Mutational analysis of patient data indicated that UTX mutations occur simultaneously with TP53 mutations in myeloid malignancies, and combined inactivation of Utx and Trp53 accelerated the development of CMML in a cell-autonomous manner.
Dysregulation of p53 was uncommon in CMML-F. CMML-F patients tended to have a shorter median overall survival compared with other CMML patients (P=0.079).