The current concept of the role of papillomavirus infection in the development of cervical intraepitelial neoplasia


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Abstract

Cervical cancer remains an important indicator of global health inequities. There are estimated 569,000 new cases and 310,000deaths annually, among which approximately 85% occur in low- and middle-income countries. In developing countries, cervical cancer is often the most common cancer in women and can account for about 25% of all cancers in them. In 1996, the World Health Association recognized human papillomavirus (HPV) as an important cause of cervical cancer. Materials and methods: The authors have analyzed the data available in the literature on studies of cervical cancer and HPV. The keywords have been used to search for data in international databases. A total of 31 sources were selected on relevant topics. Conclusion: It should be noted that the problem of human papillomavirus infection in gynecology is still far from being solved, and many issues are the subject of ongoing investigations. The complexity of the problem involves mainly the significant prevalence of infection, the emergence of new HPV genotypes and the presence of considerable differences in their malignant potency, as well as changes in the strength of the patient’s antiviral immunity that determines the stability of cure or the onset of relapse. The accumulated knowledge about the mechanism of viral carcinogenesis in the development of dysplasia and cervical cancer necessitates further investigation to develop the most effective etiopathogenetic treatment regimens that are able to have a point effect at the genetic level.

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About the authors

Gagik A. Beglaryan

University of Milan

International Medical School of the Faculty of Medicine

Armine G. Arutyunyan

M. Heratsi Yerevan State Medical University

Email: adelinatorgomyan@yahoo.com
MD, Professor, Head of the Department of Obstetrics and Gynecology No. 1

