Оценка внешних факторов риска развития гепатоцеллюлярного рака и маркеров генетической предрасположенности к его развитию в этнической группе якутов-мужчин
Оценка внешних факторов риска развития гепатоцеллюлярного рака и маркеров генетической предрасположенности к его развитию в этнической группе якутов-мужчин
Ющук Н.Д., Слепцова С.С., Малов С.И. и др. Оценка внешних факторов риска развития гепатоцеллюлярного рака и маркеров генетической предрасположенности к его развитию в этнической группе якутов-мужчин. Терапевтический архив. 2020; 92 (1): 56–61. DOI: 10.26442/00403660.2020.01.000505
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Аннотация
Цель исследования. Установить основные внешние и генетически детерминированные факторы риска развития гепатоцеллюлярного рака (ГЦР) в этнической группе якутов-мужчин, проживающих на территории Республики Саха (Якутия) [РС (Я)] в условиях эпидемиологического неблагополучия по заболеваемости вирусными гепатитами.
Материалы и методы. Обследовано 97 якутов мужского пола, в том числе с диагнозом ГЦР – 44 человека, с диагнозом хронический вирусный гепатит – 53 человека. Факторы риска ГЦР выявляли путем анализа медицинской документации и анкетированного опроса больных. В опытной и контрольной группах выполнены генетические исследования однонуклеотидных полиморфизмов генов, картированных на Х-хромосоме и участвующих в активации противовирусного иммунитета по TLR7-сигнальному пути.
Результаты и обсуждение. У 100% больных ГЦР обнаружено инфицирование вирусами гепатитов B, C, D или ко-инфекция указанными агентами. Каждый 4-й больной ГЦР в РС (Я) оказался инфицирован вирусом гепатита D (HDV). Течение ГЦР, ассоциированного с HDV, характеризовалось быстрым прогрессированием цирроза печени, развитием портальной гипертензии, кровотечением из варикозно расширенных вен желудка и пищевода и отечно-асцитическим синдромом. Кроме вирусных агентов выявлены дополнительные факторы риска развития рака печени, такие как злоупотребление алкоголем, избыточная масса тела, сахарный диабет, табакокурение. Среди исследованных вариационных сайтов генов, локализованных на Х-хромосоме и кодирующих реакции врожденного противовирусного иммунитета, не обнаружено генетического маркера с достаточной степенью достоверности детерминирующего вероятность развития ГЦР.
Заключение. Высокая заболеваемость ГЦР мужского населения в РС (Я) обусловлена широким распространением парентеральных вирусных гепатитов, в особенности HDV. В связи с внедрением в Российской Федерации массовой вакцинации населения против гепатита В, в обозримом будущем в РС (Я) следует ожидать снижение доли ГЦР, ассоциированной с вирусами гепатитов B и D, в связи с чем основное внимание должно быть уделено лечению и профилактике вирусного гепатита С и неинфекционным факторам риска.
Ключевые слова: гепатоцеллюлярный рак, факторы риска, однонуклеотидные полиморфизмы, Х-хромосома, TLR-7, мужской пол, якуты.
Materials and methods. A total of 97 male Yakuts were examined, including 44 people diagnosed with hepatocellular cancer and 53 people diagnosed with chronic viral hepatitis. HCC risk factors were identified by analyzing medical records and questioning patients. In the experimental and control groups, genetic studies of single nucleotide polymorphisms of genes mapped on the X-chromosome and involved in the activation of antiviral immunity along the TLR7 signaling pathway were performed.
Results and discussion. In 100% of patients with hepatocellular cancer, infection with hepatitis B, C, D viruses or co-infection with these agents was detected. Every fourth patient with HCC in the RS (Y) was infected with hepatitis D. The course of hepatocellular cancer associated with HDV was characterized by rapid progression of liver cirrhosis, development of portal hypertension, bleeding from varicose veins of the stomach and esophagus (36.4%) and edematous ascitic syndrome (63.6%). In addition to viral agents, additional risk factors for liver cancer were identified, such as alcohol abuse, overweight, diabetes mellitus, and smoking. Among the studied variation sites of genes localized on the X-chromosome and encoding the reaction of innate antiviral immunity, no genetic marker was found with a sufficient degree of confidence determining the likelihood of hepatocellular cancer developing.
Conclusions. The high incidence of hepatocellular carcinoma of the male population in the RS (Y) is due to the widespread prevalence of parenteral viral hepatitis, especially viral hepatitis D. Due to the introduction of mass vaccination of the population against hepatitis B in the Russian Federation in the foreseeable future in the RS (Y) we should see a decrease in the proportion of hepatocellular cancer associated with hepatitis B and D viruses, and therefore the focus should be on the treatment and prevention of hepatitis C virus and non-infectious risk factors.
Keywords: hepatocellular cancer, risk factors, single nucleotide polymorphisms, X chromosome, TLR-7, male gender, Yakuts.
