全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

Evidences Suggesting Involvement of Viruses in Oral Squamous Cell Carcinoma

DOI: 10.1155/2013/642496

Full-Text   Cite this paper   Add to My Lib

Abstract:

Oral cancer is one of the most common cancers and it constitutes a major health problem particularly in developing countries. Oral squamous cell carcinoma (OSCC) represents the most frequent of all oral neoplasms. Several risk factors have been well characterized to be associated with OSCC with substantial evidences. The etiology of OSCC is complex and involves many factors. The most clearly defined potential factors are smoking and alcohol, which substantially increase the risk of OSCC. However, despite this clear association, a substantial proportion of patients develop OSCC without exposure to them, emphasizing the role of other risk factors such as genetic susceptibility and oncogenic viruses. Some viruses are strongly associated with OSCC while the association of others is less frequent and may depend on cofactors for their carcinogenic effects. Therefore, the exact role of viruses must be evaluated with care in order to improve the diagnosis and treatment of OSCC. Although a viral association within a subset of OSCC has been shown, the molecular and histopathological characteristics of these tumors have yet to be clearly defined. 1. Introduction The significant role of viruses in cancer was acknowledged finally in the second half of the past century after various rodent tumorigenic viruses were discovered, and evidence had accumulated supporting an association between viruses and human cancer. Indeed, the Nobel Prize was awarded to Rous in 1966 in recognition of his seminal discovery of tumor-inducing viruses. In addition, almost at the same time, a Special Virus Cancer Program (VCP) was launched by the US Congress in 1964 providing enormous funds for intensive research into the supposed role of viruses in human cancer. This program, criticized by some investigators as being a political moonshot-style plan, failed to identify candidate human cancer-causing viruses yet generated fundamental information about the molecular biology and mechanisms underlying, in particular, virus-related animal cancer and cancer in general [1]. The strong cohort effect that accounted for the increased incidence of head and neck cancers after 1915 indicates that oral cancer is a disease largely attributable to behaviors that expose an individual to environmental carcinogens. The majority of oral cancers in individuals above and below the age of 45 can be attributed to the combined effects of alcohol and tobacco smoking. Other risk factors for oral cancers include diet, Body Mass Index, oral hygiene, and viral infections [2]. The most commonly implicated viruses in oral

References

[1]  R. T. Javier and J. S. Butel, “The history of tumor virology,” Cancer Research, vol. 68, no. 19, pp. 7693–7706, 2008.
[2]  M. E. McLaughlin-Drubin and K. Munger, “Viruses associated with human cancer,” Biochimica et Biophysica Acta, vol. 1782, no. 3, pp. 127–150, 2008.
[3]  S. M. Gondivkar, R. V. Parikh, A. R. Gadbail et al., “Involvement of viral factors with head and neck cancers,” Oral Oncology, vol. 48, no. 3, pp. 195–199, 2012.
[4]  R. O. Greer Jr., J. M. Douglas Jr., P. Breese, and L. K. Crosby, “Evaluation of oral and laryngeal specimens for human papillomavirus (HPV) DNA by dot blot hybridization,” Journal of Oral Pathology and Medicine, vol. 19, no. 1, pp. 35–38, 1990.
[5]  R. O. Greer, K. Shroyer, and L. Crosby, “Identification of human papillomavirus DNA in smokeless tobacco keratoses and premalignant and malignant oral lesions by PCR amplification with consensus sequence primers,” NIH Publication No. 92-3461, US Department of Health and Human Services, Public Health Service, National Institutes of Health, Bethesda, Md, USA, 1992.
[6]  N. H. Park, M. M. Byung, and L. L. Sheng, “Role of viruses in oral carcinogenesis,” NIH Publication No. 92-3461, US Department of Health and Human Services, Public Health Service, National Institutes of Health, Bethesda, Md, USA, 1992.
[7]  N. W. Johnson, Risk Markers for Oral Disease, Oral Cancer Detection of Patients and Lesions at Risk, Cambridge University Press, Cambridge, UK, 1991.
[8]  Y. Nagao, M. Sata, K. Tanikawa, K. Itoh, and T. Kameyama, “High prevalence of hepatitis C virus antibody and RNA in patients with oral cancer,” Journal of Oral Pathology and Medicine, vol. 24, no. 8, pp. 354–360, 1995.
[9]  S. R. Porter, G. Lodi, K. Chandler, and N. Kumar, “Development of squamous cell carcinoma in hepatitis C virus-associated lichen planus,” Oral Oncology, vol. 33, no. 1, pp. 58–59, 1997.
[10]  Y. Chang, E. Cesarman, M. S. Pessin et al., “Identification of herpesvirus-like DNA sequences in AIDS-associated Kaposi's sarcoma,” Science, vol. 266, no. 5192, pp. 1865–1869, 1994.
[11]  S. M. Cohen, Microbes and MAlignancy: Infection as a Cause of Human Cancers, Oxford University Press, Oxford, UK, 1999, J. Parsonnet (Ed.).
[12]  R. Koch, in Vernhandlungen des X Internationalen Medicinischen Congresses, vol. 1, pp. 35–47, Berlin, 1890.
[13]  A. S. Evans and N. E. Mueller, “Viruses and cancer. Causal associations,” Annals of Epidemiology, vol. 1, no. 1, pp. 71–92, 1990.
[14]  A. B. HILL, “The environment and disease: association or causation?” Proceedings of the Royal Society of Medicine, vol. 58, pp. 295–300, 1965.
[15]  A. B. Hill and I. D. Hill, Bradford Hill's Principles of Medical Statistics, Edward Arnold, London, UK, 12th edition, 1991.
[16]  H. Z. Zur Hausen and E.-M. De Villiers, “Human papillomaviruses,” Annual Review of Microbiology, vol. 48, pp. 427–447, 1994.
[17]  C. C. R. Ragin, F. Modugno, and S. M. Gollin, “The epidemiology and risk factors of head and neck cancer: a focus on human papillomavirus,” Journal of Dental Research, vol. 86, no. 2, pp. 104–114, 2007.
[18]  Y. Yabe, H. Sadakane, and H. Isono, “Connection between capsomeres in human papilloma virus,” Virology, vol. 96, no. 2, pp. 547–552, 1979.
[19]  L. Gissmann, H. Pfister, and H. Zur Hausen, “Human papilloma viruses (HPV): characterization of four different isolates,” Virology, vol. 76, no. 2, pp. 569–580, 1977.
[20]  O. Danos, M. Katinka, and M. Yaniv, “Human papillomavirus 1a complete DNA sequence: a novel type of genome organization among papovaviridae,” The EMBO Journal, vol. 1, no. 2, pp. 231–236, 1982.
