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Review

Progress in studies of the mechanisms and clinical diagnosis of cervical carcinoma associated with genomic integration of high-risk human papillomavirus DNA

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  • 1 Guangdong Medical University, Zhanjiang 524023, China
    2 Capital Corporation Clinical & Translational Science Institute, Beijing 102206, China
    3 Laboratory of Shenzhen Third People’s Hospital, Shenzhen 518112, China

Received date: 2017-04-24

  Revised date: 2017-07-17

  Online published: 2017-10-21

Supported by

Supported by Shenzhen Key Laboratory of Biochip(ZDSYS201504301534057);Funds of Shenzhen for Introduced High-Level Medical Team

Abstract

High-risk human papillomavirus (hrHPV) has been identified as a key factor in the development of cervical cancer. Integration of viral DNA into the host genome has been postulated as an important etiological event during cervical carcinogenesis. High-risk HPV DNA integration frequently results in either the deletion or interruption of the large fragment of E1 and E2 region and the overexpression of oncogenes E6 and E7 in the viral genome, and the activation of oncogenes and the inactivation of tumor suppressors in host genome. Recent studies have showed that hrHPV integration can be used as a predictive biomarker in high-quality cervical lesion screening. Most effective diagnostic approaches are based on fluorescence in situ hybridization, real-time quantitative PCR and Sanger sequencing of hybrid captured viral DNA. This review highlights the primary mechanisms of hrHPV DNA integration associated with cervical carcinogenesis, illustrates recent advances in predictive biomarkers in cervical lesion screening and the development and popularization of prophylactic HPV vaccines, and summarizes the various methods of detecting hrHPV DNA integration.

Cite this article

Shasha Huang,Dengzai Hao,Yan Zhang,Houming Liu,Wanshui Shan . Progress in studies of the mechanisms and clinical diagnosis of cervical carcinoma associated with genomic integration of high-risk human papillomavirus DNA[J]. Hereditas(Beijing), 2017 , 39(9) : 775 -783 . DOI: 10.16288/j.yczz.17-151

References

[1] Forouzanfar MH, Foreman KJ, Delossantos AM, Lozano R, Lopez AD, Murray CJL, Naghavi M. Breast and cervical cancer in 187 countries between 1980 and 2010: a systematic analysis. Lancet, 2011, 378(9801): 1461-1484.
[2] Ferlay J, Shin HR, Bray F, Forman D, Mathers C, Parkin DM. Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. Int J Cancer, 2010, 127(12): 2893-2917.
[3] Wang H, Xu FZ, Zhao QY. Application of three-stage diagnosis and treatment process in screening of cervical precancerous lesion. Mater Child Health Care China, 2011, 26(5): 769-770.
[3] 王红, 徐福智, 赵秋艳. 三阶梯诊疗程序筛查宫颈癌前病变. 中国妇幼保健, 2011, 26(5): 769-770.
[4] Datta SD, Saraiya M. Cervical cancer screening among women who attend sexually transmitted diseases (STD) clinics: background paper for 2010 STD Treatment Guidelines. Clin Infect Dis, 2011, 53(Suppl. 3): S153-S159.
[5] Zhang RY, Shen C, Zhao LJ, Wang JL, McCrae M, Chen XM, Lu FM. Dysregulation of host cellular genes targeted by human papillomavirus (HPV) integration contributes to HPV-related cervical carcinogenesis. Int J Cancer, 2016, 138(5): 1163-1174.
[6] Liu Y, Lu ZM, Xu RP, Ke Y. Comprehensive mapping of the human papillomavirus (HPV) DNA integration sites in cervical carcinomas by HPV capture technology. Oncotarget, 2016, 7(5): 5852-5864.
[7] Schmitz M, Driesch C, Beer-Grondke K, Jansen L, Runnebaum IB, Dürst M. Loss of gene function as a consequence of human papillomavirus DNA integration. Int J Cancer, 2012, 131(5): E593-E602.
[8] Seedorf K, Kr?mmer G, Dürst M, Suhai S, R?wekamp WG. Human papillomavirus type 16 DNA sequence. Virology, 1985, 145(1): 181-185.
[9] Matsukura T, Kanda T, Furuno A, Yoshikawa H, Kawana T, Yoshiike K. Cloning of monomeric human papillomavirus type 16 DNA integrated within cell DNA from a cervical carcinoma. J Virol, 1986, 58(3): 979-982.
[10] Howie HL, Katzenellenbogen RA, Galloway DA. Papillomavirus E6 proteins. Virology, 2009, 384(2): 324-334.
[11] McLaughlin-Drubin ME, Münger K. The human papillomavirus E7 oncoprotein. Virology, 2009, 384(2): 335-344.
[12] Moody CA, Laimins LA. Human papillomavirus oncoproteins: pathways to transformation. Nat Rev Cancer, 2010, 10(8): 550-560.
[13] Zhao YJ, Cheng D, Wang SW, Zhu JY. Dual roles of c-Myc in the regulation of hTERT gene. Nucleic Acids Res, 2014, 42(16): 10385-10398.
[14] Oh ST, Kyo S, Laimins LA. Telomerase activation by human papillomavirus type 16 E6 protein: induc
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