期刊
LEUKEMIA
卷 14, 期 1, 页码 40-46出版社
STOCKTON PRESS
DOI: 10.1038/sj.leu.2401636
关键词
B-CLL; apoptosis; cell cycle; DNA repair
B cell chronic lymphocytic leukemia (B-CLL) cannot be cured with conventional chemotherapy, This clinical enigma appears to be at least partially due to the fact that B-CLL cells are resistant to programmed cell death (apoptosis) and that they are arrested in G0/G1 phase of the cell cycle. The reasons for the dysregulation of these two key cellular events in B-CLL are unclear. The present study aimed at determining correlations between the expression levels of proteins regulating apoptosis, cell cycle and DNA repair in B-CLL cells and normal B cells. In addition, the differential sensitivity of B-CLL cells to drug-induced apoptosis was quantified. We show that in B-CLL cells levels of the death-suppressor Bcl-2 correlated positively with those of the pro-apoptotic protein Bar and of the cyclin-dependent kinase (cdk) inhibitor p27(Kip1). I, B-CLL cells levels of the anti-apoptotic Bcl-x(L) showed a positive correlation with levels of the 80 kDa regulatory component (Ku80) of the DNA-dependent protein kinase that is involved in DNA double-stranded break repair. These correlations were not detected in normal B cells. The sensitivity of leukemic cells to FLUD but not to ADM, CPM or to DEX was reduced in pre-treated patients. These data support the hypothesis that in B-CLL cells death-modulators and molecules modulating cell cycle and DNA repair are regulated in a coordinated manner.
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