The Influence of Biologically Active Substances Secreted by the Adipose Tissue on Endometrial Cancer

Diagnostics

Kaja Michalczyk¹  Natalia Niklas¹  Aneta Cymbaluk-Płoska¹  Małgorzata Rychlicka¹ 

[1] Department of Gynecological Surgery and Gynecological Oncology of Adults and Adolescents, Pomeranian Medical University, Al. Powstańców Wielkopolskich 72, 70-111 Szczecin, Poland;

关键词: endometrial cancer;    adipokines;    cytokines;    inflammation;    angiogenesis;    leptin;   

DOI  :  10.3390/diagnostics11030494

来源: DOAJ

【 摘 要 】

Endometrial cancer is one of the most frequently diagnosed gynecological neoplasms in developed countries and its incidence is rising. Usually, it is diagnosed in the early stages of the disease and has a good prognosis; however, in later stages, the rate of recurrence reaches up to 60%. The discrepancy in relapse rates is due to the heterogeneity of the group related to the presence of prognostic factors affecting survival parameters. Increased body weight, diabetes, metabolic disturbances and estrogen imbalance are important factors for the pathogenesis of endometrial cancer. Even though prognostic factors such as histopathological grade, clinical stage, histological type and the presence of estrogen and progesterone receptors are well known in endometrial cancer, the search for novel prognostic biomarkers continues. Adipose tissue is an endocrine organ involved in metabolism, immune response and the production of biologically active substances participating in cell growth and differentiation, angiogenesis, apoptosis and carcinogenesis. In this manuscript, we review the impact of factors secreted by the adipose tissue involved in the regulation of glucose and lipid metabolism (leptin, adiponectin, omentin, vaspin, galectins) and factors responsible for homeostasis maintenance, inflammatory processes, angiogenesis and oxidative stress (IL-1β, 6, 8, TNFα, Vascular endothelial growth factor (VEGF), Fibroblast growth factors (FGFs)) in the diagnosis and prognosis of endometrial cancer.

【 授权许可】

Unknown