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Trisomy 12 CLL
which was associated with aggressive disease, and CD38 and ZAP70 positivity.47 Unfortunately, this study did not assess the association between NT5E expression and cyto- genetic status. Our findings suggest that targeting this pathway may be an effective therapy in patients with +12 CLL.
In summary, we have demonstrated, by whole tran- scriptome profiling, that CLL cases with +12 as the only cytogenetic abnormality demonstrate a unique set of dif- ferentially expressed genes and pathways compared to cases with del(13q) or del(11q). Our data support the hypothesis that these differences contribute, in part, to the
unique pathophysiology of +12 CLL. Finally, we have identified genes and pathways, such as the checkpoint inhibitor molecule, NT5E (CD73), and the NFAT signaling pathway that may represent new therapeutic targets.
Acknowledgments
The authors thank the patients who donated their blood. The authors also thank Dr. David Lucas for helpful discussions and comments.
Funding
This work was supported in part by grants from the CLL Global Research Foundation and NIH/NCI 1 R01 CA182905-01.
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