A feedforward loop between ACLY and MYC supports T-ALL progression in vivo

Abstract excerpt

• MYC transcription is supported by ACLY-generated acetyl-CoA, and ACLY is a direct target of MYC, establishing a feedforward loop in T-ALL. • Secondary Acly loss or ACLY inhibition results in significant therapeutic effects in vivo, unveiling ACLY as a novel target in T-ALL. T-cell acute lymphoblastic leukemia (T-ALL) is a hematological malignancy in need of novel therapeutic approaches. Here, we identify...

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