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The purpose of the current project is to study the candidate genes and immunological factors involved in the pathogenesis of endometriosis. Endometriosis is oestrogen-dependent disease in which endometrial tissue grows outside the uterus. Endometriosis occurs in 10% of women of reproductive age and up to 50% of infertile women. Despite the intensive research, the molecular mechanisms underlying the endometriosis are still poorly understood. However, the previous studies have clearly confirmed that endometriosis is a polygenic and multifactorial disease. Therefore, the aim of the current project is to investigate the genetic variations of the genes possibly involved in the development of endometriosis. The special emphasis is given to the study of the genetic variations of the genes of oestrogen metabolism (17β-HSD1), hormone receptors (ERα and ERβ), angiogenic factors (ACE, VEGF and VEGFR), extracellular matrix degrading enzymes (MMP-2 and -9), immunogenetic markers (HLA-DR4 and CTLA-4) and antiapoptotic factors (survivin). In addition, the importance of the survivin as a new marker for non-invasive diagnosis of endometriosis will be evaluated. In order to find out the putative role of the immunological factors in the aetiology of endometriosis, the autoantibodies directed towards the endometrium as well as the organ-nonspecific autoantibodies will be determined in the blood serum samples of patients with endometriosis. The results of the current project provide us a better understanding of the risk factors leading to the endometriosis and help to design more effective therapies for the treatment of endometriosis. |