LAUSR

(P< .0001), low hemoglobin (P5 .0009), high absolute lymphocyte count (P5 .02), higher serum lactate dehydrogenase levels (P5 .023), PB blast % (P< .0001), BM blast % (P< .0001), 2016WHO morphological subtype CMML-2 (P< .0001), abnormal cytogenetics (P5 .002), Mayo-French cytogenetic risk stratification (P5 .01), NPM1 (P5 .0004), and Tp53 (P5 .002) mutations. ASXL1, DNMT3A, TET2, and FLT3 ITD mutations did not impact LFS; in multivariable analysis that included the aforementioned significant variables, only PB blasts % (P< .0001, HR 1.2, 95% CI 1.13–1.3), NPM1 mutations (P5 .03, HR 4.7, 95% CI 1.7–12.8), and Tp53 mutations (P5 .001, HR 5.4, 95% CI 1.6–18.4) remained significant. The current study confirms the infrequent occurrence of NPM1 mutations in CMML; also, the number of informative cases was large enough to allow demonstration of clustering of NPM1 mutations in CMML with normal cytogenetics, “dysplastic CMML phenotype” and DNTM3A mutations. More importantly, we show a significantly higher risk of BT in patients with CMML harboring NPM1 mutations.