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High Prevalence of High Risk HPV with Low Frequency of Tp53 Mutations in Esophageal Squamous Cell Carcinoma and Adenocarcinoma Patients in Tangshan China
International Journal of Genetics and Genomics
Volume 4, Issue 2, April 2016, Pages: 11-15
Received: May 4, 2016; Published: May 5, 2016
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Authors
Vania H. M. Teofilo, Beijing Key Lab. of Environmental & Viral Oncology, College of Life Science & Bioengineering, Beijing Univ. of Technology, Beijing, China
Jintao Li, Beijing Key Lab. of Environmental & Viral Oncology, College of Life Science & Bioengineering, Beijing Univ. of Technology, Beijing, China; State Key Laboratory for Infectious Disease Prevention and Control, National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, China
Mohammadreza Mohammadzad Mephryar, Beijing Key Lab. of Environmental & Viral Oncology, College of Life Science & Bioengineering, Beijing Univ. of Technology, Beijing, China
Si Ye, Beijing Key Lab. of Environmental & Viral Oncology, College of Life Science & Bioengineering, Beijing Univ. of Technology, Beijing, China
Shaomei Zhou, Beijing Key Lab. of Environmental & Viral Oncology, College of Life Science & Bioengineering, Beijing Univ. of Technology, Beijing, China
Rugang Zhong, Beijing Key Lab. of Environmental & Viral Oncology, College of Life Science & Bioengineering, Beijing Univ. of Technology, Beijing, China
Yi Zeng, Beijing Key Lab. of Environmental & Viral Oncology, College of Life Science & Bioengineering, Beijing Univ. of Technology, Beijing, China; State Key Laboratory for Infectious Disease Prevention and Control, National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, China
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Abstract
Esophageal cancer, including Squamous Cell Carcinoma and Adenocarcinoma, is one of the most common causes of cancer and cancer death globally, with China alone accounting for about half of the new cases worldwide in 2012. In this study we analyzed the presence of human papilloma virus (HPV) DNA and Tp53 mutations in 52 cancer patients, including 26 Squamous Cell Carcinoma cases, 21 Adenocarcinomas and 5 of non-described histology from Tangshan China. Overall 44 patients were positive for HPV L1 consensus, 28 were positive for HPV16 and 34 for HPV18 (84.62%, 53.82% and 65.38% respectively); 23 samples (44.23%) were positive for both HPV16 and HPV 18. We detected however a very low rate of Tp53 mutations in exons 5 through 8, which may possible be related to the elevated percentage of high risk HPV. Our findings corroborate our previous study on Esophageal Squamous Cell carcinoma in the same area but a further analysis on other Tp53 exons polymorphisms are necessary to understand the reason behind the low level of Tp53 mutations we reported.
Keywords
Esophageal Cancer, HPV, Tp53 Mutations
To cite this article
Vania H. M. Teofilo, Jintao Li, Mohammadreza Mohammadzad Mephryar, Si Ye, Shaomei Zhou, Rugang Zhong, Yi Zeng, High Prevalence of High Risk HPV with Low Frequency of Tp53 Mutations in Esophageal Squamous Cell Carcinoma and Adenocarcinoma Patients in Tangshan China, International Journal of Genetics and Genomics. Vol. 4, No. 2, 2016, pp. 11-15. doi: 10.11648/j.ijgg.20160402.12
References
[1]
J. Ferlay, I. Soerjomataram, M. Ervik, R. Dikshit, S. Eser, C. Mathers, M. Rebelo, D. M. Parkin, D. Forman and F. Bray, GLOBOCAN 2012 v1.0, Cancer Incidence and Mortality Worldwide: IARC Cancer Base No. 11 [http://globocan.iarc.fr/Pages/fact_sheets_cancer.aspx]. Lyon, France: International Agency for Research on Cancer; 2013. Available from: http://globocan.iarc.fr, accessed on 11/03/2016.
[2]
G. Edgren, H. O. Adami, E. Weiderpass and O. Nyren, “A global assessment of the oesophageal adenocarcinoma epidemic,” Gut, 2013, vol. 62(10), pp.1406–14.
[3]
M. Arnold, I. Soerjomataram, J. Ferlay and D. Forman, “Global incidence of oesophageal cancer by histo-logical subtype in 2012,” Gut, 2015, vol. 64, pp. 381-387.
[4]
M. P. Curado, B. Edwards, H. R. Shin, H. Storm, J. Ferlay, M. Heanue and P. Boyle, Cancer incidence in five continents, vol. IX, IARC Scientific Publications No. 160. Lyon: IARC, 2007.
[5]
Y. Zhang, “Epidemiology of esophageal cancer,” World J. Gastroentrol, 2013, vol. 19(34), pp. 5598-5606.
[6]
W. Chen, R. Zheng, S. Zhang, P. Zhao, H. Zeng, X. Zou, and J. He, “Annual report on status of cancer in China, 2010,” Chin. J. Cancer Res., 2014, vol. 26(1), pp. 48-58.
