17p Deletion is associated with resistance of B-cell chronic lymphocytic leukemia cells to in vitro fludarabine-induced apoptosis

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dc.authorwosidTurgut, Burhan/A-2517-2016
dc.authorwosidSoysal, Teoman/C-8223-2017
dc.contributor.authorTurgut, Burhan
dc.contributor.authorVural, Ozden
dc.contributor.authorPala, Funda S.
dc.contributor.authorPamuk, Gulsum E.
dc.contributor.authorTabakcioglu, Kiymet
dc.contributor.authorDemir, Muzaffer
dc.contributor.authorOngoren, Seniz
dc.date.accessioned2024-06-12T10:56:30Z
dc.date.available2024-06-12T10:56:30Z
dc.date.issued2007
dc.departmentTrakya Üniversitesien_US
dc.description.abstractWe explored the relationship between the cytogenetic/biologic characteristics of B-chronic lymphocytic leukemia (B-CLL) cells and their tendency to undergo spontaneous or fludarabine-induced apoptosis in vitro. B cells from 36 B-CLL patients were incubated with or without fluclarabine for 48 h. Apoptosis was determined by two assays: annexin V staining and DNA staining. Fluorescence in situ hybridization was used for detection of trisomy 12, 11q deletion, and 17p deletion. Bcl-2 and CD38 expressions were determined by flow cytometry. Five patients had 17p deletion, 6 had trisomy 12, and another 6 had 11q deletion. B-CLL cells with 17p deletion had significant resistance to apoptosis induced by fludarabine and a slight spontaneous resistance to apoptosis. Bcl-2 and CD38 were not associated with in vitro spontaneous and fludarabine-induced apoptosis. In conclusion, 17p deletion, which causes loss of p53 gene, is associated with resistance to fludarabine-induced apoptosis in vitro. New treatment modalities should be tried in B-CLL patients with 17p deletion.en_US
dc.identifier.doi10.1080/10428190601059829
dc.identifier.endpage320en_US
dc.identifier.issn1042-8194
dc.identifier.issue2en_US
dc.identifier.pmid17325891en_US
dc.identifier.scopus2-s2.0-34247842875en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage311en_US
dc.identifier.urihttps://doi.org/10.1080/10428190601059829
dc.identifier.urihttps://hdl.handle.net/20.500.14551/19796
dc.identifier.volume48en_US
dc.identifier.wosWOS:000244528300017en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTaylor & Francis Ltden_US
dc.relation.ispartofLeukemia & Lymphomaen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectChronic Lymphocytic Leukemiaen_US
dc.subjectApoptosisen_US
dc.subjectFludarabineen_US
dc.subject17p Deletionen_US
dc.subjectGene Mutation Statusen_US
dc.subjectDrug-Resistanceen_US
dc.subjectCd38 Expressionen_US
dc.subjectPurine Analogsen_US
dc.subjectGenomic Aberrationsen_US
dc.subjectP53 Dysfunctionen_US
dc.subjectBcl-2 Geneen_US
dc.subjectT-Cellsen_US
dc.subjectCllen_US
dc.subjectSurvivalen_US
dc.title17p Deletion is associated with resistance of B-cell chronic lymphocytic leukemia cells to in vitro fludarabine-induced apoptosisen_US
dc.typeArticleen_US

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