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.

76 Dysregulation of the COX pathway: Many tumors, including MPNs, show hyperactivity of cyclooxygenases (COX-1/COX-2), leading to excessive production of prostaglandins, especially PGE₂. Immunomodulation: PGE₂ suppresses the antitumor immune response by reducing the activity of NK cells, CD8⁺ T lymphocytes, and stimulating regulatory T cells. This creates an immunosuppressive microenvironment favorable for clonal growth. PGs support chronic inflammation in the bone marrow, which is a key factor in the progression of MPN. They stimulate angiogenesis, stromal remodeling and myeloid cell proliferation. Interaction with JAK2, CALR, MPL mutations: Although PGs are not the primary cause of MPN, they amplify the effects of mutations, promoting the survival and expansion of pathological clones. That is, PGs, especially PGE₂, act as key mediators of immune dysfunction and the inflammatory microenvironment in MPN. They do not directly trigger the disease, but significantly contribute to its progression and complications [9]. PGE₂ acts as a ―double-edged sword‖: on the one hand, it supports angiogenesis and cell survival, on the other hand, it suppresses antitumor immunity. This gives a clear picture: in MPN, PGs contribute to inflammation and immune dysfunction, thromboxanes to thrombosis, and prostacyclin to protective anticoagulant effects. PGs (PGE₂, PGF₂α, PGD₂) are responsible for inflammation, pain, and immunomodulation. In MPN, excessive production of PGE₂ is observed → chronic inflammation and immune dysfunction. Thromboxanes (TXA₂) — stimulate platelet aggregation and vasoconstriction. In MPN, their activity increases the risk of thrombosis. Prostacyclin (PGI₂) — counteracts thromboxanes, causes vasodilation, and inhibits platelet aggregation. In MPN, its level is often reduced, which disrupts the balance and contributes to thrombotic complications.