[21]  E. Schwarz, M. Dürst, C. Demankowski et al., “DNA sequence and genome organization of genital human papillomavirus type 6b,” The EMBO Journal, vol. 2, no. 12, pp. 2341–2348, 1983.
[22]  D. Kremsdorf, M. Favre, and S. Jablonska, “Molecular cloning and characterization of the genomes of nine newly recognized human papillomavirus types associated with epidermodysplasia verruciformis,” Journal of Virology, vol. 52, no. 3, pp. 1013–1018, 1984.
[23]  K. Seedorf, G. Krammer, and M. Durst, “Human papillomavirus type 16 DNA sequence,” Virology, vol. 145, no. 1, pp. 181–185, 1985.
[24]  N. Munoz, F. X. Bosch, and X. Castellsague, “Against which human papillomavirus types shall we vaccinate and screen? The international perspective,” International Journal of Cancer, vol. 111, pp. 278–285, 2004.
[25]  M. Schiffman, P. E. Castle, J. Jeronimo, A. C. Rodriguez, and S. Wacholder, “Human papillomavirus and cervical cancer,” The Lancet, vol. 370, no. 9590, pp. 890–907, 2007.
[26]  H. Zur Hausen, E. M. De Villiers, and L. Gissmann, “Papillomavirus infections and human genital cancer,” Gynecologic Oncology, vol. 12, no. 2, pp. S124–S128, 1981.
[27]  F. X. Bosch, A. Lorincz, N. Mu?oz, C. J. L. M. Meijer, and K. V. Shah, “The causal relation between human papillomavirus and cervical cancer,” Journal of Clinical Pathology, vol. 55, no. 4, pp. 244–265, 2002.
[28]  I. O. C. Thompson, P. van der Bijl, C. W. van Wyk, and A. D. van Eyk, “A comparative light-microscopic, electron-microscopic and chemical study of human vaginal and buccal epithelium,” Archives of Oral Biology, vol. 46, no. 12, pp. 1091–1098, 2001.
[29]  K. J. Syrj?nen, S. Pyrh?nen, S. M. Syrj?nen, and M. A. Lamberg, “Immunohistochemical demonstration of human Papilloma virus (HPV) antigens in oral squamous cell lesions,” British Journal of Oral Surgery, vol. 21, no. 2, pp. 147–153, 1983.
[30]  M. L. Gillison, W. M. Koch, R. B. Capone et al., “Evidence for a causal association between human papilloma virus and a subset of head and neck cancers,” Journal of the National Cancer Institute, vol. 92, no. 9, pp. 709–720, 2000.
[31]  E. M. Smith, H. T. Hoffman, K. S. Summersgill, H. L. Kirchner, L. P. Turek, and T. H. Haugen, “Human papillomavirus and risk of oral cancer,” Laryngoscope, vol. 108, no. 7, pp. 1098–1103, 1998.
[32]  C. S. Miller and B. M. Johnstone, “Human papillomavirus as a risk factor for oral squamous cell carcinoma: a meta-analysis, 1982–1997,” Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics, vol. 91, no. 6, pp. 622–635, 2001.
[33]  S. M. Schwartz, J. R. Daling, D. R. Doody et al., “Oral cancer risk in relation to sexual history and evidence of human papillomavirus infection,” Journal of the National Cancer Institute, vol. 90, no. 21, pp. 1626–1636, 1998.
[34]  T. Bjorge, E. M. Hennig, G. B. Skare, O. Soreide, and S. O. Thoresen, “Second primary cancers in patients with carcinoma in situ of the uterine cervix. The Norwegian experience 1970–1992,” International Journal of Cancer, vol. 62, no. 1, pp. 29–33, 1995.
[35]  C. S. Rabkin, R. J. Biggar, M. Melbye, and R. E. Curtis, “Second primary cancers following anal and cervical carcinoma: evidence of shared etiologic factors,” American Journal of Epidemiology, vol. 136, no. 1, pp. 54–58, 1992.
[36]  M. Frisch and R. J. Biggar, “Aetiological parallel between tonsillar and anogenital squamous-cell carcinomas,” The Lancet, vol. 354, no. 9188, pp. 1442–1443, 1999.
[37]  K. Hemminki, C. Dong, and M. Frisch, “Tonsillar and other upper aerodigestive tract cancers among cervical cancer patients and their husbands,” European Journal of Cancer Prevention, vol. 9, no. 6, pp. 433–437, 2000.
[38]  S. Syrj?nen, “Current concepts on human papillomavirus infections in children,” APMIS, vol. 118, no. 6-7, pp. 494–509, 2010.
[39]  M. Scheffner, J. M. Huibregtse, R. D. Vierstra, and P. M. Howley, “The HPV-16 E6 and E6-AP complex functions as a ubiquitin-protein ligase in the ubiquitination of p53,” Cell, vol. 75, no. 3, pp. 495–505, 1993.
[40]  M. Scheffner and N. J. Whitaker, “Human papillomavirus-induced carcinogenesis and the ubiquitin-proteasome system,” Seminars in Cancer Biology, vol. 13, no. 1, pp. 59–67, 2003.
[41]  M. Scheffner, B. A. Werness, J. M. Huibregtse, A. J. Levine, and P. M. Howley, “The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53,” Cell, vol. 63, no. 6, pp. 1129–1136, 1990.
[42]  R. R. Reddel, “Alternative lengthening of telomeres, telomerase, and cancer,” Cancer Letters, vol. 194, no. 2, pp. 155–162, 2003.
[43]  B. Damania, “DNA tumor viruses and human cancer,” Trends in Microbiology, vol. 15, no. 1, pp. 38–44, 2007.
[44]  R. H. Kim, M. K. Kang, K.-H. Shin et al., “Bmi-1 cooperates with human papillomavirus type 16 E6 to immortalize normal human oral keratinocytes,” Experimental Cell Research, vol. 313, no. 3, pp. 462–472, 2007.
[45]  X. Liu, G. L. Disbrow, H. Yuan, V. Tomai?, and R. Schlegel, “Myc and human papillomavirus type 16 E7 genes cooperate to immortalize human keratinocytes,” Journal of Virology, vol. 81, no. 22, pp. 12689–12695, 2007.
[46]  W.-M. Chien, F. Noya, H. M. Benedict-Hamilton, T. R. Broker, and L. T. Chow, “Alternative fates of keratinocytes transduced by human papillomavirus type 18 E7 during squamous differentiation,” Journal of Virology, vol. 76, no. 6, pp. 2964–2972, 2002.
[47]  S. G. Hwang, D. Lee, J. Kim, T. Seo, and J. Choe, “Human papillomavirus type 16 E7 binds to E2F1 and activates E2F1-driven transcription in a retinoblastoma protein-independent manner,” Journal of Biological Chemistry, vol. 277, no. 4, pp. 2923–2930, 2002.
