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Метаболизм эстрогенов: почему так важно сохранять равновесие?
Метаболизм эстрогенов: почему так важно сохранять равновесие?
Якушевская О.В., Юренева С.В., Протасова А.Э. Метаболизм эстрогенов: почему так важно сохранять равновесие? Гинекология. 2019; 21 (6): 31–35.
DOI: 10.26442/20795696.2019.6.190752
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Аннотация
Цель. Провести анализ и систематизировать имеющуюся информацию относительно патогенетических механизмов гормонального канцерогенеза.
Материалы и методы. В обзор включены данные зарубежных статей, опубликованных в PubMed и Medline, и отечественные работы, помещенные на elibrary.ru за последние 20 лет.
Результаты. В настоящее время термин «эстрогены» достаточно часто употребляется в контексте гормонального канцерогенеза. По мнению большинства исследователей, осознание его тонкостей не должно укладываться в узкие рамки рецептор-опосредуемой пролиферации, индуцируемой эстрогенами в тканях-мишенях. Понятие «эстробиом» как совокупность всех механизмов, обеспечивающих реализацию эффектов эстрогенов, должно включать в себя не только сами гормоны и «родные» рецепторы, но и ферменты, участвующие в их синтезе, метаболиты эстрогенов, микробиоту кишечника, а также генетические и эпигенетические факторы.
Заключение. При анализе онкологического риска необходимо комплексно оценивать предрасполагающие факторы и гормонально-метаболические предпосылки развития неопластического процесса.
Ключевые слова: гормональный канцерогенез, эстрогены, метаболиты эстрогенов, рецепторы эстрогенов, микробиота.
Materials and methods. The review includes data from foreign articles published in PubMed and Medline and national works posted on elibrary.ru over the past 20 years.
Results. Currently, the term "estrogen" is often used in the context of hormonal carcinogenesis. According to most researchers, it should not fit into the narrow framework of receptor-mediated proliferation induced by estrogens in target tissues. The concept of “estrobiome” as a combination of all mechanisms providing the realization of estrogen effects should include not only hormones and “native” receptors themselves, but also the enzymes involved in their synthesis, estrogen metabolites, intestinal microbiota, as well as genetic and epigenetic factors.
Conclusions. When analyzing cancer risk, it is necessary to comprehensively assess contributing factors and hormonal-metabolic preconditions for neoplastic process.
Key words: carcinogenesis, estrogen, estrogen metabolites, estrogen receptors, microbiome.
Материалы и методы. В обзор включены данные зарубежных статей, опубликованных в PubMed и Medline, и отечественные работы, помещенные на elibrary.ru за последние 20 лет.
Результаты. В настоящее время термин «эстрогены» достаточно часто употребляется в контексте гормонального канцерогенеза. По мнению большинства исследователей, осознание его тонкостей не должно укладываться в узкие рамки рецептор-опосредуемой пролиферации, индуцируемой эстрогенами в тканях-мишенях. Понятие «эстробиом» как совокупность всех механизмов, обеспечивающих реализацию эффектов эстрогенов, должно включать в себя не только сами гормоны и «родные» рецепторы, но и ферменты, участвующие в их синтезе, метаболиты эстрогенов, микробиоту кишечника, а также генетические и эпигенетические факторы.
Заключение. При анализе онкологического риска необходимо комплексно оценивать предрасполагающие факторы и гормонально-метаболические предпосылки развития неопластического процесса.
Ключевые слова: гормональный канцерогенез, эстрогены, метаболиты эстрогенов, рецепторы эстрогенов, микробиота.
________________________________________________
Materials and methods. The review includes data from foreign articles published in PubMed and Medline and national works posted on elibrary.ru over the past 20 years.