Материалы и методы. Обследовано 97 якутов мужского пола, в том числе с диагнозом ГЦР – 44 человека, с диагнозом хронический вирусный гепатит – 53 человека. Факторы риска ГЦР выявляли путем анализа медицинской документации и анкетированного опроса больных. В опытной и контрольной группах выполнены генетические исследования однонуклеотидных полиморфизмов генов, картированных на Х-хромосоме и участвующих в активации противовирусного иммунитета по TLR7-сигнальному пути.
Результаты и обсуждение. У 100% больных ГЦР обнаружено инфицирование вирусами гепатитов B, C, D или ко-инфекция указанными агентами. Каждый 4-й больной ГЦР в РС (Я) оказался инфицирован вирусом гепатита D (HDV). Течение ГЦР, ассоциированного с HDV, характеризовалось быстрым прогрессированием цирроза печени, развитием портальной гипертензии, кровотечением из варикозно расширенных вен желудка и пищевода и отечно-асцитическим синдромом. Кроме вирусных агентов выявлены дополнительные факторы риска развития рака печени, такие как злоупотребление алкоголем, избыточная масса тела, сахарный диабет, табакокурение. Среди исследованных вариационных сайтов генов, локализованных на Х-хромосоме и кодирующих реакции врожденного противовирусного иммунитета, не обнаружено генетического маркера с достаточной степенью достоверности детерминирующего вероятность развития ГЦР.
Заключение. Высокая заболеваемость ГЦР мужского населения в РС (Я) обусловлена широким распространением парентеральных вирусных гепатитов, в особенности HDV. В связи с внедрением в Российской Федерации массовой вакцинации населения против гепатита В, в обозримом будущем в РС (Я) следует ожидать снижение доли ГЦР, ассоциированной с вирусами гепатитов B и D, в связи с чем основное внимание должно быть уделено лечению и профилактике вирусного гепатита С и неинфекционным факторам риска.
Ключевые слова: гепатоцеллюлярный рак, факторы риска, однонуклеотидные полиморфизмы, Х-хромосома, TLR-7, мужской пол, якуты.
________________________________________________
Materials and methods. A total of 97 male Yakuts were examined, including 44 people diagnosed with hepatocellular cancer and 53 people diagnosed with chronic viral hepatitis. HCC risk factors were identified by analyzing medical records and questioning patients. In the experimental and control groups, genetic studies of single nucleotide polymorphisms of genes mapped on the X-chromosome and involved in the activation of antiviral immunity along the TLR7 signaling pathway were performed.
Results and discussion. In 100% of patients with hepatocellular cancer, infection with hepatitis B, C, D viruses or co-infection with these agents was detected. Every fourth patient with HCC in the RS (Y) was infected with hepatitis D. The course of hepatocellular cancer associated with HDV was characterized by rapid progression of liver cirrhosis, development of portal hypertension, bleeding from varicose veins of the stomach and esophagus (36.4%) and edematous ascitic syndrome (63.6%). In addition to viral agents, additional risk factors for liver cancer were identified, such as alcohol abuse, overweight, diabetes mellitus, and smoking. Among the studied variation sites of genes localized on the X-chromosome and encoding the reaction of innate antiviral immunity, no genetic marker was found with a sufficient degree of confidence determining the likelihood of hepatocellular cancer developing.
Conclusions. The high incidence of hepatocellular carcinoma of the male population in the RS (Y) is due to the widespread prevalence of parenteral viral hepatitis, especially viral hepatitis D. Due to the introduction of mass vaccination of the population against hepatitis B in the Russian Federation in the foreseeable future in the RS (Y) we should see a decrease in the proportion of hepatocellular cancer associated with hepatitis B and D viruses, and therefore the focus should be on the treatment and prevention of hepatitis C virus and non-infectious risk factors.
Keywords: hepatocellular cancer, risk factors, single nucleotide polymorphisms, X chromosome, TLR-7, male gender, Yakuts.
Список литературы
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2. Bugaeva TT, Ivanov PM, Alexeeva MN, Karatayev PD, Smetanina VD. Primary liver cancer morbidity of the Republic Sakha (Yakutia) population. Yakut medical journal. 2011;(1):87-9 (In Russ.)
3. Sleptsova SS. Parenteral viral hepatitis and their origin in the Republic of Sakha (Yakutia). Moscow, 2017:216 p (In Russ.)
4. Pimenov NN, Komarova SV, Karandashova IV, Tsapkova NN, Volchkova EV, Chulanov VP. Hepatitis С and its outcomes in Russia: analysis of incidence, prevalence and mortality rates before the start of the programme of infection elimination. Infekc bolezni (Infectious diseases). 2018;16(3):37-45 (In Russ.) doi: 10.20953/1729-9225-2018-3-37-45
5. Calvaruso V, Cabibbo G, Cacciola I, et al. Incidence of Hepatocellular Carcinoma in Patients With HCV-Associated Cirrhosis Treated With Direct-Acting Antiviral Agents. Gastroenterol. 2018;155(2):411-21. doi: 10.1053/j.gastro.2018.04.008
6. EASL Clinical Practice Guidelines: Management of hepatocellular carcinoma. J Hepatol. 2018;69(1):182-236. doi: 10.1016/j.jhep.2018.03.019
7. General Assembly of the World Medical Association. World Medical Association Declaration of Helsinki: ethical principal for medical research involving human subject. J Am Coll Dent. 2014;81(3):14-8.
