[p53 alterations and HPV status in oral squamous cell carcinomas] M Barten, C Ostwald, P Muller, T Loning, K Milde-Langosch, Y Wukasch. Verh Dtsch Ges Pathol 1994;78:255-259. 28/40 (70%) oral carcinomas contained HPV-16 or 18.
Barten / Verh Dtsch Ges Pathol 1994 abstract
Detection of HPV DNA in oral carcinoma using polymerase chain reaction together with in situ hybridization. CS Miller, MS Zeuss, DK White. Oral Surg Oral Med Oral Pathol 1994 May;77(5):480-486. HPV was detected in 20/30 specimens (66.7%).
Miller / Oral Surg Oral Med Oral Pathol 1994 abstract
Human papillomavirus DNA in oral squamous cell carcinomas and normal mucosa. C Ostwald, P Muller, M Barten, K Rutsatz, M Sonnenberg, K Milde-Langosch, T Loning. J Oral Pathol Med 1994 May;23(5):220-225. 16/26 (61.5%) OSCCs were positive, and “The frequency of HPV detection in non-neoplastic mucosa of tumor patients decreased claerly with increasing distance from the tumor… In contrast, normal buccal mucosa of a group of healthy volunteers contained HPV DNA only in 1% (1/97).”
Ostwald / J Oral Pathol Med 1994 abstract
H-ras oncogene mutation and human papillomavirus infection in oral carcinomas. JA Anderson, JC Irish, CM McLachlin, BY Ngan. Arch Otolaryngol Head Neck Surg 1994 Jul;120(7):755-760. 6/27 OSCCs (22%) were positive for HPV DNA.
Anderson / Arch Otolaryngol Head Neck Surg 1994 abstract
Detection of HPV DNA by in situ hybridization in benign, premalignant and malignant lesions of the oral mucosa. MA Gonzalez-Moles, I Ruiz-Avila, S Gonzalez-Moles, I Martinez, A Ceballos, F Nogales. Bull Group Int Rech Sci Stomatol Odontol 1994 Sep-Dec;37(3-4):79-85. HPV was found in 37% of 27 oral squamous cell carcinomas.
Gonzalez-Moles / Bull Group Int Rech Sci Stomatol Odontol 1994 abstract
Presence of human papillomavirus sequences in tumour-derived human oral keratinocytes expressing mutant p53. WA Yeudall, IC Paterson, V Patel, SS Prime. Oral Oncol, Eur J Cancer 1995 Mar;31B(2):136-143. 2/8 OSCC early passaged cell lines were positive for HPV-16. “HPV sequences were undetectable in cells at later passage (12-15), suggesting that viral sequences had been lost during growth in vitro, or that negative selection of HPV-containing cells had occurred.”
Yeudall / Oral Oncol Eur J Cancer 1995 abstract
Human papillomavirus in 91 oral cancers from Indian betel quid chewers — high prevalence and multiplicity of infections. P Balaram, KR Nalinnakumari, E Abraham, A Balan, NK Hareendran, HU Bernard, SY Chan. Int J Cancer 1995 May 16;61(4):450-454. “HPV DNA was detected in 74% of these lesions, of which 41% had multiple HPV infections,” and 9/11 (99%) of tongue lesions were HPV positive.
Balaram / Int J Cancer 1995 abstract
Detection of human papillomavirus DNA sequences in oral squamous cell carcinomas and their relation to p53 and proliferating cell nuclear antigen expression. M Shindoh, I Chiba, M Yasuda, T Saito, K Funaoka, T Kohgo, A Amemiya, Y Sawada, K Fujinaga. Cancer 1995 Nov 1;76(9):1513-1521. 23/77 (30%) OSCCs were positive for HPV.
Shindoh / Cancer 1995 abstract
Age-dependence of human papillomavirus DNA presence in oral squamous cell carcinomas. IB Cruz, PJ Snijders, RD Steenbergen, CJ Meijer, GB Snow, JM Walboomers, I van der Waal. Eur J Cancer B Oral Oncol 1996 Jan;32B(1):55-62. 54.3% of 35 OSCCs were positive for HPV, and the prevalence of the virus was higher in patients less than 60 years old.
Cruz / Eur J Cancer B Oral Oncol 1996 abstract
Mutations in the p53 gene and human papillomavirus infection as significant prognostic factors in squamous cell carcinomas of the oral cavity. I Chiba, M Shindoh, M Yasuda, Y Yamazaki, A Amemiya, Y Sato, K Fujinaga, K Notani, H Fukuda. Oncogene 1996 Apr 18;12(8):1663-1668. 8/38 cases (21%) were positive for HPV-16.
Chiba / Oncogene 1996 abstract
Human papillomavirus and cancers of the upper aerodigestive tract: a review of epidemiological and experimental evidence. S Franceschi, N Munoz, XF Bosch, PJ Snijders, JM Walboomers. Cancer Epidemiol Biomarkers Prev 1996 Jul;5(7):567-575. “Largest and most accurate case series )i.e., >15 UADT cancer cases, based on best HPV detection techniques) showed HPV in 46% of cancers of the oral cavity and pharynx, 15% of cancers of the esophagus, and 24% of cancers of the larynx, with, however, great discrepancies from one study to another. An additional 14 case series with a comparison group of noncancer patients revealed approximately a 4-fold higher HPV prevalence in UADT cancer tissues than in normal ones.”