Results. Currently, the term "estrogen" is often used in the context of hormonal carcinogenesis. According to most researchers, it should not fit into the narrow framework of receptor-mediated proliferation induced by estrogens in target tissues. The concept of “estrobiome” as a combination of all mechanisms providing the realization of estrogen effects should include not only hormones and “native” receptors themselves, but also the enzymes involved in their synthesis, estrogen metabolites, intestinal microbiota, as well as genetic and epigenetic factors.
Conclusions. When analyzing cancer risk, it is necessary to comprehensively assess contributing factors and hormonal-metabolic preconditions for neoplastic process.
Key words: carcinogenesis, estrogen, estrogen metabolites, estrogen receptors, microbiome.
Полный текст
Список литературы
1. Сметник В.П. Эстрогены: от синтеза до клинического применения. М.: Практическая медицина, 2012.
[Smetnik V.P. Estrogens: from synthesis to clinical use. Moscow: Prakticheskaia meditsina, 2012 (in Russian).]
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7. Lee JR, Zava D, Hopkins V. What your doctor may not tell you about breast cancer. How hormone balance may save your life. Warner Books, Inc., New York, NY, 2002.
8. Samavat H, Kurzer MS. Estrogen Metabolism and Breast Cancer. Cancer Lett 2015; 356: 231.
9. Lakhani NJ, Sarkar MA. 2-methoxyestradiol, a promising anticancer agent. Pharmacother 2003; 23: 165–72.
10. Lavigne JA, Goodman JE, Fonong T. The effects of catechol-O-methyltransferase inhibition on estrogen metabolite and oxidative DNA damage levels in estradiol-treated MCF-7 cells. Cancer Res 2017; 61: 488–94.
11. Arslan AA, Shore RE, Afanasyeva Y, Koenig KL. Circulating estrogen metabolites and risk for breast cancer in premenopausal women. Can Epid Biom Prev 2009; 18: 2273–9.
12. Bjornstrom L, Sjoberg M. Mechanisms of Estrogen Receptor Signaling: convergence of genomic and nongenomic action on target genes. Mol Endocr 2005; 19 (14): 833.
13. Weikum ER, Liu X, Ortlund EA. The nuclear receptor superfamily: A structural perspective. Protein Sci 2018; 27 (11): 1876–92. DOI: 10.1002/pro.3496
14. Safe S, Jin UH, Hedrick E et al. Minireview: role of orphan nuclear receptors in cancer and potential as drug targets. Mol Endocrinol 2014; 28 (2): 157–72.
15. Bezerra MG, Latronico AC, Fragoso MC. Endocrine tumors association to protein Gs alpha\Gialpha mutations. Arq Bras Endocrinol Metabol 2005; 49 (5): 784–90.
16. Shanle EK, Xu W. Endocrine disrupting chemicals targeting estrogen receptors signaling: identification and mechanisms of action. J Chem Res Tox 2011; 24 (1): 6.
17. Berger C, Qian Y, Chen X. The p53-estrogen receptor loop in cancer. Curr Mol Med 2013; 13 (8): 1229–40.
18. Oh H, Eliassen AH, Beck AH et al. Breast cancer risk factors in relation to estrogen receptor, progesterone receptor, insulin-like growth factor-1 receptor, and Ki67 expression in normal breast tissue. NPJ Breast Cancer 2017; 3: 39.
19. Hsu LH, Chu NM, Kao SH. Estrogen, Estrogen Receptor and Lung Cancer. Int J Mol Sci 2017; 18 (8): 1713.
20. Swisshelm K. Concepts of immortalization in human mammary epithelial cells. Prog Mol Subcell Biol 2000; 24: 155–72.
21. Якушевская О.В. Менопауза – новый старт в женской судьбе. Медицинский совет. 2019; 7: 126–32.
[Iakushevskaia O.V. Menopauza – novyi start v zhenskoi sud'be. Meditsinskii sovet. 2019; 7: 126–32 (in Russian).]
22. Сухих Г.Т., Сметник В.П., Юренева С.В. и др. Менопауза и климактерическое состояние у женщин. Клинические рекомендации. М., 2016.
