TP53 mutations are frequent in adult acute lymphoblastic leukemia cases negative for recurrent fusion genes and correlate with poor response to induction therapy

Acute lymphoblastic leukemia (ALL) is a disease of either B-cell (80–85%) or T-cell (20–25%) derivation. Several molecular aberrations (i.e. BCR-ABL1, MLL/AFF1, SIL/TAL1 and E2A/PBX1) confer an overall poor outcome.1,2 However, a proportion of patients do not carry known genetic abnormalities and have a heterogeneous clinical course. P53 plays a crucial role in cell cycle regulation and apoptosis after DNA damage, and its role in tumorigenesis is well-recognized in solid and hematologic malignancies, particularly acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL), in which its deregulation represents an important predictor of poor outcome.3–10