Developmental genetics of endometriosis

Published on November 29, 2018   20 min

A selection of talks on Genetics & Epigenetics

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Today, I wish to present a lecture about "Developmental Genetics of Endometriosis". In the present lecture, I wish to call your attention to our new hypothesis of endometriosis, which we call "developmental genomics of endometriosis".
The title of my lecture is proved by a well-known fact that almost 100 years past since endometriosis, as a chronic disease, was first described by Karl Rokitiansky in 1860 as a chronic estrogen-dependent inflammatory heritable disease, affecting and debilitating approximately five to 10 percent of all women in their early reproductive age. The problem of endometriosis remains in the focus of intensive clinical and medical inspection as scientifical studies. In spite of enormous effort, a lot of information on numerous genetic, epigenetic, endocrine, immunological studies, the pathogenesis of endometriosis still remains enigmatical. In our famous Ott's Institute of Obstetrics, Gynecology and Reproductology in Saint-Petersburg, Russia, the problem of endometriosis is in the focus of clinical laboratory and theoretical studies for over 30 years.
This slide shows basic theories and hypotheses of endometriosis known so far, but there are a lot of them. Over 10 of these basic hypotheses and theories tried to provide the clue to solve the endometriosis problem. They include the old but still widely accepted transplantation theory, suggested by J.A. Sampson in 1922. Latest implemented as different immunological-toxicology location, and hormonal dysregulation theory. Genetic and epigenetic views of endometriosis pathology are especially numerous and prevailed at the present endometriosis study. With a suggestion made by Dr. Meyer on the dormant stem cells in peritoneum and abnormalities altering the development suspected by the Italian scientist's Signorile group in 2012, deserve special attention in view of our recent hypothesis, postulating the existence of special genetic program, operative in the development of endometriosis. Their basic conclusion drawn from this theory is quite obvious. Clinical studies identified in today's genes specific microRNA called human sequencing, expression profile, immunological, and hormonal. And epigenetic data on the pathogenesis of endometriosis are numerous, but they are still full of contradiction, and unanimously confirm the general hormonal, monologic biochemical deregulation of endometriosis effect in human. But, none of these theories or hypotheses provide suitable guides on understanding the intimate pathophysiological mechanism of endometriosis, its origin and progression.