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dc.contributor.authorBrito-Babapulle, Ven_US
dc.contributor.authorBaou, Men_US
dc.contributor.authorMatutes, Een_US
dc.contributor.authorMorilla, Ren_US
dc.contributor.authorAtkinson, Sen_US
dc.contributor.authorCatovsky, Den_US
dc.date.accessioned2018-09-24T15:54:48Z
dc.date.issued2001-08en_US
dc.identifier2en_US
dc.identifier.citationBRITISH JOURNAL OF HAEMATOLOGY, 2001, 114 pp. 327 - 332en_US
dc.identifier.issn0007-1048en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2851
dc.identifier.doi10.1046/j.1365-2141.2001.02935.xen_US
dc.description.abstractDeletions of 13q14.3 are well known in several malignancies and are thought to be associated with tumour suppressor function. The RB-1 gene is a tumour suppressor gene, but other loci including D13S319 and D13S25 telomeric to this within 13q14.3 axe deleted in B-cell chronic lymphocytic leukaemia (B-CLL), multiple myeloma and non-Hodgkin’s lymphoma, with varying clinical significance. The fluorescence in situ hybridization screening of 22 patients with T-prolymphocytic leukaemia (T-PLL) for deletions of 13q14.3 revealed loss of D13S25 in 17 cases (mean 40% range 13-98%), with 11 patients having at least a 20% deletion. Mapping the deletions for the RB-1, D13S319,and D13S25 loci revealed D13S25 as the most frequently deleted marker. However, patients with only the D13S25 deletion had low percentages of cells with the deletion (12-13%), suggesting that loss of D13S25 on its own may not provide sufficient growth advantage. The use of the YAC 954c12, which maps immediately adjacent to D13S25, defined the telomeric border of the deletion in some of the cases. Inv(14)(q11q32) and t(14;14)(q11;q32) are characteristic of T-PLL, but are also observed in premalignant T-cell clones in patients with ataxia telangiectasia. Transition to overt leukaemia may result from loss of suppressor function. Thus, 13q14.3 deletions could contribute to the development of overt leukaemia in T-PLL, but the involvement of more than one gene in the region cannot be excluded.en_US
dc.format.extent327 - 332en_US
dc.languageEnglishen_US
dc.language.isoEnglishen_US
dc.publisherBLACKWELL SCIENCE LTDen_US
dc.titleDeletions of D13S25, D13S319 and RB-1 mapping to 13q14.3 in T-cell prolymphocytic leukaemiaen_US
dc.typeJournal Article
rioxxterms.versionofrecord10.1046/j.1365-2141.2001.02935.xen_US
rioxxterms.licenseref.startdate2001-08en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfBRITISH JOURNAL OF HAEMATOLOGYen_US
pubs.notesaffiliation: Brito-Babapulle, V (Reprint Author), Royal Marsden Hosp, Fulham Rd, London SW3 6JJ, England. Inst Canc Res, Acad Dept Haematol & Cytogenet, London SW3 6JB, England. keywords: T-PLL; B-CLL; 13q14.3 deletions; suppressor genes; trisomy 12 keywords-plus: CHRONIC LYMPHOCYTIC-LEUKEMIA; IN-SITU-HYBRIDIZATION; TUMOR-SUPPRESSOR GENE; ATAXIA-TELANGIECTASIA; MULTIPLE-MYELOMA; CHROMOSOME 13Q14; MANTLE CELL; BAND 13Q14; REGION; IDENTIFICATION research-areas: Hematology web-of-science-categories: Hematology number-of-cited-references: 21 times-cited: 3 usage-count-last-180-days: 0 usage-count-since-2013: 0 journal-iso: Br. J. Haematol. doc-delivery-number: 465CB unique-id: ISI:000170570200012 oa: gold_or_bronze da: 2018-09-24en_US
pubs.notesNot knownen_US
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Molecular Haematology (including Cytogenetics Group and Cell Markers)
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Molecular Haematology (including Cytogenetics Group and Cell Markers)
pubs.volume114en_US
pubs.embargo.termsNot knownen_US
icr.researchteamMolecular Haematology (including Cytogenetics Group and Cell Markers)en_US
dc.contributor.icrauthorCatovsky, Danielen_US
dc.contributor.icrauthorMatutes, Estellaen_US
dc.contributor.icrauthorMorilla, Ricardoen_US


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