Proceedings of the International scientific and practical conference ―Science at the Frontier of Progress‖ (June 8-10, 2026) / Publisher website: www.naukainfo.com. – Paris, France, 2026. - 178 p.

21 BIOLOGYAND BIOTECHNOLOGY UDC 577 213/.216: 577.213/.215 Voroniak Myroslav candidate of biological sciences, senior scientist; Shurko Nataliya candidate of biological sciences; senior scientist Khudzii Sofiia scientist; Kokoruz Maryana scientist; Laboratory of Molecular Genetics State Institution ―Institute of Blood Pathology and Transfusion Medicine of the National Academy of Medical Sciences of Ukraine‖, Lviv, Ukraine ROLE OF THE JAK/STAT SIGNALING PATHWAY IN PN-NEGATIVE CHRONIC MYELOPROLIFERATIVE DISEASES Abstract. The Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway is a fundamental intracellular mechanism that mediates cytokine and growth factor signaling. Dysregulation of this pathway through genetic mutations, polymorphisms, or persistent activation is closely associated with autoimmune diseases, inflammatory disorders, and a wide range of hematological and solid malignancies. Accordingly, the JAK/STAT pathway has become a major therapeutic and diagnostic target in precision medicine. The paper reviews the current understanding of the mechanisms of functioning of this phenomenon in normal and pathological conditions. Keywords: JAK/STAT signaling pathway, Janus kinases, STAT protein family, cytokines, myeloproliferative neoplasias. The JAK-STAT (Janus Kinases – signal transducer and activator of transcription) signaling pathway is a widely expressed intracellular signaling pathway that plays an important role in many critical biological processes, including immune system control, cell division, differentiation, and apoptosis. This pathway involves receptor-ligand complexes, Janus kinases (JAKs), signal transducers and activators of transcription (STAT) proteins, and the SOCS/CIS-containing protein family, which signals cytokines/cytokine-induced Src homology 2 (SH2), which play a critical role in the fine modulation of JAK/STAT pathway function. The JAK family includes JAK1, JAK2, JAK3, and TYK2, and the STAT family includes STAT1, STAT2, STAT3, STAT4, STAT5a, STAT5b, and STAT6. The SOCS/CIS protein family includes SOCS1–SOCS7 and CIS [1]. The signal transducer and activator of transcription (JAK-STAT) is an evolutionarily conserved transmembrane signal transduction mechanism that allows cells to communicate with the external environment. Various cytokines, interferons, growth factors, and other specific molecules activate JAK-STAT signaling to trigger a variety of physiological and pathological processes, including proliferation, metabolism, immune response, inflammation, and malignancy. Disrupted JAK-STAT signaling and associated genetic mutations are closely associated with immune activation and cancer progression. It is an evolutionarily conserved signaling pathway that functions in several key physiological processes, including hematopoiesis, differentiation, metabolism, and immune modulation [2, 3, 4, 5]. n mammals, the JAK/STAT pathway is a major signaling mechanism for a wide range of cytokines and growth factors. JAK/STAT signaling plays a key role in cell proliferation, stem cell maintenance, differentiation, and regulation of the immune system. More than 50 cytokines and growth factors, such as hormones, interferons (IFNs), interleukins (ILs), and colony-stimulating factors, have been identified in the JAK/STAT signaling pathway. Events mediated by JAK/STAT are diverse and include hematopoiesis, immune fitness, tissue repair, inflammation, apoptosis, and adipogenesis. Loss or mutation of JAK/STAT components is associated with many human diseases. The JAK/STAT signaling pathway was discovered in 1989, but only in the past three decades has significant progress been made in understanding the role of this process in myeloproliferative neoplasms (MPNs). The Janus kinase-transducer and activator of transcription (JAK-STAT) signaling pathway plays a key role in mediating signals from a wide range of cytokines and