References

  1. Bray F., Ferlay J., Soerjomataram I., Siegel R.L., Torre L.A., Jemal A. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J. Clin. 2018; 68(6): 394424. https://dx.doi.org/10.3322/caac.21492.
  2. National Institutes of Health. Human papilloma virus subtypes. In: Human papilloma virus database. Bethesda, MA, USA : NIH; 2019.
  3. Kuguyo O., Tsikai N., Thomford N.E., Magwali T., Madziyire M.G., Nhachi C.F.B. et al. Genetic susceptibility for cervical cancer in African populations: what are the host genetic drivers? Omics. 2018; 22(7): 468-83. https://dx.doi.org/10.1089/omi.2018.0075.
  4. von Minckwitz G., Procter M., de Azambuja E., Zardavas D., Benyunes M., Viale G. et al. Improved survival with bevacizumab in advanced cervical cancer. N. Engl. J. Med. 2017; 377(2): 122-31. https://dx.doi.org/10.1056/NEJMoa1703643. Erratum in: Improved survival with bevacizumab in advanced cervical cancer. N. Engl. J. Med. 2017; 377:(7): 702. https://dx.doi.org/10.1056/NEJMx170011.
  5. Yao S., Xu J., Zhao K., Song P., Yan Q., Fan W. et al. Down-regulation of HPGD by miR-146b-3p promotes cervical cancer cell proliferation, migration and anchorage-independent growth through activation of STAT3 and AKT pathways. Cell Death Dis. 2018; 9(11): 1055. https://dx.doi.org/10.1038/s41419-018-1059-y.
  6. Fang F, Huang B., Sun S., Xiao M., Guo J., Yi X. et al. miR-27a inhibits cervical adenocarcinoma progression by downregulating the TGF-_RI signaling pathway. Cell Death Dis. 2018; 9(3): 395. https://dx.doi.org/10.1038/s41419-018-0431-2.
  7. Huang J., Qian Z., Gong Y., Wang Y., Guan Y., Han Y. et al. Comprehensive genomic variation profiling of cervical intraepithelial neoplasia and cervical cancer identifies potential targets for cervical cancer early warning. J. Med. Genet. 2018; 56(3): 186-94. https://dx.doi.org/10.1136/jmedgenet-2018-105745
  8. Nuryadi E., Sasaki Y., Hagiwara Y., Permata T.B.M., Sato H., Komatsu S. et al. Mutational analysis of uterine cervical cancer that survived multiple rounds of radiotherapy. Oncotarget. 2018; 9(66): 32642-52. https://dx.doi.org/10.18632/oncotarget.25982.
  9. Lyng H., Beigi M., Svendsrud D.H., Brustugun O.T., Stokke T., Kristensen G.B. et al. Intratumor chromosomal heterogeneity in advanced carcinomas of the uterine cervix. Int. J. Cancer. 2004; 111(3): 358-66. https://dx.doi.org/10.1002/ijc.20258.
  10. Cancer Genome Atlas Research Network; Albert Einstein College of Medicine; Analytical Biological Services et al. Integrated genomic and molecular characterization of cervical cancer. Nature. 2017; 543(7645): 378-84. https://dx.doi.org/10.1038/nature21386.
  11. Paaso A., Jaakola A., Syrjanen S., Louvanto K. From HPV infection to lesion progression: the role of HLA alleles and host immunity. Acta Cytol. 2019; 63: 148-58. https://dx.doi.org/10.1159/000494985.
  12. Ding B., Sun W, Han S., Cai Y., Ren M., Shen Y. Cytochrome P450 1A1 gene polymorphisms and cervical cancer risk: A systematic review and meta-analysis. Medicine (Baltimore). 2018; 97(13): e0210. https://dx.doi.org/10.1097/MD.0000000000010210.
  13. Wang L., Yi T., Kortylewski M., Pardoll D.M., Zeng D., Yu H. IL-17 can promote tumor growth through an IL-6-Stat3 signaling pathway. J. Exp. Med. 2009; 206(7): 1457-64. https://dx.doi.org/10.1084/jem.20090207.
  14. Tewari K.S., Sill M.W., Long H.J. 3rd, Penson R.T., Huang H., Ramondetta L.M. et al. Improved survival with bevacizumab in advanced cervical cancer. N. Engl. J. Med. 2014; 370(8): 734-43. https://dx.doi.org/10.1056/NEJMoa1309748.
  15. Giroglu T., Florin L., Schafer F., Streeck R.E., Sapp M. Human papillomavirus infection requires cell surface heparan sulfate. J. Virol. 2001; 75(3): 1565-70. https://dx.doi.org/10.1128/JVI.75.3.1565-1570.2001.
  16. Muntean M., Simionescu C., Taslica R., Gruia C., Comanescu A., Patrana N., Fota G. Cytological and histopathological aspects concerning pre-invasive squamous cervical lesions. Curr. Health Sci. J. 2010; 36(1): 26-32.
  17. Szymonowicz K.A., Chen J. Biological and clinical aspects of HPV-related cancers. Cancer Biol. Med. 2020; 17(4): 864-78. https://dx.doi.org/10.20892/j.issn.2095-3941.2020.0370.
  18. Ferenczy A., Franco E. Persistent human papillomavirus infection in cervical neoplasia. Lancet Oncol. 2002; 3: 11-6. https://dx.doi.org/10.1016/s1470-2045(01)00617-9.
  19. Doorbar J. Molecular biology of human papillomavirus infection and cervical cancer. Clin. Sci. (Lond.). 2006; 110(5): 525-41. https://dx.doi.org/10.1042/CS20050369.
  20. Ghittoni R., Accardi R., Chiocca S., Tommasino M. Role of human papillomaviruses in carcinogenesis. Ecancermedicalscience. 2015; 9: 526. https://dx.doi.org/10.3332/ecancer.2015.526.
  21. zur Hausen H. Papillomaviruses and cancer: from basic studies to clinical application. Nat. Rev. Cancer. 2002; 2(5): 342-50. https://dx.doi.org/10.1038/nrc798.
  22. Yang A., Jeang J., Cheng K., Cheng T., Yang B., Wu T.C., Hung C.F. Current state in the development of candidate therapeutic HPV vaccines. Expert Rev. Vaccines. 2016; 15(8): 989-1007. https://dx.doi.org/10.1586/14760584.2016.1157477.
  23. Perkins R.B., Guido R.S., Castle P.E., Chelmow D., Einstein M.H., Garcia F. et al. 2019 ASCCP risk-based management consensus guidelines for abnormal cervical cancer screening tests and cancer precursors..J. Low. Genit. Tract Dis. 2020; 24(2): 102-31. 10.1097/LGT.0000000000000525.
  24. Mello V., Sundstrom R.K. Cancer, cervicaliIntraepithelial neoplasia (CIN). Treasure Island, FL: StatPearls Publishing; 2021.
  25. Adams A.K., Wise-Draper T.M., Wells S.I. Human papillomavirus induced transformation in cervical and head and neck cancers. Cancers (Basel). 2014; 6(3): 1793-820. https://dx.doi.org/10.3390/cancers6031793.
  26. Peitsaro P., Johansson B., Syrjanen S. Integrated human papillomavirus type 16 is frequently found in cervical cancer precursors as demonstrated by a novel quantitative real-time PCR technique. J. Clin. Microbiol. 2002; 40(3): 886-91. https://dx.doi.org/10.1128/JCM.40.3.886-891.2002.
  27. Barr A. R., Cooper S., Heldt FS., But era F, Stoy H., Mansfeld J. et al. DNA damage during S-phase mediates the proliferation-quiescence decision in the subsequent G1 via p21 expression. Nat. Commun. 2017; 8: 14728. https://dx.doi.org/10.1038/ncomms14728.
  28. Oh K-J., Kalinina A., Wang J., Nakayama K., Nakayama K.I., Bagchi S. The papillomavirus E7 oncoprotein is ubiquitinated by UbcH7 and cullin 1- and Skp2-containing E3 ligase. J. Virol. 2004; 78(10): 5338-46. https://dx.doi.org/10.1128/jvi.78.10.5338-5346.2004.
  29. Huh K, Zhou X., Hayakawa H., Cho J.Y., Libermann T.A., Jin J. et al. Human papillomavirus type 16 E7 oncoprotein associates with the cullin 2 ubiquitin ligase complex, which contributes to degradation of the retinoblastoma tumor suppressor. J. Virol. 2007; 81(18): 9737-47. https://dx.doi.org/10.1128/JVI.00881-07.
  30. Булатова И.А., Шевлюкова Т.П., Ненашева О.Ю., Щекотова А.П., Спирина А.Б. Оценка инфицированности высококанцерогенными типами вируса папилломы человека по данным скрининга. Акушерство и гинекология. 2021; 10: 112-7. https://dx.doi.org/10.18565/aig.2021.10.112-117.
  31. Harro C.D., Pang Y.Y., Roden R.B., Hildesheim A., Wang Z., Reynolds M.J. et al. Safety and immunogenicity trial in adult volunteers of a human papillomavirus 16 L1 virus-like particle vaccine. J. Natl. Cancer Inst. 2001; 93(4): 284-92. https://dx.doi.org/10.1093/jnci/93.4.284.
  32. Canfell K. Towards the global elimination of cervical cancer. Papillomavirus Res. 2019 Dec 8: 100170. https://dx.doi.org/10.1016/j.pvr.2019.100170.

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