[Sukhikh G.T., Smetnik V.P., Yureneva S.V. et al. Menopause and menopause in women. Clinical recommendations. Moscow, 2016 (in Russian).]
23. Юренева С.В., Ильина Л. М., Якушевская О.В. Менопаузальная гормональная терапия: качество жизни сегодня и в долгосрочной перспективе. Гинекология. 2016; 18 (1): 24–9.
[Yureneva S.V., Ilyina L.M., Yakushevskaya O.V. Menopausal hormone therapy in postmenopausal women: the quality of life today and in the long term. Gynecology. 2016; 18 (1): 24–9 (in Russian).]
24. Madak-Erdogan et al. Design of pathway-preferential estrogens that provide beneficial metabolic and vascular effects without stimulating reproductive tissues. Sci Signal. Author manuscript; available in PMC 2016 June 07.
25. Plottel CS, Blaser MJ. Microbiome and Malignancy. Cell Host & Microbe 10. Elsevier Inc., 2011; р. 324.
26. Benson AK, Kelly SA. Individuality in gut microbiota composition is a complex polygenic trait shaped by multiple environmental and host genetic factors. PNAS 2010; 107 (44): 18933–8.
27. Arumugam M, Raes J, Pelletier E et al. MetaHIT Consortium. Enterotypes of the human gut microbiome. Nature 2011; 473: 174–80.
2. Barnes RB, Levrant SG. In: Treatment of the postmenopausal women. Basic and clinical aspects, 3d edn. By R.A.Lobo, 2007; p. 767–77.
3. Santen R, Song R, Zhang Z, Kumar R. Adaptive hypersensitivity to estrogen: mechanisms for superiority of aromatase inhibitors over selective estrogen receptor modulators for brest cancer treatment and prevention. Endoc-Relat Cancer 2003; 10: 111–30.
4. Hecker M, Park JW. Effects of atrazine on CYP19 gene expression and aromatase activity in testes and on plasma sex steroid concentrations of male African clawed frogs. ToxSci (United States) 2005; 86 (2): 273–80.
5. Yao J, Li Y, Chang M et al. Catechol estrogen 4-hydroxyequilenin is a substrate and an inhibitor of catechol-O-methyltransferase. Chem Res Toxicol (United States) 2003; 16 (5): 668–75.
6. Matthews CE, Fowke JH, Dai Q, Leon Bradlow H. Physical activity, body size, and estrogen metabolism in women. Cancer Causes Control (Netherlands) 2004; 15 (5): 473–81.
7. Lee JR, Zava D, Hopkins V. What your doctor may not tell you about breast cancer. How hormone balance may save your life. Warner Books, Inc., New York, NY, 2002.
8. Samavat H, Kurzer MS. Estrogen Metabolism and Breast Cancer. Cancer Lett 2015; 356: 231.
9. Lakhani NJ, Sarkar MA. 2-methoxyestradiol, a promising anticancer agent. Pharmacother 2003; 23: 165–72.
10. Lavigne JA, Goodman JE, Fonong T. The effects of catechol-O-methyltransferase inhibition on estrogen metabolite and oxidative DNA damage levels in estradiol-treated MCF-7 cells. Cancer Res 2017; 61: 488–94.
11. Arslan AA, Shore RE, Afanasyeva Y, Koenig KL. Circulating estrogen metabolites and risk for breast cancer in premenopausal women. Can Epid Biom Prev 2009; 18: 2273–9.
12. Bjornstrom L, Sjoberg M. Mechanisms of Estrogen Receptor Signaling: convergence of genomic and nongenomic action on target genes. Mol Endocr 2005; 19 (14): 833.
