Uterine myoma and adenomyosis: molecular characterization by steroid receptor gene expression


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Abstract

Objective. To study the characteristics of endometrial and myometrial responses to steroid stimulation by determining the level of steroid receptor gene expression in the myomatous nodules, adenomyosis, and the surrounding myometrium in uterine myoma, combined and isolated adenomyosis. Material and methods. Steroid receptor gene expression was comparatively analyzed in 48 patients with cellular myoma (n = 11), simple myoma (n = 15), adenomyosis (n = 12), and myoma concurrent with adenomyosis (n = 10). The investigators used uterine tissue samples removed during surgery, such as those of myomatous nodules, adenomyosis and their surrounding myometrium. The expression level of the studied genes was determined using real-time PCR. The latter employed sequence-specific primers for estrogen receptor and progesterone receptor genes. Results. The level of steroid receptor gene expression in the nodules was 2-9 times greater than that in the myometrium. There was the highest expression of estrogen receptor genes in the nodules of patients with adenomyosis and the lowest one in those with simple myoma. The expression of progesterone receptor genes in the nodules and myometrium was determined to be highest in patients with cellular myoma and to be lowest in those with adenomyosis. Conclusion. The foci of adenomyosis were characterized by the high expression of estrogen receptor genes with the insufficient expression of progesterone receptor genes. The significantly high level of estrogen receptor gene expression in the myometrium of patients with cellular myoma may have important pathogenetic value, by determining recurrence rates and propensity. The concurrent pathology was characterized by the equivalent and low expression of steroid receptor genes, which can explain the lack of therapeutic effects. The f indings will assist in personifying therapeutic approaches to choosing treatment policy for patients with both combined and isolated benign proliferative uterine diseases.

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About the authors

Svetlana Vladimirovna Shramko

Novokuznetsk State Institute for Postgraduate Training of Physicians; Branch, Russian Medical Academy of Continuing Professional Education, Ministry of Health of Russia

Email: shramko_08@mail.ru
PhD (medical science), Associate Professor of Teaching assistant of Department of obstetrics and gynecology

Lyudmila Fedorovna Gulyaeva

Institute of Molecular Biology and Biophysics, Siberian Branch, Russian Academy of Medical Sciences

Email: gulyaeva@niimbb.ru
PhD (Doctor of Biology), Professor, Institute of Molecular Biology and Biophysics.

Lyudmila Grigoryevna Bazhenova

Novokuznetsk State Institute for Postgraduate Training of Physicians; Branch, Russian Medical Academy of Continuing Professional Education, Ministry of Health of Russia

Email: l_bagenova@mail.ru
M.D. (Doctor of medical science), Professor, Head of Department of obstetrics and gynecology

Vladimir Grigorevich Levchenko

Novokuznetsk State Institute for Postgraduate Training of Physicians; Branch, Russian Medical Academy of Continuing Professional Education, Ministry of Health of Russia

Email: vglev@yandex.ru
PhD (medical science), Associate Professor of Teaching assistant of Department of Department of obstetrics and gynecology

