of diagnostic and prognostic relevance. However, a proportion of acute myeloid leukaemia (AML) cases have an apparently normal karyotype despite comprehensive cytogenetic analysis. Based on conventional cytogenetic analysis of banded chromosomes, we selected a series of 23 paediatric patients with acute myeloid leukaemia and performed whole genome array comparative genome hybridization (aCGH) using DNA samples derived from the same patients. Imbalances involving large chromosomal regions or entire chromosomes were detected by aCGH in seven of the patients studied. Results were validated by fluorescence in situ hybridization (FISH) to both interphase nuclei and metaphase chromosomes using appropriate bacterial artificial chromosome (BAC) probes. The majority of these copy number alterations (CNAs) were confirmed by FISH and found to localize to the interphase rather than metaphase nuclei. Furthermore, the proliferative states of the cells analyzed by FISH were tested by immunofluorescence using an antibody against the proliferation marker pKi67. Interestingly, these experiments showed that, in the vast majority of cases, the changes appeared to be confined to interphase nuclei in a non-proliferative status.en_US
dc.description.sponsorshipThis work was supported by a grant from Leukaemia Research UK (grant no. 0253). SJLK and RR were supported by the NIHR Biomedical Research Centre, Oxford, with funding from the Department of Health’s NIHR Biomedical Research Centres funding scheme-
dc.description.sponsorshipThis article is available through the Brunel Open Access Publishing Fund.-
dc.publisherPublic Library of Scienceen_US
dc.titleGenomic imbalances are confined to non-proliferating cells in paediatric patients with acute myeloid leukaemia and a normal or incomplete karyotypeen_US
dc.typeResearch Paperen_US
pubs.organisational-data/Brunel/Brunel (Active)-
pubs.organisational-data/Brunel/Brunel (Active)/School of Health Science & Social Care-
pubs.organisational-data/Brunel/Research Centres-
pubs.organisational-data/Brunel/Research Centres/BIAS-
pubs.organisational-data/Brunel/Research Centres/CCCB-
pubs.organisational-data/Brunel/School of Health Sciences and Social Care-
pubs.organisational-data/Brunel/School of Health Sciences and Social Care/BIAS-
pubs.organisational-data/Brunel/School of Health Sciences and Social Care/CCCB-
Appears in Collections:Biological Sciences
Community Health and Public Health
Brunel OA Publishing Fund
Dept of Life Sciences Research Papers

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