8. Babor T, Higgins-Biddle JC, Saunders JB, Monteiro MG. AUDIT – The Alcohol Use Disorders Identification Test: Guidelines for Use in Primary Health Care (2nd edn). Geneva: World Health Organization, 2001.
9. Akaike H. A new look at the statistical model identification. IEEE Transactions on Automatic Control. 1974;19(6):716-23.
10. Mentha N, Clément S, Negro F, Alfaiate D. A review on hepatitis D: From virology to new therapies. J Adv Res. 2019;17:3-15. doi: 10.1016/j.jare.2019.03.009
11. Shchanitcyna SE, Burnevich EZ, Nikulkina EN, et al. Risk factors of unfavorable prognosis of chronic hepatitis C. Therapeutic Archive. 2019;91(2):59-66 (In Russ.) doi: 10.26442/00403660.2019.02.000082
12. Budny A, Kozłowski P, Kamińska M, et al. Epidemiology and risk factors of hepatocellular carcinoma. Pol Merkur Lekarski. 2017;43(255):133-9 (In Polish).
13. Kim HS, El-Serag HB. The Epidemiology of Hepatocellular Carcinoma in the USA. Curr Gastroenterol Rep. 2019;21(4):17. doi: 10.1007/s11894-019-0681-x
14. Sleptsova SS. A role of the genotypes of hepatitis B, C and D viruses in primary liver cancer progression. HIV Infection and Immunosuppressive Disorders. 2012;4(4):67-73 (In Russ.)
15. Zhu RX, Seto WK, Lai CL, Yuen MF. Epidemiology of Hepatocellular Carcinoma in the Asia-Pacific Region. Gut Liver. 2016;10(3):332-9. doi: 10.5009/gnl15257
16. Yuschuk ND, Malov IV, Baatarkhuu O, et al. Clinical and epidemiological manifestation of hepatocellular carcinoma in patients belonging to ethnic groups of Caucasians and Asians of North-East Asia. Zh Mikrobiol Epidemiol Immunobiol. 2018;6:25-31 (In Russ.)
17. Stroffolini T, Sagnelli E, Sagnelli C, et al. Decreasing role of HCV and HBV infections as aetiological factors of hepatocellular carcinoma in Italy. Infection. 2019. doi: 10.1007/s15010-019-01308-3 [Epub ahead of print].
18. Schegolev AI, Tumanova U.N. The role of alcohol in the occurrence of liver cancer. International J Applied and Fundamental Research. 2017;11-2:223-7 (In Russ.)
19. Agyemang-Yeboah F, Eghan BAJ, Annani-Akollor ME, et al. Evaluation of Metabolic Syndrome and Its Associated Risk Factors in Type 2 Diabetes: A Descriptive Cross-Sectional Study at the Komfo Anokye Teaching Hospital, Kumasi, Ghana. Biomed Res Int. 2019;2019:4562904. doi: 10.1155/2019/4562904
20. Ioannou GN, Green P, Lowy E, et al. Differences in hepatocellular carcinoma risk, predictors and trends over time according to etiology of cirrhosis. PLoS One. 2018;13(9):e0204412. doi: 10.1371/journal.pone.0204412
21. Rawla P, Sunkara T, Muralidharan P, Raj JP. Update in global trends and aetiology of hepatocellular carcinoma. Contemp Oncol (Pozn). 2018; 22(3):141-50. doi: 10.5114/wo.2018.78941
22. Motawi TMK, Sadik NAH, Sabry D, Shahin NN, Fahim SA. rs2267531, a promoter SNP within glypican-3 gene in the X chromosome, is associated with hepatocellular carcinoma in Egyptians. Sci Rep. 2019;9(1):6868. doi: 10.1038/s41598-019-43376-3
23. Fakhir FZ, Lkhider M, Badre W, et al. Genetic variations in toll-like receptors 7 and 8 modulate natural hepatitis C outcomes and liver disease progression. Liver Int. 2018;38(3):432-42. doi: 10.1111/liv.13533
24. Maglione PJ, Simchoni N, Cunningham-Rundles C. Toll-like receptor signaling in primary immune deficiencies. Ann NY Acad Sci. 2015;1356:1-21. doi: 10.1111/nyas.12763
25. Miki D, Ochi H, Hayes CN, et al. Variation in the DEPDC5 locus is associated with progression to hepatocellular carcinoma in chronic hepatitis C virus carriers. Nat Genet. 2011;43(8):797-800. doi: 10.1038/ng.876
26. Lo PH, Urabe Y, Kumar V, et al. Identification of a functional variant in the MICA promoter which regulates MICA expression and increases HCV-related hepatocellular carcinoma risk. PLoS One. 2013;8(4):e61279. doi: 10.1371/journal.pone.0061279