[48]  T. Loning, H. Ikenberg, and J. Becker, “Analysis of oral papillomas, leukoplakias, and invasive carcinomas for human papillomavirus type related DNA,” Journal of Investigative Dermatology, vol. 84, no. 5, pp. 417–420, 1985.
[49]  N. J. Maitland, M. F. Cox, C. Lynas, S. S. Prime, C. A. Meanwell, and C. Scully, “Detection of human papillomavirus DNA in biopsies of human oral tissue,” British Journal of Cancer, vol. 56, no. 3, pp. 245–250, 1987.
[50]  A. Gassenmaier and O. P. Hornstein, “Presence of human papillomavirus DNA in benign and precancerous oral leukoplakias and squamous cell carcinomas,” Dermatologica, vol. 176, no. 5, pp. 224–233, 1988.
[51]  S. M. Syrj?nen, K. J. Syrj?nen, and R. P. Happonen, “Human papillomavirus (HPV) DNA sequences in oral precancerous lesions and squamous cell carcinoma demonstrated by in situ hybridization,” Journal of Oral Pathology, vol. 17, no. 6, pp. 273–278, 1988.
[52]  F. Chang, S. Syrjanen, J. Nuutinen, J. Karja, and K. Syrjanen, “Detection of human papillomavirus (HPV) DNA in oral squamous cell carcinomas by in sity hybridization and polymerase chain reaction,” Archives of Dermatological Research, vol. 282, no. 8, pp. 493–497, 1990.
[53]  R. O. Greer Jr., L. R. Eversole, and L. K. Crosby, “Detection of human papillomavirus-genomic DNA in oral epithelial dysplasias, oral smokeless tobacco-associated leukoplakias, and epithelial malignancies,” Journal of Oral and Maxillofacial Surgery, vol. 48, no. 11, pp. 1201–1205, 1990.
[54]  H. K. Kashima, L. S. Levin, M. Kutcher, E.-M. De Villiers, T. Kessis, and K. Shah, “Human papillomavirus in squamous cell carcinoma, leukoplakia, lichen planus, and clinically normal epithelium of the oral cavity,” Annals of Otology, Rhinology and Laryngology, vol. 99, no. 1, pp. 55–61, 1990.
[55]  S. K. Young and K. W. Min, “In situ DNA hybridization analysis of oral papillomas, leukoplakias, and carcinomas for human papillomavirus,” Oral Surgery Oral Medicine and Oral Pathology, vol. 71, no. 6, pp. 726–9, 1991.
[56]  M. S. Zeuss, C. S. Miller, and D. K. White, “In situ hybridization analysis of human papillomavirus DNA in oral mucosal lesions,” Oral Surgery Oral Medicine and Oral Pathology, vol. 71, no. 6, pp. 714–720, 1991.
[57]  E. B. Holladay and W. L. Gerald, “Viral gene detection in oral neoplasms using the polymerase chain reaction,” American Journal of Clinical Pathology, vol. 100, no. 1, pp. 36–40, 1993.
[58]  M. Cox, N. Maitland, and C. Scully, “Human herpes simplex-1 and papillomavirus type 16 homologous DNA sequences in normal, potentially malignant and malignant oral mucosa,” European Journal of Cancer B, vol. 29, no. 3, pp. 215–219, 1993.
[59]  M. Brandwein, J. Zeitlin, G. J. Nuovo et al., “HPV detection using “hot start” polymerase chain reaction in patients with oral cancer: a clinicopathological study of 64 patients,” Modern Pathology, vol. 7, no. 7, pp. 720–727, 1994.
[60]  M. A. González-Moles, I. Ruiz-Avila, S. González-Moles, I. Martinez, A. Ceballos, and F. Nogales, “Detection of HPV DNA by in situ hybridization in benign, premalignant and malignant lesions of the oral mucosa,” Bulletin du Groupement International pour la Recherche Scientifique en Stomatologie & Odontologie, vol. 37, no. 3-4, pp. 79–85, 1994.
[61]  C. Ostwald, P. Muller, M. Barten et al., “Human papillomavirus DNA in oral squamous cell carcinomas and normal mucosa,” Journal of Oral Pathology and Medicine, vol. 23, no. 5, pp. 220–225, 1994.
[62]  P. Balaram, K. R. Nalinakumari, E. Abraham et al., “Human papillomaviruses in 91 oral cancers from indican betel quid chewers—High prevalence and multiplicity of infections,” International Journal of Cancer, vol. 61, no. 4, pp. 450–454, 1995.
[63]  M. Shindoh, I. Chiba, M. Yasuda, et al., “Detection of human papillomavirus DNA sequences in oral squamous cell carcinomas and their relation to p53 and proliferating cell nuclear antigen expression,” Cancer, vol. 76, pp. 1513–1521, 1995.
[64]  E. J. van Rensburg, W. F. P. van Heerden, E. H. Venter, and E. J. Raubenheimer, “Detection of human papillomavirus DNA with in situ hybridisation in oval squamous carcinoma in a rural black population,” South African Medical Journal, vol. 85, no. 9, pp. 894–896, 1995.
[65]  I. B. F. Cruz, P. J. F. Snijders, R. D. M. Steenbergen et al., “Age-dependence of human papillomavirus DNA presence in oral squamous cell carcinomas,” European Journal of Cancer B, vol. 32, no. 1, pp. 55–62, 1996.
[66]  E. J. Mao, S. M. Schwartz, J. R. Daling, et al., “Human papilloma viruses and p53 mutations in normal pre-malignant and malignant oral epithelia,” International Journal of Cancer, vol. 69, pp. 152–158, 1996.
[67]  E. J. van Rensburg, S. Engelbrecht, W. F. P. van Heerden, E. J. Raubennheimer, and B. D. Schoub, “Human papillomavirus DNA in oral squamous cell carcinomas from an African population sample,” Anticancer Research, vol. 16, no. 2, pp. 969–973, 1996.
[68]  I. Chiba, M. Shindoh, M. Yasuda et al., “Mutations in the p53 gene and human papillomavirus infection as significant prognostic factors in squamous cell carcinomas of the oral cavity,” Oncogene, vol. 12, no. 8, pp. 1663–1668, 1996.
[69]  S. Wen, T. Tsuji, X. Li, Y. Mizugaki, Y. Hayatsu, and F. Shinozaki, “Detection and analysis of human papillomavirus 16 and 18 homologous DNA sequences in oral lesions,” Anticancer Research, vol. 17, no. 1 A, pp. 307–311, 1997.
[70]  R. Gopalakrishnan, C. M. Weghorst, T. A. Lehman et al., “Mutated and wild-type p53 expression and HPV integration in proliferative verrucous leukoplakia and oral squamous cell carcinoma,” Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics, vol. 83, no. 4, pp. 471–477, 1997.
