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Significance Capicua (CIC) is a protein that regulates gene transcription, and its dysfunction leads to several neurological diseases.CIC is frequently mutated in several cancers, but mechanistic studies on its tumor suppressor function have been limited. Here, we showed that deletion ofCic in mice causes T cell acute lymphoblastic leukemia/lymphoma (T-ALL) and disrupts early T cell development. We also found that loss of CIC up-regulates the oncogenic RAS program, both before and after the onset of T-ALL. Moreover, we detected activation of the NOTCH1 and MYC transcriptional programs, which we propose cooperate with the RAS pathway to drive tumor development. Our study demonstrates that CIC is a tumor suppressor for lymphoid malignancies and elucidates the tumorigenic events upon loss of CIC.

Loss of Capicua alters early T cell development and predisposes mice to T cell lymphoblastic leukemia/lymphoma