27. Carmo RF, Aroucha D, Vasconcelos LR, et al. Genetic variation in PTX3 and plasma levels associated with hepatocellular carcinoma in patients with HCV. J Viral Hepat. 2016;23(2):116-22. doi: 10.1111/jvh.12472
28. Luo X, Wang Y, Shen A, et al. Relationship between the rs2596542 polymorphism in the MICA gene promoter and HBV/HCV infection-induced hepatocellular carcinoma: a meta-analysis. BMC Med Genet. 2019; 20(1):142. doi: 10.1186/s12881-019-0871-2
29. Tan C, Bei C, Zhu X, et al. Single Nucleotide Polymorphisms of CBX4 and CBX7 Decrease the Risk of Hepatocellular Carcinoma. Biomed Res Int. 2019;2019:6436825. doi: 10.1155/2019/6436825
30. Wang H, Cao H, Xu Z, et al. SNP rs2596542G>A in MICA is associated with risk of hepatocellular carcinoma: a meta-analysis. Biosci Rep. 2019; 39(5). pii: BSR20181400. doi: 10.1042/BSR20181400
31. Zhu X, Wang Z, Qiu X, et al. Rs2303428 of MSH2 Is Associated with Hepatocellular Carcinoma Prognosis in a Chinese Population. DNA Cell Biol. 2018;37(7):634-41. doi: 10.1089/dna.2018.4224
32. Yazici H, Zipprich J, Peng T, et al. Investigation of the miR16-1 (C > T) + 7 Substitution in Seven Different Types of Cancer from Three Ethnic Groups. J Oncol. 2009;2009:827532. doi: 10.1155/2009/827532
33. Hu M, Zhao L, Hu S, Yang J. The association between two common polymorphisms in MicroRNAs and hepatocellular carcinoma risk in Asian population. PLoS One. 2013;8(2):e57012. doi: 10.1371/journal.pone.0057012
34. Kim LH, Cheong HS, Namgoong S, et al. Replication of genome wide association studies on hepatocellular carcinoma susceptibility loci of STAT4 and HLA-DQ in a Korean population. Infect Genet Evol. 2015;33: 72-6. doi: 10.1016/j.meegid.2015.04.013
35. Akhdar H, El Shamieh S, Musso O, et al. The rs3957357C>T SNP in GSTA1 Is Associated with a Higher Risk of Occurrence of Hepatocellular Carcinoma in European Individuals. PLoS One. 2016;11(12):e0167543. doi: 10.1371/journal.pone.0167543
2. Бугаева Т.Т., Иванов П.М., Алексеева М.Н., Каратаев П.Д., Сметанина В.Д. Заболеваемость населения Республики Саха (Якутия) первичным раком печени. Якутский медицинский журнал. 2011;(1):87-9 [Bugaeva TT, Ivanov PM, Alexeeva MN, Karatayev PD, Smetanina VD. Primary liver cancer morbidity of the Republic Sakha (Yakutia) population. Yakut medical journal. 2011;(1):87-9 (In Russ.)].
3. Слепцова С.С. Парентеральные вирусные гепатиты и их исходы в Республике Саха (Якутия). М., 2017:216 с. [Sleptsova SS. Parenteral viral hepatitis and their origin in the Republic of Sakha (Yakutia). Moscow, 2017:216 p (In Russ.)].
4. Пименов Н.Н., Комарова С.В., Карандашова И.В., Цапкова Н.Н., Волчкова Е.В., Чуланов В.П. Гепатит С и его исходы в России: анализ заболеваемости распространенности и смертности до начала программы элиминации инфекции. Инфекционные болезни. 2018; 16(3):37-45 [Pimenov NN, Komarova SV, Karandashova IV, Tsapkova NN, Volchkova EV, Chulanov VP. Hepatitis С and its outcomes in Russia: analysis of incidence, prevalence and mortality rates before the start of the programme of infection elimination. Infekc bolezni (Infectious diseases). 2018;16(3):37-45 (In Russ.)]. doi: 10.20953/1729-9225-2018-3-37-45
5. Calvaruso V, Cabibbo G, Cacciola I, et al. Incidence of Hepatocellular Carcinoma in Patients With HCV-Associated Cirrhosis Treated With Direct-Acting Antiviral Agents. Gastroenterol. 2018;155(2):411-21. doi: 10.1053/j.gastro.2018.04.008
6. EASL Clinical Practice Guidelines: Management of hepatocellular carcinoma. J Hepatol. 2018;69(1):182-236. doi: 10.1016/j.jhep.2018.03.019
7. General Assembly of the World Medical Association. World Medical Association Declaration of Helsinki: ethical principal for medical research involving human subject. J Am Coll Dent. 2014;81(3):14-8.