[71]  S. O. Ibrahim, B. Bertelsen, M. B. Kalvenes et al., “Expression of keratin 13, 14 and 19 in oral squamous cell carcinomas from Sudanese snuff dippers: lack of association with human papillomavirus infection,” APMIS, vol. 106, no. 10, pp. 959–969, 1998.
[72]  J. Y. Koh, N. P. Cho, G. Kong, J. D. Lee, and K. Yoon, “p53 mutations and human papillomavirus DNA in oral squamous cell carcinoma: correlation with apoptosis,” British Journal of Cancer, vol. 78, no. 3, pp. 354–359, 1998.
[73]  G. Premoli-De-Percoco, J. L. Ramírez, and I. Galindo, “Correlation between HPV types associated with oral squamous cell carcinoma and cervicovaginal cytology: an in situ hybridization study,” Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics, vol. 86, no. 1, pp. 77–81, 1998.
[74]  J. D'Costa, D. Saranath, P. Dedhia, V. Sanghvi, and A. R. Mehta, “Detection of HPV-16 genome in human oral cancers and potentially malignant lesions from India,” Oral Oncology, vol. 34, no. 5, pp. 413–420, 1998.
[75]  F. Elamin, H. Steingrimsdottir, S. Wanakulasuriya, N. Johnson, and M. Tavassoli, “Prevalence of human papillomavirus infection in premalignant and malignant lesions of the oral cavity in U.K. subjects: a novel method of detection,” Oral Oncology, vol. 34, no. 3, pp. 191–197, 1998.
[76]  E. P. Aggelopoulou, D. Skarlos, C. Papadimitriou, C. Kittas, and C. Troungos, “Human papilloma virus DNA detection in oral lesions in the Greek population,” Anticancer Research, vol. 19, no. 2B, pp. 1391–1395, 1999.
[77]  M. R. Pillai, A. Phanidhara, A. L. Kesari, et al., “Cellular manifestations of human papillomavirus infection in the oral mucosa,” Journal of Surgical Oncology, vol. 71, pp. 10–15, 1999.
[78]  J. Pintos, E. L. Franco, M. J. Black, J. Bergeron, and M. Arella, “Human papillomavirus and prognoses of patients with cancers of the upper aerodigestive tract,” Cancer, vol. 85, pp. 1903–1909, 1999.
[79]  G. Badaracco, A. Venuti, R. Morello, A. Muller, and M. L. Marcante, “Human papillomavirus in head and neck carcinomas: prevalence, physical status and relationship with clinical/pathological parameters,” Anticancer Research, vol. 20, no. 2 B, pp. 1301–1305, 2000.
[80]  M. Bouda, V. G. Gorgoulis, N. G. Kastrinakis et al., “‘High risk’ HPV types are frequently detected in potentially malignant and malignant oral lesions, but not in normal oral mucosa,” Modern Pathology, vol. 13, no. 6, pp. 644–653, 2000.
[81]  J. Cao, Z. Y. Zhang, P. Patima, Y. X. Zhang, and W. T. Chen, “Human papillomavirus infection and p53 alteration in oral squamous cell carcinoma,” The Chinese Journal of Dental Research, vol. 3, no. 3, pp. 44–49, 2000.
[82]  J. Patima Cao, W. T. Chen, and Z. Y. Zhang, “Detection of high risk human papillomavirus DNA in oral squamous cell carcinoma,” Shanghai Kou Qiang Yi Xue, vol. 9, pp. 212–215, 2000.
[83]  L. Sand, J. Jalouli, P.-A. Larsson, and J.-M. Hirsch, “Human papilloma viruses in oral lesions,” Anticancer Research, vol. 20, no. 2B, pp. 1183–1188, 2000.
[84]  K. Tsuhako, I. Nakazato, J. Miyagi et al., “Comparative study of oral squamous cell carcinoma in Okinawa, Southern Japan and Sapporo in Hokkaido, Northern Japan; with special reference to human papillomavirus and Epstein-Barr virus infection,” Journal of Oral Pathology and Medicine, vol. 29, no. 2, pp. 70–79, 2000.
[85]  G. Premoli-De-Percoco and J. L. Ramirez, “High risk human papillomavirus in oral squamous carcinoma: evidence of risk factors in a Venezuelan rural population. Preliminary report,” Journal of Oral Pathology and Medicine, vol. 30, no. 6, pp. 355–361, 2001.
[86]  S. R. Schwartz, B. Yueh, J. K. McDougall, J. R. Daling, and S. M. Schwartz, “Human papillomavirus infection and survival in oral squamous cell cancer: a population-based study,” Otolaryngology, vol. 125, no. 1, pp. 1–9, 2001.
[87]  P. C.-H. Chen, C. Kuo, C.-C. Pan, and M.-Y. Chou, “Risk of oral cancer associated with human papillomavirus infection, betel quid chewing, and cigarette smoking in Taiwan—an integrated molecular and epidemiological study of 58 cases,” Journal of Oral Pathology and Medicine, vol. 31, no. 6, pp. 317–322, 2002.
[88]  A. Kojima, H. Maeda, Y. Sugita, S. Tanaka, and Y. Kameyama, “Human papillomavirus type 38 infection in oral squamous cell carcinomas,” Oral Oncology, vol. 38, no. 6, pp. 591–596, 2002.
[89]  J. K. Nagpal, S. Patnaik, and B. R. Das, “Prevalence of high-risk human papilloma virus types and its association with p53 codon 72 polymorphism in tobacco addicted oral squamous cell carcimona (OSCC) patients of Eastern India,” International Journal of Cancer, vol. 97, no. 5, pp. 649–653, 2002.
[90]  J. Y.-F. Chang, M.-C. Lin, and C.-P. Chiang, “High-risk human papillomaviruses may have an important role in non-oral habits-associated oral squamous cell Carcinomas in Taiwan,” American Journal of Clinical Pathology, vol. 120, no. 6, pp. 909–916, 2003.
[91]  P. A. G. Fregonesi, D. B. Teresa, R. A. Duarte, C. B. Neto, M. R. B. De Oliveira, and C. P. Soares, “p16INK4A immunohistochemical overexpression in premalignant and malignant oral lesions infected with human papillomavirus,” Journal of Histochemistry and Cytochemistry, vol. 51, no. 10, pp. 1291–1297, 2003.
[92]  A. A. Kansky, M. Poljak, K. Seme et al., “Human papillomavirus DNA in oral squamous cell carcinomas and normal oral mucosa,” Acta Virologica, vol. 47, no. 1, pp. 11–16, 2003.
[93]  J. M. Ritchie, E. M. Smith, K. F. Summersgill et al., “Human papillomavirus infection as a prognostic factor in carcinomas of the oral cavity and oropharynx,” International Journal of Cancer, vol. 104, no. 3, pp. 336–344, 2003.