[7]
K. J. Napier, M. Scheerer, and S. Misra, “Esophageal cancer: A review of epidemiology, pathogenesis, staging workup and treatment modalities,” World J. Gastrointest. Oncol., 2014, vol. 6(5), pp. 112-120.
[8]
M. Olivier, M. Hollstein, and P. Hainaut, “TP53 mutations in human cancers: origins, consequences and clinical use”. Cold Spring Harb. Prespect. Biol., 2010, vol. 2 a0001008.
[9]
C. Whibley, P. D. Pharoah, and M. Hollstein, “p53 polymorphisms: cancer implications,” Nat. Rev. Cancer, 2009, vol. 9, pp. 99-107.
[10]
M. C. Hollstein, R. A. Metcalf, J. A. Welsh, R. Montesano, and C. C. Harris, “Frequent mutation of the p53 gene in human esophageal cancer,” Proc. Natl. Acad. Sci. USA, 1990, vol. 87(24), pp. 9958–9961.
[11]
M. C. Hollstein, L. Peri, A. M. Mandard, J. A. Welsh, R. Montesano, R. A. Metcalf, M. Bak and C. C. Harris, “Genetic analysis of human esophageal tumors from two high incidence geographic areas: frequent p53 base substitutions and absence of ras mutations,” Cancer Res., 1991, vol. 51(15) pp. 4102–4106.
[12]
N. Agrawal, Y. Jiao, C. Bettegowda, S. M. Hutfless, Y. Wang, S. David, Y. Cheng, W. S. Twaddell, N. L. Latt, E. J. Shin, L. D. Wang, L. Wang, W. Yang, V. E. Velculescu, B. Vogelstein, N. Papadopoulos, K. W. Kinzler, and S. J. Meltzer, “Comparative genomic analysis of esophageal adenocarcinoma and squamous cell carcinoma,” Cancer Discov., 2012, vol. 2(10), pp. 899-905.
[13]
A. M. Dulak, P. Stojanov, S. Peng, M. S. Lawrence, C. Fox, C. Stewart, S. Bandla, Y. Imamura, S. E. Schumacher, E. Shefler, A. McKenna, S. L. Carter, K. Cibulskis, A. Sivachenko, G. Saksena, D. Voet, A. H. Ramos, D. Auclair, K. Thompson, C. Sougnez, R. C. Onofrio, C. Guiducci, R. Beroukhim, Z. Zhou, L. Lin, J. Lin, R. Reddy, A. Chang, R. Landrenau, A. Pennathur, S. Ogino, J. D. Luketich, T. R. Golub, S. B. Gabriel, E. S. Lander, D. G. Beer, T. E. Godfrey, G. Getz, and A. J. Bass, "Exome and whole-genome sequencing of esophageal adenocarcinoma identifies recurrent driver events and mutational complexity," Nat. Genet., 2013,vol. 45(5), pp. 478-86.
[14]
C. A. Moody and A. L. Laimins, “Human papillomavirus oncoproteins: pathways to transformation,” Nat. Rev. Cancer, 2010, vol. 10, pp. 550-560.
[15]
H. L. Howie, R. A. Katzenellenbogen and D. A. Galloway, “Papillomavirus E6 proteins. Minireview,” Virol., 2001, vol. 384, pp.324-334.
[16]
K. J. Syrjanen, “Histological changes identical to those of condylomatous lesions found in esophageal squamous cell carcinomas,” Arch Geschwolstforsh, 1982, vol. 15, pp. 415-425.
[17]
S. S. Liyanage, B. Rahman, I. Ridda, A. T. Newall, S. N. Tabrizi, S. M. Garland, E. Segelov, H. Seale, P. J. Crowe, A. Moa, and C. R. Macintyre, “The aetiological role of human papillomavirus in oesophageal squamous cell carcinoma: A meta-Analysis,” PLoS One, 2013, vol. 8(7), pp. 1-12.
[18]
J. Koshiol, W. Q. Wei, A. R. Kreimer, W. Chen, P. Gravitt, J. S. Ren, C. C. Abnet, J. B. Wang, F. Kamangar, D. M. Lin, M. von Knebel-Doeberitz, Y. Zhang, R. Viscidi, G. Q. Wang, M. L. Gillison, M. J. Roth, Z. W. Dong, E. Kim, P. R. Taylor, Y. L. Qiao, and S. M. Dawsey, “No role for human papillomavirus in esophageal squamous cell carcinoma in China,” Int. J. Cancer, 2010, vol. 127(1), pp. 93-100.
[19]
F. Kamangar, Y. L. Qiao, J. T. Schiller, S. M. Dawsey, T. Fears, X. D. Sun, C. C. Abnet, P. Zhao, P. R. Taylor, and S. D. Mark, “Human papillomavirus serology and the risk of esophageal and gastric cancers: results from a cohort in a high-risk region in China,” Int. J. Cancer, 2006,vol. 119(3), pp. 579-584.