13. Weikum ER, Liu X, Ortlund EA. The nuclear receptor superfamily: A structural perspective. Protein Sci 2018; 27 (11): 1876–92. DOI: 10.1002/pro.3496
14. Safe S, Jin UH, Hedrick E et al. Minireview: role of orphan nuclear receptors in cancer and potential as drug targets. Mol Endocrinol 2014; 28 (2): 157–72.
15. Bezerra MG, Latronico AC, Fragoso MC. Endocrine tumors association to protein Gs alpha\Gialpha mutations. Arq Bras Endocrinol Metabol 2005; 49 (5): 784–90.
16. Shanle EK, Xu W. Endocrine disrupting chemicals targeting estrogen receptors signaling: identification and mechanisms of action. J Chem Res Tox 2011; 24 (1): 6.
17. Berger C, Qian Y, Chen X. The p53-estrogen receptor loop in cancer. Curr Mol Med 2013; 13 (8): 1229–40.
18. Oh H, Eliassen AH, Beck AH et al. Breast cancer risk factors in relation to estrogen receptor, progesterone receptor, insulin-like growth factor-1 receptor, and Ki67 expression in normal breast tissue. NPJ Breast Cancer 2017; 3: 39.
19. Hsu LH, Chu NM, Kao SH. Estrogen, Estrogen Receptor and Lung Cancer. Int J Mol Sci 2017; 18 (8): 1713.
20. Swisshelm K. Concepts of immortalization in human mammary epithelial cells. Prog Mol Subcell Biol 2000; 24: 155–72.
21. Iakushevskaia O.V. Menopauza – novyi start v zhenskoi sud'be. Meditsinskii sovet. 2019; 7: 126–32 (in Russian).
22. Sukhikh G.T., Smetnik V.P., Yureneva S.V. et al. Menopause and menopause in women. Clinical recommendations. Moscow, 2016 (in Russian).
23. Yureneva S.V., Ilyina L.M., Yakushevskaya O.V. Menopausal hormone therapy in postmenopausal women: the quality of life today and in the long term. Gynecology. 2016; 18 (1): 24–9 (in Russian).
24. Madak-Erdogan et al. Design of pathway-preferential estrogens that provide beneficial metabolic and vascular effects without stimulating reproductive tissues. Sci Signal. Author manuscript; available in PMC 2016 June 07.
25. Plottel CS, Blaser MJ. Microbiome and Malignancy. Cell Host & Microbe 10. Elsevier Inc., 2011; р. 324.
26. Benson AK, Kelly SA. Individuality in gut microbiota composition is a complex polygenic trait shaped by multiple environmental and host genetic factors. PNAS 2010; 107 (44): 18933–8.
27. Arumugam M, Raes J, Pelletier E et al. MetaHIT Consortium. Enterotypes of the human gut microbiome. Nature 2011; 473: 174–80.
[Smetnik V.P. Estrogens: from synthesis to clinical use. Moscow: Prakticheskaia meditsina, 2012 (in Russian).]
2. Barnes RB, Levrant SG. In: Treatment of the postmenopausal women. Basic and clinical aspects, 3d edn. By R.A.Lobo, 2007; p. 767–77.
3. Santen R, Song R, Zhang Z, Kumar R. Adaptive hypersensitivity to estrogen: mechanisms for superiority of aromatase inhibitors over selective estrogen receptor modulators for brest cancer treatment and prevention. Endoc-Relat Cancer 2003; 10: 111–30.
4. Hecker M, Park JW. Effects of atrazine on CYP19 gene expression and aromatase activity in testes and on plasma sex steroid concentrations of male African clawed frogs. ToxSci (United States) 2005; 86 (2): 273–80.
5. Yao J, Li Y, Chang M et al. Catechol estrogen 4-hydroxyequilenin is a substrate and an inhibitor of catechol-O-methyltransferase. Chem Res Toxicol (United States) 2003; 16 (5): 668–75.
6. Matthews CE, Fowke JH, Dai Q, Leon Bradlow H. Physical activity, body size, and estrogen metabolism in women. Cancer Causes Control (Netherlands) 2004; 15 (5): 473–81.
