Proceedings of the International scientific and practical conference ― Cambridge Science and Education Conference‖ (February 23-25, 2026) / Publisher website: www.naukainfo.com. – Cambridge, United Kingdom, 2026. - 289 p.

73 [3]. These frequently observed concomitant mutations include genes encoding epigenetic modifiers, transcriptional regulators, and mRNA splicing machinery. Current therapeutic approaches in MPN aim to limit the risk of thrombosis with antiplatelet agents, anticoagulants, therapeutic venesection, and cytoreductive therapies, including hydroxycarbamide and interferon-alpha, all with proven benefits in certain circumstances [4]. JAK inhibitors, particularly ruxolitinib, have provided additional targeted therapy with clear symptomatic and clinical benefits but limited disease-modifying activity [5]. Hematopoietic stem cell transplantation is the only option for treatment, but is rarely appropriate due to significant toxicity and risk of mortality. It is usually reserved for younger, more resilient individuals with high-risk myelofibrosis or blast phase disease, and outcomes in these populations remain poor [6]. The clinical and genetic similarities and differences in this heterogeneous population provide an opportunity to characterize and elucidate the contribution of various genetic and epigenetic factors to the pathogenesis of the diseases. The improved availability of such genetic and phenotypic data has made it possible to generate individualized probabilities of prognosis for patients with MPN [3]. It is clear that in addition to the main driver mutations, other mutations and many other factors play an important role in the occurrence and development of these diseases. Such factors include prostaglandins (PGs). PGs are biologically active lipid mediators that are formed from arachidonic acid and belong to the class of eicosanoids. PGs were first isolated from semen and were thought to be involved in many reproductive processes. Initially, it was assumed that these substances originate in the prostate gland, but in fact it turned out that they are formed in the seminal vesicles. PG formation is not limited to the reproductive system; they are produced by all tissues. There are several classes of PGs, which are designated by letters of the Latin alphabet. They have a wide range of actions: they regulate inflammation, immune response, vascular tone, platelet aggregation and cell growth. Recent studies have highlighted the involvement of these lipids in various types of cancer [7].