[94]  M. Sugiyama, U. K. Bhawal, T. Dohmen, S. Ono, M. Miyauchi, and T. Ishikawa, “Detection of human papillomavirus-16 and HPV-18 DNA in normal, dysplastic, and malignant oral epithelium,” Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics, vol. 95, no. 5, pp. 594–600, 2003.
[95]  R. Herrero, X. Castellsagué, M. Pawlita et al., “Human papillomavirus and oral cancer: the international agency for research on cancer multicenter study,” Journal of the National Cancer Institute, vol. 95, no. 23, pp. 1772–1783, 2003.
[96]  C. Ostwald, K. Rutsatz, J. Schweder, W. Schmidt, K. Gundlach, and M. Barten, “Human papillomavirus 6/11, 16 and 18 in oral carcinomas and benign oral lesions,” Medical Microbiology and Immunology, vol. 192, no. 3, pp. 145–148, 2003.
[97]  M. Correnti, H. Rivera, and M. E. Cavazza, “Detection of human papillomaviruses of high oncogenic potential in oral squamous cell carcinoma in a Venezuelan population,” Oral Diseases, vol. 10, no. 3, pp. 163–166, 2004.
[98]  L. Dahlgren, H. Dahlstrand, D. Lindquist et al., “Human papillomavirus is more common in base of tongue than in mobile tongue cancer and is a favorable prognostic factor in base of tongue cancer patients,” International Journal of Cancer, vol. 112, no. 6, pp. 1015–1019, 2004.
[99]  E. M. Smith, J. M. Ritche, K. F. Summersgill et al., “Human papillomavirus in oral exfoliated cells and risk of head and neck cancer,” Journal of the National Cancer Institute, vol. 96, no. 6, pp. 449–455, 2004.
[100]  Z.-Y. Zhang, P. Sdek, J. Cao, and W.-T. Chen, “Human papillomavirus type 16 and 18 DNA in oral squamous cell carcinoma and normal mucosa,” International Journal of Oral and Maxillofacial Surgery, vol. 33, no. 1, pp. 71–74, 2004.
[101]  Y.-Y. Yang, L.-W. Koh, J.-H. Tsai et al., “Involvement of viral and chemical factors with oral cancer in Taiwan,” Japanese Journal of Clinical Oncology, vol. 34, no. 4, pp. 176–183, 2004.
[102]  P. Koppikar, E.-M. De Villiers, and R. Mulherkar, “Identification of human papillomaviruses in tumors of the oral cavity in an Indian community,” International Journal of Cancer, vol. 113, no. 6, pp. 946–950, 2005.
[103]  L. Lo Muzio, M. D'Angelo, M. Procaccini et al., “Expression of cell cycle markers and human papillomavirus infection in oral squamous cell carcinoma: Use of fuzzy neural networks,” International Journal of Cancer, vol. 115, no. 5, pp. 717–723, 2005.
[104]  S. Boy, E. J. V. Rensburg, S. Engelbrecht, L. Dreyer, M. van Heerden, and W. van Heerden, “HPV detection in primary intra-oral squamous cell carcinomas—commensal, aetiological agent or contamination?” Journal of Oral Pathology and Medicine, vol. 35, no. 2, pp. 86–90, 2006.
[105]  S. K. El-Mofty and S. Patil, “Human papillomavirus (HPV)-related oropharyngeal nonkeratinizing squamous cell carcinoma: characterization of a distinct phenotype,” Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology, vol. 101, no. 3, pp. 339–345, 2006.
[106]  J. A. Nemes, L. Deli, Z. Nemes, and I. J. Márton, “Expression of p16INK4A, p53, and Rb proteins are independent from the presence of human papillomavirus genes in oral squamous cell carcinoma,” Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology, vol. 102, no. 3, pp. 344–352, 2006.
[107]  E. R. C. Rivero and F. D. Nunes, “HPV in oral squamous cell carcinomas of a Brazilian population: amplification by PCR,” Brazilian Oral Research, vol. 20, no. 1, pp. 21–24, 2006.
[108]  G. Campisi, L. Giovannelli, F. Calvino et al., “HPV infection in relation to OSCC histological grading and TNM stage. Evaluation by traditional statistics and fuzzy logic model,” Oral Oncology, vol. 42, no. 6, pp. 638–645, 2006.
[109]  V. E. Furrer, M. B. Benitez, M. Furnes, H. E. Lanfranchi, and N. M. Modesti, “Biopsy versus superficial scraping: detection of human papillomavirus 6, 11, 16, and 18 in potentially malignant and malignant oral lesions,” Journal of Oral Pathology and Medicine, vol. 35, no. 6, pp. 338–344, 2006.
[110]  K. Koyama, K. Uobe, and A. Tanaka, “Highly sensitive detection of HPV-DNA in paraffin sections of human oral carcinomas,” Journal of Oral Pathology and Medicine, vol. 36, no. 1, pp. 18–24, 2007.
[111]  M. Sugiyama, U. K. Bhawal, M. Kawamura et al., “Human papillomavirus-16 in oral squamous cell carcinoma: clinical correlates and 5-year survival,” British Journal of Oral and Maxillofacial Surgery, vol. 45, no. 2, pp. 116–122, 2007.
[112]  C.-W. Luo, C.-H. Roan, and C.-J. Liu, “Human papillomaviruses in oral squamous cell carcinoma and pre-cancerous lesions detected by PCR-based gene-chip array,” International Journal of Oral and Maxillofacial Surgery, vol. 36, no. 2, pp. 153–158, 2007.
[113]  S.-O. P. Khovidhunkit, W. Buajeeb, S. Sanguansin, S. Poomsawat, and W. Weerapradist, “Detection of human papillomavirus in oral squamous cell carcinoma, leukoplakia and lichen planus in Thai patients,” Asian Pacific Journal of Cancer Prevention, vol. 9, no. 4, pp. 771–775, 2008.
[114]  K. Szarka, I. Tar, E. Feher et al., “Progressive increase of human papillomavirus carriage rates in potentially malignant and malignant oral disorders with increasing malignant potential,” Oral Microbiology and Immunology, vol. 24, no. 4, pp. 314–318, 2009.
[115]  D. Zhao, Q.-G. Xu, X.-M. Chen, and M.-W. Fan, “Human papillomavirus as an independent predictor in oral squamous cell cancer,” International journal of oral science, vol. 1, no. 3, pp. 119–125, 2009.
[116]  P. Attner, J. Du, A. N?sman et al., “The role of human papillomavirus in the increased incidence of base of tongue cancer,” International Journal of Cancer, vol. 126, no. 12, pp. 2879–2884, 2010.
[117]  K. J. Elango, A. Suresh, E. M. Erode et al., “Role of human papilloma virus in oral tongue squamous cell carcinoma,” Asian Pacific Journal of Cancer Prevention, vol. 12, no. 4, pp. 889–896, 2011.
