title: 17p Deletion is associated with resistance of B-cell chronic lymphocytic leukemia cells to in vitro fludarabine-induced apoptosis.
abstract: We 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 fludarabine 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.
authors.affiliation: Division of Hematology, Trakya University Medical Faculty, Edirne, Turkey. burhanturgut@trakya.edu.tr
authors.forename: Burhan
authors.initials: B
authors.lastname: Turgut
authors.forename: Ozden
authors.initials: O
authors.lastname: Vural
authors.forename: Funda S
authors.initials: FS
authors.lastname: Pala
authors.forename: Gülsüm E
authors.initials: GE
authors.lastname: Pamuk
authors.forename: Kiymet
authors.initials: K
authors.lastname: Tabakcioğlu
authors.forename: Muzaffer
authors.initials: M
authors.lastname: Demir
authors.forename: Seniz
authors.initials: S
authors.lastname: Ongören
authors.forename: Teoman
authors.initials: T
authors.lastname: Soysal
authors.forename: Cetin
authors.initials: C
authors.lastname: Algüneş
mesh_terms: D051997:ADP-ribosyl Cyclase 1 / Q000378:metabolism; D000368:Aged; D000369:Aged, 80 and over; D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D002872:Chromosome Deletion; D002886:Chromosomes, Human, Pair 17 / Q000235:genetics*; D004248:DNA (Cytosine-5-)-Methyltransferases / Q000037:antagonists & inhibitors; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D014740:Vidarabine / Q000031:analogs & derivatives* / Q000494:pharmacology
chemical_list: D000970:Antineoplastic Agents; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D004248:DNA (Cytosine-5-)-Methyltransferases; D051997:ADP-ribosyl Cyclase 1; D014740:Vidarabine; C024352:fludarabine