8. Babor T, Higgins-Biddle JC, Saunders JB, Monteiro MG. AUDIT – The Alcohol Use Disorders Identification Test: Guidelines for Use in Primary Health Care (2nd edn). Geneva: World Health Organization, 2001.
9. Akaike H. A new look at the statistical model identification. IEEE Transactions on Automatic Control. 1974;19(6):716-23.
10. Mentha N, Clément S, Negro F, Alfaiate D. A review on hepatitis D: From virology to new therapies. J Adv Res. 2019;17:3-15. doi: 10.1016/j.jare.2019.03.009
11. Щаницына С.Е., Бурневич Э.З., Никулкина Е.Н. и др. Факторы риска неблагоприятного прогноза хронического гепатита С. Терапевтический архив. 2019;91(2):59-66 [Shchanitcyna SE, Burnevich EZ, Nikulkina EN, et al. Risk factors of unfavorable prognosis of chronic hepatitis C. Therapeutic Archive. 2019;91(2):59-66 (In Russ.)]. doi: 10.26442/00403660.2019.02.000082
12. Budny A, Kozłowski P, Kamińska M, et al. Epidemiology and risk factors of hepatocellular carcinoma. Pol Merkur Lekarski. 2017;43(255):133-9 (In Polish).
13. Kim HS, El-Serag HB. The Epidemiology of Hepatocellular Carcinoma in the USA. Curr Gastroenterol Rep. 2019;21(4):17. doi: 10.1007/s11894-019-0681-x
14. Слепцова С.С. Роль генотипов вирусов гепатитов В, С и D в развитии первичного рака печени. ВИЧ-инфекция и иммуносупрессии. 2012; 4(4):67-73 [Sleptsova SS. A role of the genotypes of hepatitis B, C and D viruses in primary liver cancer progression. HIV Infection and Immunosuppressive Disorders. 2012;4(4):67-73 (In Russ.)].
15. Zhu RX, Seto WK, Lai CL, Yuen MF. Epidemiology of Hepatocellular Carcinoma in the Asia-Pacific Region. Gut Liver. 2016;10(3):332-9. doi: 10.5009/gnl15257
16. Ющук Н.Д., Малов И.В., Baatarkhuu O. и др. Клинико-эпидемиологические проявления гепатоцеллюлярной карциномы в этнических группах европеоидов и монголоидов, проживающих на территории Северо-Восточной Азии. Журнал микробиологии, эпидемиологии и иммунобиологии. 2018;6:25-31 [Yuschuk ND, Malov IV, Baatarkhuu O, et al. Clinical and epidemiological manifestation of hepatocellular carcinoma in patients belonging to ethnic groups of Caucasians and Asians of North-East Asia. Zh Mikrobiol Epidemiol Immunobiol. 2018;6:25-31 (In Russ.)].
17. Stroffolini T, Sagnelli E, Sagnelli C, et al. Decreasing role of HCV and HBV infections as aetiological factors of hepatocellular carcinoma in Italy. Infection. 2019. doi: 10.1007/s15010-019-01308-3 [Epub ahead of print].
18. Щеголев А.И., Туманова У.Н. Роль алкоголя в развитии рака печени. Международный журнал прикладных и фундаментальных исследований. 2017;11-2:223-7 [ Schegolev AI, Tumanova U.N. The role of alcohol in the occurrence of liver cancer. International J Applied and Fundamental Research. 2017;11-2:223-7 (In Russ.)].
