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

[Guest guest]

Blank

17p Deletion is associated with resistance of B-cell chronic lymphocytic

leukemia cells to in vitro fludarabine-induced apoptosis.

B Turgut, O Vural, FS Pala, GE Pamuk, K Tabakcioglu, M Demir, S Ongoren, T

Soysal, and C Algunes

Leuk Lymphoma, February 1, 2007; 48(2): 311-20.

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.

PMID: 17325891