7. Lee JR, Zava D, Hopkins V. What your doctor may not tell you about breast cancer. How hormone balance may save your life. Warner Books, Inc., New York, NY, 2002.
8. Samavat H, Kurzer MS. Estrogen Metabolism and Breast Cancer. Cancer Lett 2015; 356: 231.
9. Lakhani NJ, Sarkar MA. 2-methoxyestradiol, a promising anticancer agent. Pharmacother 2003; 23: 165–72.
10. Lavigne JA, Goodman JE, Fonong T. The effects of catechol-O-methyltransferase inhibition on estrogen metabolite and oxidative DNA damage levels in estradiol-treated MCF-7 cells. Cancer Res 2017; 61: 488–94.
11. Arslan AA, Shore RE, Afanasyeva Y, Koenig KL. Circulating estrogen metabolites and risk for breast cancer in premenopausal women. Can Epid Biom Prev 2009; 18: 2273–9.
12. Bjornstrom L, Sjoberg M. Mechanisms of Estrogen Receptor Signaling: convergence of genomic and nongenomic action on target genes. Mol Endocr 2005; 19 (14): 833.
13. Weikum ER, Liu X, Ortlund EA. The nuclear receptor superfamily: A structural perspective. Protein Sci 2018; 27 (11): 1876–92. DOI: 10.1002/pro.3496
14. Safe S, Jin UH, Hedrick E et al. Minireview: role of orphan nuclear receptors in cancer and potential as drug targets. Mol Endocrinol 2014; 28 (2): 157–72.
15. Bezerra MG, Latronico AC, Fragoso MC. Endocrine tumors association to protein Gs alpha\Gialpha mutations. Arq Bras Endocrinol Metabol 2005; 49 (5): 784–90.
16. Shanle EK, Xu W. Endocrine disrupting chemicals targeting estrogen receptors signaling: identification and mechanisms of action. J Chem Res Tox 2011; 24 (1): 6.
17. Berger C, Qian Y, Chen X. The p53-estrogen receptor loop in cancer. Curr Mol Med 2013; 13 (8): 1229–40.
18. Oh H, Eliassen AH, Beck AH et al. Breast cancer risk factors in relation to estrogen receptor, progesterone receptor, insulin-like growth factor-1 receptor, and Ki67 expression in normal breast tissue. NPJ Breast Cancer 2017; 3: 39.
19. Hsu LH, Chu NM, Kao SH. Estrogen, Estrogen Receptor and Lung Cancer. Int J Mol Sci 2017; 18 (8): 1713.
20. Swisshelm K. Concepts of immortalization in human mammary epithelial cells. Prog Mol Subcell Biol 2000; 24: 155–72.
21. Якушевская О.В. Менопауза – новый старт в женской судьбе. Медицинский совет. 2019; 7: 126–32.
[Iakushevskaia O.V. Menopauza – novyi start v zhenskoi sud'be. Meditsinskii sovet. 2019; 7: 126–32 (in Russian).]
22. Сухих Г.Т., Сметник В.П., Юренева С.В. и др. Менопауза и климактерическое состояние у женщин. Клинические рекомендации. М., 2016.
[Sukhikh G.T., Smetnik V.P., Yureneva S.V. et al. Menopause and menopause in women. Clinical recommendations. Moscow, 2016 (in Russian).]
23. Юренева С.В., Ильина Л. М., Якушевская О.В. Менопаузальная гормональная терапия: качество жизни сегодня и в долгосрочной перспективе. Гинекология. 2016; 18 (1): 24–9.
[Yureneva S.V., Ilyina L.M., Yakushevskaya O.V. Menopausal hormone therapy in postmenopausal women: the quality of life today and in the long term. Gynecology. 2016; 18 (1): 24–9 (in Russian).]
