IMMUNE MODULATION AND METASTASIS IN OVARIAN CANCER

The review article presents data on the predominant mechanisms of metastatic progression in ovarian cancer. It highlights the morphological and functional features of the greater omentum, detailing how these contribute to the spread of cancer cells as well as exert anti-tumor effects. The balance between these opposing properties is influenced by the cellular composition, the content of extracellular matrix molecules, and the biomechanical characteristics of the greater omentum during carcinogenesis. The milk spots serve as the primary sites for cancer cell implantation and differ from lymph nodes due to their simpler structure and unique cellular composition (including macrophages, B cells, CD4+ and CD8+ T lymphocytes, and other immune cells), which undergoes significant changes during metastasis. M2 macrophages, adipocytes, CD33+ cells, and CD4+ CD25high CD127low T suppressor cells promote the migration, invasion, growth, and colonization of cancer cells. Most molecules synthesized in the greater omentum during metastasis also stimulate these processes, with exceptions including E-cadherin, CXCL10, CXCL11, and CXCR3, which inhibit tumor growth.