19. Agyemang-Yeboah F, Eghan BAJ, Annani-Akollor ME, et al. Evaluation of Metabolic Syndrome and Its Associated Risk Factors in Type 2 Diabetes: A Descriptive Cross-Sectional Study at the Komfo Anokye Teaching Hospital, Kumasi, Ghana. Biomed Res Int. 2019;2019:4562904. doi: 10.1155/2019/4562904
20. Ioannou GN, Green P, Lowy E, et al. Differences in hepatocellular carcinoma risk, predictors and trends over time according to etiology of cirrhosis. PLoS One. 2018;13(9):e0204412. doi: 10.1371/journal.pone.0204412
21. Rawla P, Sunkara T, Muralidharan P, Raj JP. Update in global trends and aetiology of hepatocellular carcinoma. Contemp Oncol (Pozn). 2018; 22(3):141-50. doi: 10.5114/wo.2018.78941
22. Motawi TMK, Sadik NAH, Sabry D, Shahin NN, Fahim SA. rs2267531, a promoter SNP within glypican-3 gene in the X chromosome, is associated with hepatocellular carcinoma in Egyptians. Sci Rep. 2019;9(1):6868. doi: 10.1038/s41598-019-43376-3
23. Fakhir FZ, Lkhider M, Badre W, et al. Genetic variations in toll-like receptors 7 and 8 modulate natural hepatitis C outcomes and liver disease progression. Liver Int. 2018;38(3):432-42. doi: 10.1111/liv.13533
24. Maglione PJ, Simchoni N, Cunningham-Rundles C. Toll-like receptor signaling in primary immune deficiencies. Ann NY Acad Sci. 2015;1356:1-21. doi: 10.1111/nyas.12763
25. Miki D, Ochi H, Hayes CN, et al. Variation in the DEPDC5 locus is associated with progression to hepatocellular carcinoma in chronic hepatitis C virus carriers. Nat Genet. 2011;43(8):797-800. doi: 10.1038/ng.876
26. Lo PH, Urabe Y, Kumar V, et al. Identification of a functional variant in the MICA promoter which regulates MICA expression and increases HCV-related hepatocellular carcinoma risk. PLoS One. 2013;8(4):e61279. doi: 10.1371/journal.pone.0061279
27. Carmo RF, Aroucha D, Vasconcelos LR, et al. Genetic variation in PTX3 and plasma levels associated with hepatocellular carcinoma in patients with HCV. J Viral Hepat. 2016;23(2):116-22. doi: 10.1111/jvh.12472
28. Luo X, Wang Y, Shen A, et al. Relationship between the rs2596542 polymorphism in the MICA gene promoter and HBV/HCV infection-induced hepatocellular carcinoma: a meta-analysis. BMC Med Genet. 2019; 20(1):142. doi: 10.1186/s12881-019-0871-2
29. Tan C, Bei C, Zhu X, et al. Single Nucleotide Polymorphisms of CBX4 and CBX7 Decrease the Risk of Hepatocellular Carcinoma. Biomed Res Int. 2019;2019:6436825. doi: 10.1155/2019/6436825
30. Wang H, Cao H, Xu Z, et al. SNP rs2596542G>A in MICA is associated with risk of hepatocellular carcinoma: a meta-analysis. Biosci Rep. 2019; 39(5). pii: BSR20181400. doi: 10.1042/BSR20181400
31. Zhu X, Wang Z, Qiu X, et al. Rs2303428 of MSH2 Is Associated with Hepatocellular Carcinoma Prognosis in a Chinese Population. DNA Cell Biol. 2018;37(7):634-41. doi: 10.1089/dna.2018.4224
32. Yazici H, Zipprich J, Peng T, et al. Investigation of the miR16-1 (C > T) + 7 Substitution in Seven Different Types of Cancer from Three Ethnic Groups. J Oncol. 2009;2009:827532. doi: 10.1155/2009/827532
33. Hu M, Zhao L, Hu S, Yang J. The association between two common polymorphisms in MicroRNAs and hepatocellular carcinoma risk in Asian population. PLoS One. 2013;8(2):e57012. doi: 10.1371/journal.pone.0057012
34. Kim LH, Cheong HS, Namgoong S, et al. Replication of genome wide association studies on hepatocellular carcinoma susceptibility loci of STAT4 and HLA-DQ in a Korean population. Infect Genet Evol. 2015;33: 72-6. doi: 10.1016/j.meegid.2015.04.013
35. Akhdar H, El Shamieh S, Musso O, et al. The rs3957357C>T SNP in GSTA1 Is Associated with a Higher Risk of Occurrence of Hepatocellular Carcinoma in European Individuals. PLoS One. 2016;11(12):e0167543. doi: 10.1371/journal.pone.0167543
________________________________________________
2. Bugaeva TT, Ivanov PM, Alexeeva MN, Karatayev PD, Smetanina VD. Primary liver cancer morbidity of the Republic Sakha (Yakutia) population. Yakut medical journal. 2011;(1):87-9 (In Russ.)
3. Sleptsova SS. Parenteral viral hepatitis and their origin in the Republic of Sakha (Yakutia). Moscow, 2017:216 p (In Russ.)
4. Pimenov NN, Komarova SV, Karandashova IV, Tsapkova NN, Volchkova EV, Chulanov VP. Hepatitis С and its outcomes in Russia: analysis of incidence, prevalence and mortality rates before the start of the programme of infection elimination. Infekc bolezni (Infectious diseases). 2018;16(3):37-45 (In Russ.) doi: 10.20953/1729-9225-2018-3-37-45
5. Calvaruso V, Cabibbo G, Cacciola I, et al. Incidence of Hepatocellular Carcinoma in Patients With HCV-Associated Cirrhosis Treated With Direct-Acting Antiviral Agents. Gastroenterol. 2018;155(2):411-21. doi: 10.1053/j.gastro.2018.04.008
6. EASL Clinical Practice Guidelines: Management of hepatocellular carcinoma. J Hepatol. 2018;69(1):182-236. doi: 10.1016/j.jhep.2018.03.019
7. General Assembly of the World Medical Association. World Medical Association Declaration of Helsinki: ethical principal for medical research involving human subject. J Am Coll Dent. 2014;81(3):14-8.