24. Madak-Erdogan et al. Design of pathway-preferential estrogens that provide beneficial metabolic and vascular effects without stimulating reproductive tissues. Sci Signal. Author manuscript; available in PMC 2016 June 07.
25. Plottel CS, Blaser MJ. Microbiome and Malignancy. Cell Host & Microbe 10. Elsevier Inc., 2011; р. 324.
26. Benson AK, Kelly SA. Individuality in gut microbiota composition is a complex polygenic trait shaped by multiple environmental and host genetic factors. PNAS 2010; 107 (44): 18933–8.
27. Arumugam M, Raes J, Pelletier E et al. MetaHIT Consortium. Enterotypes of the human gut microbiome. Nature 2011; 473: 174–80.
________________________________________________
2. Barnes RB, Levrant SG. In: Treatment of the postmenopausal women. Basic and clinical aspects, 3d edn. By R.A.Lobo, 2007; p. 767–77.
3. Santen R, Song R, Zhang Z, Kumar R. Adaptive hypersensitivity to estrogen: mechanisms for superiority of aromatase inhibitors over selective estrogen receptor modulators for brest cancer treatment and prevention. Endoc-Relat Cancer 2003; 10: 111–30.
4. Hecker M, Park JW. Effects of atrazine on CYP19 gene expression and aromatase activity in testes and on plasma sex steroid concentrations of male African clawed frogs. ToxSci (United States) 2005; 86 (2): 273–80.
5. Yao J, Li Y, Chang M et al. Catechol estrogen 4-hydroxyequilenin is a substrate and an inhibitor of catechol-O-methyltransferase. Chem Res Toxicol (United States) 2003; 16 (5): 668–75.
6. Matthews CE, Fowke JH, Dai Q, Leon Bradlow H. Physical activity, body size, and estrogen metabolism in women. Cancer Causes Control (Netherlands) 2004; 15 (5): 473–81.
7. Lee JR, Zava D, Hopkins V. What your doctor may not tell you about breast cancer. How hormone balance may save your life. Warner Books, Inc., New York, NY, 2002.
8. Samavat H, Kurzer MS. Estrogen Metabolism and Breast Cancer. Cancer Lett 2015; 356: 231.
9. Lakhani NJ, Sarkar MA. 2-methoxyestradiol, a promising anticancer agent. Pharmacother 2003; 23: 165–72.
10. Lavigne JA, Goodman JE, Fonong T. The effects of catechol-O-methyltransferase inhibition on estrogen metabolite and oxidative DNA damage levels in estradiol-treated MCF-7 cells. Cancer Res 2017; 61: 488–94.
11. Arslan AA, Shore RE, Afanasyeva Y, Koenig KL. Circulating estrogen metabolites and risk for breast cancer in premenopausal women. Can Epid Biom Prev 2009; 18: 2273–9.
12. Bjornstrom L, Sjoberg M. Mechanisms of Estrogen Receptor Signaling: convergence of genomic and nongenomic action on target genes. Mol Endocr 2005; 19 (14): 833.
13. Weikum ER, Liu X, Ortlund EA. The nuclear receptor superfamily: A structural perspective. Protein Sci 2018; 27 (11): 1876–92. DOI: 10.1002/pro.3496
14. Safe S, Jin UH, Hedrick E et al. Minireview: role of orphan nuclear receptors in cancer and potential as drug targets. Mol Endocrinol 2014; 28 (2): 157–72.
15. Bezerra MG, Latronico AC, Fragoso MC. Endocrine tumors association to protein Gs alpha\Gialpha mutations. Arq Bras Endocrinol Metabol 2005; 49 (5): 784–90.
16. Shanle EK, Xu W. Endocrine disrupting chemicals targeting estrogen receptors signaling: identification and mechanisms of action. J Chem Res Tox 2011; 24 (1): 6.
