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Significance B-cell chronic lymphocytic leukemia (CLL) is the most common adult leukemia. We previously found that dysregulation of the T-cell leukemia/lymphoma 1 (TCL1 ) oncogene is a critical contributing event in the pathogenesis of this disease. In this study we investigated molecular causes ofTCL1 overexpression in CLL. We identifiedmiR-3676 as a powerful regulator ofTCL1 expression. We found thatmiR-3676 is down-regulated on all groups of CLLs and mutated in 1% of CLLs. Interestingly,miR-3676 is located at 17p13, only 500-kb centromeric of tumor protein p53 (Tp53 ), and is codeleted withTp53 in 17p-deleted CLL. Loss ofmiR-3676 causes high levels ofTCL1 expression contributing to CLL progression. Thus, this study uncovers a major mechanism in the pathogenesis of CLL.

TCL1 targeting miR-3676 is codeleted with tumor protein p53 in chronic lymphocytic leukemia