Harnessing the MYB-dependent TAL1 5’super-enhancer for targeted therapy in T-ALL

The acquisition of genetic abnormalities leading to deregulation of oncogenes is the basis for cancer development. Some proto-oncogenes have several mechanisms of deregulation. In T-cell acute lymphoblastic leukemia (T-ALL), in V. Asnafi’s team, C. Smith showed that patients carrying 5’super-enhancer (5’SE) mutations of the TAL1 oncogene constitute a specific subgroup of patients with a poor prognosis, independently of the level of oncogene deregulation. Interestingly, this anomaly may serve as a therapeutic target for the molecule Mebendazole.

Images of control and treated mice after Mebendazole administration. The tumor burden of treated mice is lower than that of control mice.