17. Berger C, Qian Y, Chen X. The p53-estrogen receptor loop in cancer. Curr Mol Med 2013; 13 (8): 1229–40.
18. Oh H, Eliassen AH, Beck AH et al. Breast cancer risk factors in relation to estrogen receptor, progesterone receptor, insulin-like growth factor-1 receptor, and Ki67 expression in normal breast tissue. NPJ Breast Cancer 2017; 3: 39.
19. Hsu LH, Chu NM, Kao SH. Estrogen, Estrogen Receptor and Lung Cancer. Int J Mol Sci 2017; 18 (8): 1713.
20. Swisshelm K. Concepts of immortalization in human mammary epithelial cells. Prog Mol Subcell Biol 2000; 24: 155–72.
21. Iakushevskaia O.V. Menopauza – novyi start v zhenskoi sud'be. Meditsinskii sovet. 2019; 7: 126–32 (in Russian).
22. Sukhikh G.T., Smetnik V.P., Yureneva S.V. et al. Menopause and menopause in women. Clinical recommendations. Moscow, 2016 (in Russian).
23. Yureneva S.V., Ilyina L.M., Yakushevskaya O.V. Menopausal hormone therapy in postmenopausal women: the quality of life today and in the long term. Gynecology. 2016; 18 (1): 24–9 (in Russian).
24. Madak-Erdogan et al. Design of pathway-preferential estrogens that provide beneficial metabolic and vascular effects without stimulating reproductive tissues. Sci Signal. Author manuscript; available in PMC 2016 June 07.
25. Plottel CS, Blaser MJ. Microbiome and Malignancy. Cell Host & Microbe 10. Elsevier Inc., 2011; р. 324.
26. Benson AK, Kelly SA. Individuality in gut microbiota composition is a complex polygenic trait shaped by multiple environmental and host genetic factors. PNAS 2010; 107 (44): 18933–8.
27. Arumugam M, Raes J, Pelletier E et al. MetaHIT Consortium. Enterotypes of the human gut microbiome. Nature 2011; 473: 174–80.
Авторы
О.В. Якушевская*1, С.В. Юренева1, А.Э. Протасова2–4
1. ФГБУ «Национальный медицинский исследовательский центр акушерства, гинекологии и перинатологии им. академика В.И. Кулакова» Минздрава России, Москва, Россия;
2. ФГБОУ ВО «Санкт-Петербургский государственный университет», Санкт-Петербург, Россия;
3. ФГБОУ ВО «Северо-Западный государственный медицинский университет им. И.И. Мечникова» Минздрава России, Санкт-Петербург, Россия;
4. ФГБУ «Национальный медицинский исследовательский центр им. В.А. Алмазова» Минздрава России, Санкт-Петербург, Россия
*aluckyone777@gmail.com
1. Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology, Moscow, Russia;
2. Saint Petersburg State University, Saint Petersburg, Russia;
3. Mechnikov North-Western State Medical University, Saint Petersburg, Russia;
4. Almazov National Medical Research Center, Saint Petersburg, Russia
*aluckyone777@gmail.com
1. ФГБУ «Национальный медицинский исследовательский центр акушерства, гинекологии и перинатологии им. академика В.И. Кулакова» Минздрава России, Москва, Россия;
2. ФГБОУ ВО «Санкт-Петербургский государственный университет», Санкт-Петербург, Россия;
3. ФГБОУ ВО «Северо-Западный государственный медицинский университет им. И.И. Мечникова» Минздрава России, Санкт-Петербург, Россия;
4. ФГБУ «Национальный медицинский исследовательский центр им. В.А. Алмазова» Минздрава России, Санкт-Петербург, Россия
*aluckyone777@gmail.com
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1. Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology, Moscow, Russia;
2. Saint Petersburg State University, Saint Petersburg, Russia;
3. Mechnikov North-Western State Medical University, Saint Petersburg, Russia;
4. Almazov National Medical Research Center, Saint Petersburg, Russia
*aluckyone777@gmail.com
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