8. Babor T, Higgins-Biddle JC, Saunders JB, Monteiro MG. AUDIT – The Alcohol Use Disorders Identification Test: Guidelines for Use in Primary Health Care (2nd edn). Geneva: World Health Organization, 2001.
9. Akaike H. A new look at the statistical model identification. IEEE Transactions on Automatic Control. 1974;19(6):716-23.
10. Mentha N, Clément S, Negro F, Alfaiate D. A review on hepatitis D: From virology to new therapies. J Adv Res. 2019;17:3-15. doi: 10.1016/j.jare.2019.03.009
11. Shchanitcyna SE, Burnevich EZ, Nikulkina EN, et al. Risk factors of unfavorable prognosis of chronic hepatitis C. Therapeutic Archive. 2019;91(2):59-66 (In Russ.) doi: 10.26442/00403660.2019.02.000082
12. Budny A, Kozłowski P, Kamińska M, et al. Epidemiology and risk factors of hepatocellular carcinoma. Pol Merkur Lekarski. 2017;43(255):133-9 (In Polish).
13. Kim HS, El-Serag HB. The Epidemiology of Hepatocellular Carcinoma in the USA. Curr Gastroenterol Rep. 2019;21(4):17. doi: 10.1007/s11894-019-0681-x
14. Sleptsova SS. A role of the genotypes of hepatitis B, C and D viruses in primary liver cancer progression. HIV Infection and Immunosuppressive Disorders. 2012;4(4):67-73 (In Russ.)
15. Zhu RX, Seto WK, Lai CL, Yuen MF. Epidemiology of Hepatocellular Carcinoma in the Asia-Pacific Region. Gut Liver. 2016;10(3):332-9. doi: 10.5009/gnl15257
16. Yuschuk ND, Malov IV, Baatarkhuu O, et al. Clinical and epidemiological manifestation of hepatocellular carcinoma in patients belonging to ethnic groups of Caucasians and Asians of North-East Asia. Zh Mikrobiol Epidemiol Immunobiol. 2018;6:25-31 (In Russ.)
17. Stroffolini T, Sagnelli E, Sagnelli C, et al. Decreasing role of HCV and HBV infections as aetiological factors of hepatocellular carcinoma in Italy. Infection. 2019. doi: 10.1007/s15010-019-01308-3 [Epub ahead of print].
18. Schegolev AI, Tumanova U.N. The role of alcohol in the occurrence of liver cancer. International J Applied and Fundamental Research. 2017;11-2:223-7 (In Russ.)
19. Agyemang-Yeboah F, Eghan BAJ, Annani-Akollor ME, et al. Evaluation of Metabolic Syndrome and Its Associated Risk Factors in Type 2 Diabetes: A Descriptive Cross-Sectional Study at the Komfo Anokye Teaching Hospital, Kumasi, Ghana. Biomed Res Int. 2019;2019:4562904. doi: 10.1155/2019/4562904
20. Ioannou GN, Green P, Lowy E, et al. Differences in hepatocellular carcinoma risk, predictors and trends over time according to etiology of cirrhosis. PLoS One. 2018;13(9):e0204412. doi: 10.1371/journal.pone.0204412
21. Rawla P, Sunkara T, Muralidharan P, Raj JP. Update in global trends and aetiology of hepatocellular carcinoma. Contemp Oncol (Pozn). 2018; 22(3):141-50. doi: 10.5114/wo.2018.78941
22. Motawi TMK, Sadik NAH, Sabry D, Shahin NN, Fahim SA. rs2267531, a promoter SNP within glypican-3 gene in the X chromosome, is associated with hepatocellular carcinoma in Egyptians. Sci Rep. 2019;9(1):6868. doi: 10.1038/s41598-019-43376-3
23. Fakhir FZ, Lkhider M, Badre W, et al. Genetic variations in toll-like receptors 7 and 8 modulate natural hepatitis C outcomes and liver disease progression. Liver Int. 2018;38(3):432-42. doi: 10.1111/liv.13533
24. Maglione PJ, Simchoni N, Cunningham-Rundles C. Toll-like receptor signaling in primary immune deficiencies. Ann NY Acad Sci. 2015;1356:1-21. doi: 10.1111/nyas.12763
25. Miki D, Ochi H, Hayes CN, et al. Variation in the DEPDC5 locus is associated with progression to hepatocellular carcinoma in chronic hepatitis C virus carriers. Nat Genet. 2011;43(8):797-800. doi: 10.1038/ng.876
26. Lo PH, Urabe Y, Kumar V, et al. Identification of a functional variant in the MICA promoter which regulates MICA expression and increases HCV-related hepatocellular carcinoma risk. PLoS One. 2013;8(4):e61279. doi: 10.1371/journal.pone.0061279
27. Carmo RF, Aroucha D, Vasconcelos LR, et al. Genetic variation in PTX3 and plasma levels associated with hepatocellular carcinoma in patients with HCV. J Viral Hepat. 2016;23(2):116-22. doi: 10.1111/jvh.12472