[118]  A. K. Kristoffersen, M. Enersen, E. Kverndokk et al., “Human papillomavirus subtypes in oral lesions compared to healthy oral mucosa,” Journal of Clinical Virology, vol. 53, no. 4, pp. 364–366, 2012.
[119]  S.-F. Chen, F.-S. Yu, Y.-C. Chang, E. Fu, S. Nieh, and Y.-S. Lin, “Role of human papillomavirus infection in carcinogenesis of oral squamous cell carcinoma with evidences of prognostic association,” Journal of Oral Pathology and Medicine, vol. 41, no. 1, pp. 9–15, 2012.
[120]  L.-A. Lee, C.-G. Huang, C.-T. Liao, et al., “Human papillomavirus-16 infection in advanced oral cavity cancer patients is related to an increased risk of distant metastases and poor survival,” PLoS ONE, vol. 7, no. 7, Article ID e40767, 2012.
[121]  K. J. Syrj?nen, S. Pyrh?nen, S. M. Syrj?nen, and M. A. Lamberg, “Immunohistochemical demonstration of Human papilloma virus (HPV) antigens in oral squamous cell lesions,” British Journal of Oral Surgery, vol. 21, no. 2, pp. 147–153, 1983.
[122]  K. Syrj?nen, S. Syrj?nen, and M. Lamberg, “Morphological and immunohistochemical evidence suggesting human papillomavirus (HPV) involvement in oral squamous cell carcinogenesis,” International Journal of Oral Surgery, vol. 12, no. 6, pp. 418–424, 1983.
[123]  C. S. Miller and D. K. White, “Human papillomavirus expression in oral mucosa, premalignant conditions, and squamous cell carcinoma a retrospective review of the literature,” Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics, vol. 82, no. 1, pp. 57–68, 1996.
[124]  S. M. Syrj?nen and K. J. Syrj?nen, “HPV infections of the oral mucosa,” in Papillomavirus Infections in Human Pathology, K. J. Syrj?nen and S. M. Syrj?nen, Eds., pp. 379–412, John Wiley & Sons, New York, NY, USA, 2000.
[125]  H. Mellin, S. Friesland, R. Lewensohn, T. Dalianis, and E. MunckWikland, “Human papillomavirus (HPV) DNA in tonsillar cancer: clinical correlates, risk of relapse, and survival,” International Journal of Cancer, vol. 89, pp. 300–304, 2000.
[126]  G. D'Souza, A. R. Kreimer, R. Viscidi et al., “Case-control study of human papillomavirus and oropharyngeal cancer,” The New England Journal of Medicine, vol. 356, no. 19, pp. 1944–1956, 2007.
[127]  K. K. Ang, J. Harris, R. Wheeler et al., “Human papillomavirus and survival of patients with oropharyngeal cancer,” The New England Journal of Medicine, vol. 363, no. 1, pp. 24–35, 2010.
[128]  S. Syrj?nen, G. Lodi, I. von Bültzingsl?wen et al., “Human papillomaviruses in oral carcinoma and oral potentially malignant disorders: a systematic review,” Oral Diseases, vol. 17, no. 1, pp. 58–72, 2011.
[129]  J. L. St Guily, A.-C. Jacquard, J.-L. Prétet et al., “Human papillomavirus genotype distribution in oropharynx and oral cavity cancer in France–the EDiTH VI study,” Journal of Clinical Virology, vol. 51, no. 2, pp. 100–104, 2011.
[130]  C. Ziegert, N. Wentzensen, S. Vinokurova et al., “A comprehensive analysis of HPV integration loci in anogenital lesions combining transcript and genome-based amplification techniques,” Oncogene, vol. 22, no. 25, pp. 3977–3984, 2003.
[131]  H. W. Haverkos, “Viruses, chemicals and co-carcinogenesis,” Oncogene, vol. 23, no. 38, pp. 6492–6499, 2004.
[132]  M. Migaldi, M. Pecorari, G. Forbicini et al., “Low prevalence of human papillomavirus infection in the healthy oral mucosa of a Northern Italian population,” Journal of Oral Pathology and Medicine, vol. 41, no. 1, pp. 16–20, 2012.
[133]  G. Pannone, A. Santoro, S. Papagerakis, L. Lo Muzio, G. De Rosa, and P. Bufo, “The role of human papillomavirus in the pathogenesis of head & neck squamous cell carcinoma: an overview,” Infectious Agents and Cancer, vol. 6, no. 1, article 4, 2011.
[134]  J. E. Burns, M. C. Baird, L. J. Clark et al., “Gene mutations and increased levels of p53 protein in human squamous cell carcinomas and their cell lines,” British Journal of Cancer, vol. 67, no. 6, pp. 1274–1284, 1993.
[135]  M. B. Gillespie, S. Rubinchik, B. Hoel, and N. Sutkowski, “Human papillomavirus and oropharyngeal cancer: what you need to know in 2009,” Current Treatment Options in Oncology, vol. 10, no. 5-6, pp. 296–307, 2009.
[136]  P. K. C. Goon, M. A. Stanley, J. Ebmeyer et al., “HPV & head and neck cancer: a descriptive update,” Head & Neck Oncology, vol. 1, article 36, 2009.
[137]  R. Kirnbauer, N. L. Hubbert, C. M. Wheeler, T. M. Becker, D. R. Lowy, and J. T. Schiller, “A virus-like particle enzyme-linked immunosorbent assay detects serum antibodies in a majority of women infected with human papillomavirus type 16,” Journal of the National Cancer Institute, vol. 86, no. 7, pp. 494–499, 1994.
[138]  J. J. Carter, L. A. Koutsky, G. C. Wipf et al., “The natural history of human papillomavirus type 16 capsid antibodies among a cohort of university women,” Journal of Infectious Diseases, vol. 174, no. 5, pp. 927–936, 1996.
[139]  W. Meschede, K. Zumbach, J. Braspenning et al., “Antibodies against early proteins of human papillomaviruses as diagnostic markers for invasive cervical cancer,” Journal of Clinical Microbiology, vol. 36, no. 2, pp. 475–480, 1998.
[140]  M. Stanley, “Antibody reactivity to HPV E6 and E7 oncoproteins and early diagnosis of invasive cervical cancer,” American Journal of Obstetrics and Gynecology, vol. 188, no. 1, pp. 3–4, 2003.
[141]  A. K. Markopoulos, “Role of human papillomavirus in the pathogenesis of oral squamous cell carcinoma,” The World Journal of Experimental Medicine, vol. 2, no. 4, pp. 65–69, 2012.
