MicroRNAs (miRNAs) have been shown to play critical roles in regulating the 
progress of leukemia. We performed miRNA expression profile in six Chinese 
patients with chronic lymphocytic leukemia (CLL), and in peripheral B cells from 
pooled 30 healthy donors, using a platform containing 866 human miRNAs. The most 
frequent changes in miRNAs in CLL cells included downregulation of miR-126, 
miR-572, miR-494, miR-923, miR-638, miR-130a, miR-181a and miR-181b and 
up-regulation of miR-29a, miR-660, miR-20a, miR-106b, miR-142-5p, miR-101, 
miR-30b, miR-34a, miR-let-7f, miR-21 and miR-155. Among the miRNAs 
down-regulated in CLL cells, we showed that miR-181a/b expression levels were 
significantly lower in poor prognostic subgroups defined by unmutated 
immunoglobulin heavy chain variable status and p53 aberrations. Furthermore, 
under-expression of miR-181a and miR-181b was associated with shorter overall 
survival and treatment-free survival in CLL patients. We further evaluated 
fludarabine-induced apoptosis after transfection of primary CLL cells from 40 
patients with miR-15a, miR-16-1, miR-34a, miR-181a and miR-181b mimics. 
Transfection of miR-34a, miR-181a and miR-181b mimics into CLL cells from p53 
wild-type patients led to significant increase in apoptosis compared with miRNA 
control. However, enforced expression of these miRNAs had no effect on B-CLL 
cells from p53-attenuated patients. We further demonstrated that miR-181a and 
miR-181b inhibiting BCL-2, MCL-1 and X-linked inhibitor of apoptosis protein by 
direct binding to 3'UTR. Thus, these results suggest that miR-181a/b may play 
important roles in the pathogenesis of CLL and may provide a possible 
therapeutic avenue and a sensitive indicator of the activity of the p53 axis in 
CLL.