Proceedings of the International scientific and practical conference ―Science at the Frontier of Civilizations‖ (March 16-18, 2026) / Publisher website: www.naukainfo.com. – Helsinki, Finland, 2026. - 145 p.

8 SFSF2 mutations were associated with leukemia progression in these cohorts, while TP53 was strongly associated in another cohort. The negative prognostic impact of ASXL1 is evident in the presence of another high-risk mutation, but not alone. A large study of 2035 patients identified eight genomic subgroups in the MPN spectrum, each representing a different proportion of patients with PV, ET, and PMF with different risks of leukemic or fibrotic transformation and overall survival. Genetic factors, including TET2, SRSF2, and ASXL1 mutations, contributed to more than 50% of the risk factors for fibrotic transformation with PV or ET using a predictive modeling approach. Similarly, more than a third of the risk of leukemic transformation was associated with genetic factors, including TP53 mutations. Individualized prognostic assessments can now be made at diagnosis based on genetic and clinical information, and molecular data are now routinely incorporated into prognostic scoring systems, including MIPPS70+ and GIPSS [2, 5]. With the use of next-generation sequencing (NGS), our knowledge of the mutational landscape in CMPN has improved significantly, and we now have a deeper understanding of the genetic basis of CMPN. Until recently, risk factors used to predict prognosis in CMPN were mostly based on clinical parameters, but information about the mutational landscape of CMPN is increasingly being added to improve and individualize prognostic assessments. The most common genetic mutations in CMPN are listed in Table 1 [6]. Only mutations with a frequency of at least 2% are listed.