References

  1. Kim J.J., Sefton E.C. The role of progesterone signaling in the pathogenesis of uterine leiomyoma. Mol. Cell. Endocrinol. 2012; 358(2): 223-31. doi: 10.1016/j. mce.2011.05.044.
  2. Буянова С.Н., Юдина Н.В., Гукасян С.А., Мгелиашвили М.В. Современные аспекты роста миомы матки. Российский вестник акушера-гинеколога. 2012; 12(4): 42-8.
  3. Duhan N., Sirohiwal D. Uterine myomas revisited. Eur. J. Obstet. Gynecol. Reprod. Biol. 2010; 152(2): 119-25. doi: 10.1016/j.ejogrb.2010.05.010.
  4. Manta L., Suciu N., Toader O., Purcârea R.M., Constantin A., Popa F. The etiopathogenesis of uterine fibromatosis. J. Med. Life. 2016; 9(1): 39-45.
  5. Дамиров М.М. Современная тактика ведения больных с аденомиозом. М.: Издательство БИНОМ; 2015. 111с.
  6. Печеникова В.А., Акопян Р.А., Кветной И.М. К вопросу о патогенетических механизмах развития и прогрессии внутреннего генитального эндометриоза - аденомиоза. Журнал акушерства и женских болезней. 2015; 64(6): 51-7.
  7. Унанян А.Л., Сидорова И.С., Коган Е.А. Активный и неактивный аденомиоз: клинико-морфологические варианты развития, дифференцированный подход к терапии. Акушерство, гинекология и репродукция. 2012; 6(2): 25-30.
  8. Сидорова И.С., Унанян А.Л., Агеев М.Б., Ведерникова Н.В., Жолобова Н.М. Современное состояние вопроса о патогенезе, клинике, диагностике и лечении миомы матки у женщин репродуктивного возраста. Акушерство, гинекология и репродукция. 2012; 6(4): 22-8.
  9. Печеникова В.А. К вопросу о нозологической значимости и правомочности использования термина «Эндометриоидная болезнь». Журнал акушерства и женских болезней. 2012; 61(5): 122-31.
  10. Leyendecker G., Kunz G., Noe M., Herberts M., Mall G. Endometriosis: a dysfunction and disease of the archimetra. Hum. Reprod. Update. 1998; 4(5): 752-62.
  11. Noe M., Kunz G., Herberts M., Mall G., Leyndecker G. The cyclic pattern of the imminocytochemical expression of estrogen and progesterone receptors inhuman myometrial and endometrial layers: characterisation of the endometrial-subendometrial unit. Hum. Reprod. 1999; 14(1): 190-7.
  12. Leyendecker G., Bilgicyildirim A., Inacker M., Stalf T., Huppert P., Mall G. et al. Adenomyosis and endometriosis. Re-visiting their association and further insights into the mechanisms of auto-traumatisation. An MRI study. Arch. Gynecol. Obstet. 2015; 291(4): 917-32. doi: 10.1007/s00404-014-3437-8.
  13. Тихомиров А.Л., Манухин И.Б., Сарсания С.И. Миома матки в сочетании с эндометриозом и гиперплазией эндометрия. Как лечить? Российский вестник акушера-гинеколога. 2014; 14(3): 76-8.
  14. Kaba M., Tokmak A., Timur H., Ozdal B., Sirvan L., Güngor T. A rare case of leiomyosarcoma originating from the left round ligament of the uterus. J. Exp. Ther. Oncol. 2016; 11(3): 237-40.
  15. Ishikawa H., Ishi K., Serna V.A., Kakazu R., Bulun S.E., Kurita T. Progesterone is essential for maintenance and growth of uterine leiomyoma. Endocrinology. 2010; 151(6): 2433-42. doi: 10.1210/en.2009-1225.
  16. Савицкий Г.А. Роль локальной гиперэсрадиолемии в патогенезе возникновения и роста миомы. Журнал акушерства и женских болезней. 2009; 58(4): 79-92.
  17. Гуриев Т.Д., Сидорова И.С., Унанян А.Л. Сочетание миомы матки и аденомиоза. М.: МИА; 2012. 251с.
  18. Steven H., Eisinger S.H., Meldrum S., Fiscella K., le Roux H.D., Guzick D.S. Low-dose mifepristone for uterine leiomyomata. Obstet. Gynecol. 2003; 101(2): 243-50.
  19. Takeuchi A., Koga K., Miyashita M., Makabe T., Sue F., Harada M. et al. Dienogest reduces proliferation, NGF expression and nerve fiber density in human adenomyosis. Eur. J. Obstet. Gynecol. Reprod. Biol. 2016; 207: 157-61. doi: 10.1016/j.ejogrb.2016.10.053.
  20. Савицкий Г.А., Савицкий А.Г. Миома матки (проблемы патогенеза и патогенетической терапии). СПб.: ЭЛБИ; 2000. 235с.
  21. Стрижаков А.Н., Давыдов А.В., Пашков В.М., Лебедев В.А. Доброкачественные заболевания матки. М.: ГЭОТАР-Медиа; 2014. 304с.

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