28. Luo X, Wang Y, Shen A, et al. Relationship between the rs2596542 polymorphism in the MICA gene promoter and HBV/HCV infection-induced hepatocellular carcinoma: a meta-analysis. BMC Med Genet. 2019; 20(1):142. doi: 10.1186/s12881-019-0871-2
29. Tan C, Bei C, Zhu X, et al. Single Nucleotide Polymorphisms of CBX4 and CBX7 Decrease the Risk of Hepatocellular Carcinoma. Biomed Res Int. 2019;2019:6436825. doi: 10.1155/2019/6436825
30. Wang H, Cao H, Xu Z, et al. SNP rs2596542G>A in MICA is associated with risk of hepatocellular carcinoma: a meta-analysis. Biosci Rep. 2019; 39(5). pii: BSR20181400. doi: 10.1042/BSR20181400
31. Zhu X, Wang Z, Qiu X, et al. Rs2303428 of MSH2 Is Associated with Hepatocellular Carcinoma Prognosis in a Chinese Population. DNA Cell Biol. 2018;37(7):634-41. doi: 10.1089/dna.2018.4224
32. Yazici H, Zipprich J, Peng T, et al. Investigation of the miR16-1 (C > T) + 7 Substitution in Seven Different Types of Cancer from Three Ethnic Groups. J Oncol. 2009;2009:827532. doi: 10.1155/2009/827532
33. Hu M, Zhao L, Hu S, Yang J. The association between two common polymorphisms in MicroRNAs and hepatocellular carcinoma risk in Asian population. PLoS One. 2013;8(2):e57012. doi: 10.1371/journal.pone.0057012
34. Kim LH, Cheong HS, Namgoong S, et al. Replication of genome wide association studies on hepatocellular carcinoma susceptibility loci of STAT4 and HLA-DQ in a Korean population. Infect Genet Evol. 2015;33: 72-6. doi: 10.1016/j.meegid.2015.04.013
35. Akhdar H, El Shamieh S, Musso O, et al. The rs3957357C>T SNP in GSTA1 Is Associated with a Higher Risk of Occurrence of Hepatocellular Carcinoma in European Individuals. PLoS One. 2016;11(12):e0167543. doi: 10.1371/journal.pone.0167543
Авторы
Н.Д. Ющук1, С.С. Слепцова2, С.И. Малов3,4, С.И. Семенов2, И.Ф. Билюкина2, Л.А. Степаненко3, О.Б. Огарков4,5, Е.Д. Савилов4,5, И.В. Малов3
1 ФГБОУ ВО «Московский государственный медико-стоматологический университет им. А.И. Евдокимова» Минздрава России, Москва, Россия;
2 Медицинский институт ФГАОУ ВО «Северо-Восточный федеральный университет им. М.К. Аммосова» Министерства науки и высшего образования России, Якутск, Россия;
3 ФГБОУ ВО «Иркутский государственный медицинский университет» Минздрава России, Иркутск, Россия;
4 Иркутская государственная медицинская академия последипломного образования – филиал ФГБОУ ДПО «Российская медицинская академия непрерывного профессионального образования» Минздрава России, Иркутск, Россия;
5 ФГБНУ «Научный центр проблем здоровья семьи и репродукции человека», Иркутск, Россия
1 A.I. Evdokimov Moscow State University of Medicine and Dentistry, Moscow, Russia;
2 M.K. Ammosov North-Eastern Federal University, Medical Institute, Yakutsk, Russia;
3 Irkutsk State Medical University, Irkutsk, Russia;
4 Irkutsk State Medical Academy of Continuing Education, Irkutsk, Russia;
5 Scientific Center of Family Health and Human Reproduction, Irkutsk, Russia
1 ФГБОУ ВО «Московский государственный медико-стоматологический университет им. А.И. Евдокимова» Минздрава России, Москва, Россия;
2 Медицинский институт ФГАОУ ВО «Северо-Восточный федеральный университет им. М.К. Аммосова» Министерства науки и высшего образования России, Якутск, Россия;
3 ФГБОУ ВО «Иркутский государственный медицинский университет» Минздрава России, Иркутск, Россия;
4 Иркутская государственная медицинская академия последипломного образования – филиал ФГБОУ ДПО «Российская медицинская академия непрерывного профессионального образования» Минздрава России, Иркутск, Россия;
5 ФГБНУ «Научный центр проблем здоровья семьи и репродукции человека», Иркутск, Россия
________________________________________________
1 A.I. Evdokimov Moscow State University of Medicine and Dentistry, Moscow, Russia;
2 M.K. Ammosov North-Eastern Federal University, Medical Institute, Yakutsk, Russia;
3 Irkutsk State Medical University, Irkutsk, Russia;
4 Irkutsk State Medical Academy of Continuing Education, Irkutsk, Russia;
5 Scientific Center of Family Health and Human Reproduction, Irkutsk, Russia
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