At the present time, it is a challenge to treat patients with uterine myomas while still preserving the surrounding organs. The aim — of the study is to consider clinical and morphological correlations and molecular mechanisms of stromal-parenchymatous relationships in uterine myoma growth to identify new pharmaceutical interventions for the disease. Material and methods. Retrospectively, 160 patients were divided into 2 groups, based on the results of morphological studies after their operations for uterine myoma: The 1st group consisted of 104 patients with simple uterine myoma, while the 2nd group numbered 56 patients with proliferative (cellular and mitotic) uterine myoma. The average age of the patients was 36.2±12.3 years. Morphological and immunohistochemical studies were performed. Immunohistochemical reactions were carried out with antigen unmasking solutions in microwave ovens on serial paraffin-infiltrated tissue slices taken from myomatous polyps and the endometrial tissue of patients. Monoclonal antibodies to proliferation markers (Ki-67 PCNA), apoptosis regulators (Ball-2, Bax CD-95), and oncoprotein c-Myc were used as primary specific antibodies; growth factors - fibroblasts (FGF-beta), epidermal growth factor (EGF), insulin-like growth factor (IGF1), platelet-derived growth factor (PDGF); extracellular matrix components (laminine and fibronectin); neo-angiogenesis marker (CD-34); EGF receptor. Results. Simple uterine myoma is characterized by slower growth and development, smaller size, and less pronounced clinical manifestations. It is more often detected in patients of later reproductive age. Proliferative (cellular, mitotic) myoma is distinguished by faster growth and more pronounced clinical manifestations (pain syndrome, and a combination of endometrial hyperplasia, uterine bleeding and anemia). It has been established that the growth of simple uterine myoma is caused by myocyte hypertrophy under the influence of a number of growth factors such as IGF-1, EGF, and PDGF; oncoproteins; and the predominance of apoptosis over hyperplasia in myocytes. The growth of such a tumor is probably the result of secondary changes and an increase in the number of stromal cells, with the most mature stromal cells comprised of the fibroblastic series. The results of the study showed that the content of epidermal growth factor (EGF) and its receptors, and platelet-derived (PDGF) and insulin-like (IGF-1) growth factors in uterine myoma tissue is significantly increased in comparison with those in simple myoma tissue. The maximum level of proliferation markers (Ki-67 and PCNA) has been established in mitotic uterine myoma. In cellular and mitotic uterine myoma there is a significant decrease in the level of apoptosis compared to its level in simple myoma. In proliferative myoma — mitotic and cellular — a less mature stroma is observed than in simple myoma. Conclusion. The results give grounds for the development of medications contributing to the inhibition of proliferation, neo-angiogenesis, expression of growth factors and stimulation of apoptosis in myoma tissue.