[142]  M. Filion, D. Skup, and M. Suh, “Specific induction of cellular gene transcription in herpes simplex virus type -2-transformed cells,” Journal of General Virology, vol. 69, no. 8, pp. 2011–2019, 1988.
[143]  N. B. La Thangue and D. S. Latchman, “A cellular protein related to heat-shock protein 90 accumulates during herpes simplex virus infection and is overexpressed in transformed cells,” Experimental Cell Research, vol. 178, no. 1, pp. 169–179, 1988.
[144]  E. L. Notarianni and C. M. Preston, “Activation of cellular stress protein genes by herpes simplex virus temperature-sensitive mutants which overproduce immediate early polypeptides,” Virology, vol. 123, no. 1, pp. 113–122, 1982.
[145]  A. D. Kwong, J. A. Kruper, and N. Frenkel, “Herpes simplex virus virion host shutoff function,” Journal of Virology, vol. 62, no. 3, pp. 912–921, 1988.
[146]  M. Fenwick, “The effects of herpes viruses on cellular macromolecular synthesis,” in Comprehensive Virology, H. Fraenkel-Conrat and R. R. Wagner, Eds., vol. 19, pp. 359–390, Plenum, New York, NY, USA, 1984.
[147]  A. D. Kwong and N. Frenkel, “Herpes simplex virus-infected cells contain a function(s) that destabilizes both host and viral mRNAs,” Proceedings of the National Academy of Sciences of the United States of America, vol. 84, no. 7, pp. 1926–1930, 1987.
[148]  G. S. Read and N. Frenkel, “Herpes simplex virus mutants defective in the virion-associated shutoff of host polypeptide synthesis and exhibiting abnormal synthesis of α (immediate early) viral polypeptides,” Journal of Virology, vol. 46, no. 2, pp. 498–512, 1983.
[149]  C. Steele and E. J. Shillitoe, “Viruses and oral cancer,” Critical Reviews in Oral Biology and Medicine, vol. 2, no. 2, pp. 153–175, 1991.
[150]  A. L. Boyd, L. Enquist, G. F. Vande Woude, and B. Hampar, “Activation of mouse retrovirus by herpes simplex virus type 1 cloned DNA fragments,” Virology, vol. 103, no. 1, pp. 228–231, 1980.
[151]  H. F. Stich, T. C. Hsu, and F. Rapp, “Viruses and mammalian chromosomes. I. Localization of chromosome aberrations after infection with herpes simplex virus,” Virology, vol. 22, no. 4, pp. 439–445, 1964.
[152]  A. Mincheva, S. Dundarov, and I. Bradvarova, “Effects of herpes simplex virus strains on human fibroblast and lymphocyte chromosomes and the localization of chromosomal aberrations,” Acta Virologica, vol. 28, no. 2, pp. 97–106, 1984.
[153]  D. S. Peat and M. A. Stanley, “Chromosome damage induced by herpes simplex virus type 1 in early infection,” Journal of General Virology, vol. 67, no. 10, pp. 2273–2277, 1986.
[154]  A. A. I. El Sissy, “Herpes simplex virus type 2 (HSV-2) proteins in oral squamous cell carcinoma—in situ detection,” Cairo Dental Journal, vol. 13, no. 2, pp. 265–270, 1997.
[155]  J. Jalouli, S. O. Ibrahim, D. Sapkota et al., “Presence of human papilloma virus, herpes simplex virus and Epstein-Barr virus DNA in oral biopsies from Sudanese patients with regard to toombak use,” Journal of Oral Pathology and Medicine, vol. 39, no. 8, pp. 599–604, 2010.
[156]  Z. Delavarian, A. Pakfetrat, F. Falaki, and M. Pazouki, “The role of viruses in oral squamous cell carcinoma in young patients in Khorasan (Northeast of Iran),” Journal of Applied Sciences, vol. 10, no. 11, pp. 981–985, 2010.
[157]  E. J. Shillitoe, D. Greenspan, J. S. Greenspan, and S. Silverman Jr., “Immunogloblin class of antibody to herpes simplex virus in patients with oral cancer,” Cancer, vol. 51, no. 1, pp. 65–71, 1983.
[158]  S. P. Schantz, E. J. Shillitoe, B. Brown, and B. Campbell, “Natural killer cell activity and head and neck cancer: a clinical assessment,” Journal of the National Cancer Institute, vol. 77, no. 4, pp. 869–875, 1986.
[159]  J. R. Starr, J. R. Daling, E. D. Fitzgibbons et al., “Serologic evidence of herpes simplex virus 1 infection and oropharyngeal cancer risk,” Cancer Research, vol. 61, no. 23, pp. 8459–8464, 2001.
[160]  R. P. Eglin, C. Scully, and T. Lehner, “Detection of RNA complementary to herpes simplex virus in human oral squamous cell carcinoma,” The Lancet, vol. 2, no. 8353, pp. 766–767, 1983.
[161]  F. Rapp and R. Duff, “Transformation of hamster embryo fibroblasts by herpes simplex viruses type I and type II,” Cancer Research, vol. 33, no. 6, pp. 1527–1534, 1973.
[162]  J. M. Hirsch, S. L. Johansson, and A. Vahlne, “Effect of snuff and herpes simplex virus-1 on rat oral mucosa: possible associations with the development of squamous cell carcinoma,” Journal of oral pathology, vol. 13, no. 1, pp. 52–62, 1984.
[163]  D. A. Galloway and J. K. McDougall, “The oncogenic potential of herpes simplex viruses: evidence for a 'hit-and-run' mechanism,” Nature, vol. 302, no. 5903, pp. 21–24, 1983.
[164]  E. J. Shillitoe, S. Zhang, G. Wang, and C. B. C. Hwang, “Functions and proteins of herpes simplex virus type-1 that are involved in raising the mutation frequency of infected cells,” Virus Research, vol. 27, no. 3, pp. 239–251, 1993.
[165]  H. Mikola, M. Waris, and J. Tenovuo, “Inhibition of herpes simplex virus type 1, respiratory syncytial virus and echovirus type 11 by peroxidase-generated hypothiocyanite,” Antiviral Research, vol. 26, no. 2, pp. 161–171, 1995.
[166]  C. B. C. Hwang and E. J. Shillitoe, “DNA sequence of mutations induced in cells by herpes simplex virus type-1,” Virology, vol. 178, no. 1, pp. 180–188, 1990.
[167]  R. Baer, A. T. Bankier, and M. D. Biggin, “DNA sequence and expression of the B95-8 Epstein-Barr virus genome,” Nature, vol. 310, no. 5974, pp. 207–211, 1984.
[168]  D. M. Parkin, “The global health burden of infection-associated cancers in the year 2002,” International Journal of Cancer, vol. 118, no. 12, pp. 3030–3044, 2006.