[20]
D. H. Zhang, Q. Y. Zhang, C. Q. Hong, J. Y. Chen, Z. Y. Shen, and Y. Zhu, “Prevalence and association of human papillomavirus 16, Epstein-Barr virus, herpes simplex virus-1 and cytomegalovirus infection with human esophageal carcinoma: a case-control study,” Oncol. Rep., 2011, vol. 25(6), pp. 1731-1738.
[21]
F. Guo, Y. Liu, X. Wang, Z. He, N. S. Weiss, M. M. Madeleine, F. Liu, X. Tian, Y. Song, Y. Pan, T. Ning, H. Yang, X. Shi, C. Lu, H. Cai, and Y. Ke,“Human papillomavirus infection and esophageal squamous cell carcinoma: a case-control study,” Cancer Epidemiol. Biomarkers Prev., 2012, vol. 21(5), pp.780-785.
[22]
M. M. Mehryar, S. Y. Li, H. W. Liu, F. Li, F. Zhang, Y. B. Zhou, Y. Zeng, and J.T. Li, “Prevalence of human papillomavirus in esophageal carcinoma in Tangshan, China,” World J. Gastroenterol., 2015, vol. 21(10), pp. 2905-2911.
[23]
W. Qu, G. Jiang, Y. Cruz, C. J. Chang, G. Y. Ho, R. S. Klein and R. D. Burk, “PCR detection of human papillomavirus: comparison between MY09/MY11 and GP5+/GP6+ primer systems, ”J. Clin. Microbiol., 1997, vol. 35, pp. 1304-1310.
[24]
A. Petitjean, E. Mathe, S. Kato, C. Ishioka, S. V. Tavtigian, P. Hainaut and M. Olivier, “Impact of mutant P53 functional properties on Tp53 Mutation Patterns and Tumor Phenotype: Lessons from recent developments in the Iarc Tp53 database,” Hum.Mutat., 2007, vol. 28, pp. 622-629. (R17, November 2013 version).
[25]
S. K. Zhang, L. W. Guo, Q. Chen, M. Zhang, S. Z. Liu, P. L. Quan, J. B. Lu, and X. B. Sun, “The Association between Human Papillomavirus 16 and Esophageal Cancer in Chinese Population: A Meta-Analysis," BMC Cancer,2015,vol. 15, pp. 1096.
[26]
B. Abedi-Ardekani,, F. Kamangar, M. Sotoudeh, S. Villar, F. Islami, K. Aghcheli, D. Nasrollahzadeh, N. Taghavi, S. M. Dawsey, C. C. Abnet, S. M. Hewitt, S. Fahimi, F. Saidi, P. Brennan, P. Boffetta, R. Malekzadeh, and P. Hainaut, "Extremely high Tp53 mutation load in esophageal squamous cell carcinoma in Golestan Province, Iran." PLoS One, 2011, vol. 6(12), e29488.
[27]
W. Cao, X. Chen, H. Dai, H. Wang, B. Shen, D. Chu, T. McAfee, and Z. F. Zhang. "Mutational spectra of P53 in geographically localized esophageal squamous cell carcinoma groups in China," Cancer, 2004, vol. 101(4), pp. 834-844.
[28]
K. Patel, S. Mining, J. Wakhisi, T. Gheit, M. Tommasino, G. Martel-Planche, P. Hainaut, and B. Abedi-Ardekani, "Tp53 mutations, human papilloma virus DNA and inflammation markers in esophageal squamous cell carcinoma from the rift valley, a high-Incidence area in Kenya," BMC Res. Notes, 2011, vol. 4, pp. 469.
[29]
W. Gamieldien, T. C. Victor, D. Mugwanya, A. Stepien, W. C. Gelderblom, W. F. Marasas, D. H. Geiger and P. D. van Helden, “p53 and p16/CDKN2 gene mutations in esophageal tumors from a high-incidence area in South Africa” Int. J. Cancer, 1998, vol. 78, pp. 544-549.
[30]
F. Chang, S. Syrjanen, A. Tervahauta, K. Kurvinen, L. Wang, and K. Syrjinen, "Frequent mutations of P53 gene in oesophageal squamous cell carcinomas with and without human papiliomavirus (Hpv) involvement suggest the dominant role of environmental carcinogens in oesophageal carcinogenesis," Br. J. Cancer,1994, vol. 70, pp. 346-351.
[31]
S. Katiyar, S. Hedau, N. Jain, P. Kar, M. S. Khuroo, J. Mohanta, S. Kumar, V. Gopalkrishna, N. Kumar and B. C. Das, "P53 gene mutation and human papillomavirus (Hpv) infection in esophageal carcinoma from three endemic geographic regions of India." Cancer Lett., 2005, vol. 218, pp. 69-79.
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