[169]  D. Wang, D. Liebowitz, and E. Kieff, “An EBV membrane protein expressed in immortalized lymphocytes transforms established rodent cells,” Cell, vol. 43, no. 3, pp. 831–840, 1985.
[170]  A. Rickinson and E. Kieff, in Fields Virology, D. M. Knipe and P. M. Howley, Eds., pp. 2575–2627, Lippincott Williams and Wilkins, Philadelphia, Pa, USA, 2001.
[171]  G. Mosialos, M. Birkenbach, R. Yalamanchili, T. VanArsdale, C. Ware, and E. Kieff, “The Epstein-Barr virus transforming protein LMP1 engages signaling proteins for the tumor necrosis factor receptor family,” Cell, vol. 80, no. 3, pp. 389–399, 1995.
[172]  E. Kieff and A. Rickinson, in Fields Virology, D. M. Knipe and P. M. Howley, Eds., pp. 2511–2573, Lippincott Williams and Wilkins, Philadelphia, Pa, USA, 2001.
[173]  W. E. Miller, J. L. Cheshire, A. S. Baldwin Jr., and N. Raab-Traub, “The NPC derived C15 LMP1 protein confers enhanced activation of NF-κB and induction of the EGFR in epithelial cells,” Oncogene, vol. 16, no. 14, pp. 1869–1877, 1998.
[174]  A. G. Eliopoulos and L. S. Young, “Activation of the cJun N-terminal kinase (JNK) pathway by the Epstein-Barr virus-encoded latent membrane protein 1 (LMP1),” Oncogene, vol. 16, no. 13, pp. 1731–1742, 1998.
[175]  A. G. Eliopoulos, N. J. Gallagher, S. M. S. Blake, C. W. Dawson, and L. S. Young, “Activation of the p38 mitogen-activated protein kinase pathway by Epstein-Barr virus-encoded latent membrane protein 1 coregulates interleukin- 6 and interleukin-8 production,” Journal of Biological Chemistry, vol. 274, no. 23, pp. 16085–16096, 1999.
[176]  L. Zhang and J. S. Pagano, “Interferon regulatory factor 7 is induced by Epstein-Barr virus latent membrane protein 1,” Journal of Virology, vol. 74, no. 3, pp. 1061–1068, 2000.
[177]  N. Wakisaka, S. Murono, T. Yoshizaki, M. Furukawa, and J. S. Pagano, “Epstein-Barr virus latent membrane protein 1 induces and causes release of fibroblast growth factor-2,” Cancer Research, vol. 62, no. 21, pp. 6337–6344, 2002.
[178]  R. G. Caldwell, J. B. Wilson, S. J. Anderson, and R. Longnecker, “Epstein-Barr virus LMP2A drives B cell development and survival in the absence of normal B cell receptor signals,” Immunity, vol. 9, no. 3, pp. 405–411, 1998.
[179]  K. Horiuchi, K. Mishima, K. Ichijima, M. Sugimura, T. Ishida, and T. Kirita, “Epstein-Barr virus in the proliferative diseases of squamous epithelium in the oral cavity,” Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and, vol. 79, no. 1, pp. 57–63, 1995.
[180]  M. González-Moles, J. Gutiérrez, I. Ruiz, J. A. Fernández, M. Rodriguez, and J. Aneiros, “Epstein-Barr virus and oral squamous cell carcinoma in patients without HIV infection: viral detection by polymerase chain reaction,” Microbios, vol. 96, no. 383, pp. 23–31, 1998.
[181]  M. Higa, T. Kinio, K. Kamiyama, T. Iwamasa, T. Hamada, and K. Iyama, “Epstein-Barr virus (EBV) subtype in EBV related oral squamous cell carcinoma in Okinawa, a subtropical island in southern Japan, compared with Kitakyushu and Kumamoto in mainland Japan,” Journal of Clinical Pathology, vol. 55, no. 6, pp. 414–423, 2002.
[182]  C. Li, C.-Y. Yen, M.-C. Lu et al., “Detection of EBV infection and gene expression in oral cancer from patients in taiwan by microarray analysis,” Journal of Biomedicine and Biotechnology, vol. 2009, Article ID 904589, 15 pages, 2009.
[183]  L. P. Sand, J. Jalouli, P.-A. Larsson, and J.-M. Hirsch, “Prevalence of Epstein-Barr virus in oral squamous cell carcinoma, oral lichen planus, and normal oral mucosa,” Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics, vol. 93, no. 5, pp. 586–592, 2002.
[184]  R. Jiang, X. Gu, T. N. Moore-Medlin, C.-A. Nathan, and L. M. Hutt-Fletcher, “Oral dysplasia and squamous cell carcinoma: correlation between increased expression of CD21, Epstein-Barr virus and CK19,” Oral Oncology, vol. 48, no. 9, pp. 836–841, 2012.
[185]  R. J. Johnson, D. R. Gretch, H. Yamabe et al., “Membranoproliferative glomerulonephritis associated with hepatitis C virus infection,” The New England Journal of Medicine, vol. 328, no. 7, pp. 465–470, 1993.
[186]  Q.-L. Choo, G. Kuo, A. J. Weiner, L. R. Overby, D. W. Bradley, and M. Houghton, “Isolation of a cDNA clone derived from a blood-borne non-A, non-B viral hepatitis genome,” Science, vol. 244, no. 4902, pp. 359–362, 1989.
[187]  M. Carrozzo, R. Quadri, P. Latorre et al., “Molecular evidence that the hepatitis C virus replicates in the oral mucosa,” Journal of Hepatology, vol. 37, no. 3, pp. 364–369, 2002.
[188]  F. Negro, K. Krawczynski, R. Quadri et al., “Detection of genomic- and minus-strand of hepatitis C virus RNA in the liver of chronic hepatitis C patients by strand-specific semiquantitative reverse-transcriptase polymerase chain reaction,” Hepatology, vol. 29, no. 2, pp. 536–542, 1999.
[189]  H. Toyoda, Y. Fukuda, I. Nakano, et al., “Quasispecies nature of hepatitis C virus (HCV) in patients with chronic hepatitis C with mixed HCV subtypes,” in Journal of Medical Virology, vol. 54, pp. 80–85, 1998.
[190]  Y. Nagao, M. Sata, K. Itoh, K. Tanikawa, and T. Kameyama, “Quantitative analysis of HCV RNA and genotype in patients with chronic hepatitis C accompanied by oral lichen planus,” European Journal of Clinical Investigation, vol. 26, no. 6, pp. 495–498, 1996.
[191]  S. Gandolfo, M. Carbone, M. Carrozzo, and V. Gallo, “Oral lichen planus and hepatitis C virus (HCV) infection: is there a relationship? A report of 10 cases,” Journal of Oral Pathology & Medicine, vol. 23, no. 3, pp. 119–122, 1994.

Full-Text

comments powered by Disqus

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133