Franceschi / Cancer Epidemiol Biomarkers Prev 1996 abstract (review)
Loss of the adenomatous polyposis coli gene and human papillomavirus infection in oral carcinogenesis. EJ Mao, D Oda, WG Haigh, AM Beckmann. Eur J Cancer B Oral Oncol 1996 Jul;32B(4):260-263. “More than half of the carcinoma cases were found to contain both LOH of APC and HPV infection.”
Mao / Eur J Cancer B Oral Oncol 1996 abstract
Increase of proliferating cell nuclear antigen (PCNA) expression in HPV-18 positive oral squamous cell carcinomas. MA Gonzalez-Moles, A Rodriguez-Archilla, I Ruiz-Avila, S Gonzalez-Moles, R Marfil-Alvarez. Acta Stomatol Belg 1996 Sep;93(3):113-118. 7/37 OSCCs (19.1%) were positive for HPV-18, and PCNA expression (a marker of cell proliferation) was greater in these tumors.
Gonzalez-Moles / Acta Stomatol Belg 1996 abstract
[Study of HPV in oral squamous cell carcinoma.] L Lei, H Li, Y Sun. Zhonghua Kou Qiang Yi Xue Za Zhi 1996 Nov;31(6):375-377. 11/23 OSCCs (47.8%) were positive for HPV, versus 20% of normal tissue (source not specified).
Lei / Zhonghua Kou Qiang Yi Xue Za Zhi 1996 abstract
Detection and analysis of human papillomavirus 16 and 18 homologous DNA sequences in oral lesions. S Wen, T Tsuji, X Li, Y Mizugaki, Y Hayatsu, F Shinozaki. Anticancer Res 1997 Jan-Feb;17(1A):307-311. 14/45 OSCCs (31.1%) were positive for HPV-16 and/or -18..
Wen / Anticancer Res 1997 abstract
Mutated and wild-type p53 expression and HPV integration in proliferative verrucous leukoplakia and oral squamous cell carcinoma. R Gopalakrishnan, CM Weghorst, TA Lehman, RJ Calvert, G Bijur, CL Sabourin, SR Mallory, DE Schuller, GD Stoner. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997 Apr;83(4):471-477. 2/7 OSCCs (29%) were positive for HPV.
Gopalakrishnan / Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997 abstract
[The presence of Human Papillomavirus (HPV) in microinvasive in situ spinocellular carcinoma of the oral cavity. Preliminary report.] MD Mignogna, R Duraccio, R Carbone, RE Mignogna, L Lo Muzio. Minerva Stomatol 1997 Jun;46(6):287-291. A variety of HPV types were found in 9 of 15 cases (60%).
Mignogna / Minerva Stomatol 1997 abstract
Human papillomavirus expression and p53 gene mutations in squamous cell carcinoma. LG Portugal, JD Goldenberg, BL Wenig, KT Ferrer, E Nodzenski, JB Sabnani, C Javier, RR Weichselbaum, EE Vokes. Arch Otolaryngol Head Neck Surg 1997 Nov;123(11):1230-1234. 11/100 patients with oral (58) and tonsillar (42) squamous cell carcinoma were positive for HPV.
Portugal / Arch Otolaryngol Head Neck Surg 1997 abstract
Low detection rate of HPV in oral and laryngeal carcinomas. T Matzow, M Boysen, M Kalantari, B Johansson, B Hagmar. Acta Oncol 1998;37(1):73-76. HPV was found in only 1/38 (2.6%) oral carcinomas.
Matzow / Acta Oncol 1998 abstract
Prevalence of human papillomavirus infection in premalignant and malignant lesions of the oral cavity in U.K. subjects: a novel method of detection. F Elamin, H Steingrimsdottir, S Wanakulasuriya, N Johnson, M Tavassoli. Oral Oncol 1998 May;34(3):191-197. HPV was detected in 14/28 oral carcinomas (50%); “HPV 6 and HPV 16 were the only HPV types detected and seven tumours harboured both types.”
Elamin / Oral Oncol 1998 abstract
p53 mutations and human papillomavirus DNA in oral squamous cell carcinoma: correlation with apoptosis. JY Koh, NP Cho, G Kong, JD Lee, K Yoon. Br J Cancer 1998 Aug;78(3):354-359. “HPV DNAs were detected from 22 out of 42 SCCs (52%) with predominance of HPV-16 (68%).”
Koh / Br J Cancer 1998 abstract
Human papilloma virus (HPV) type 16 and 18 detected in head and neck squamous cell carcinoma. H Mineta, T Ogino, HM Amano, Y Ohkawa, K Araki, S Takebayashi, K Miura. Anticancer Res 1998 Nov-Dec;18(6B):4765-4768. HPV was present in 3/14 (21%) oral cavity carcinomas.
Mineta / Anticancer Res 1998 abstract
Detection of the E7 transform gene of human papilloma virus type 16 in human oral squamous cell carcinoma. J Wang, J Li, H Huang, Y Fu. Chin J Dent Res 1998 Dec;1(3):35-37. “HPV 16 was detected in 36.7% (11/30) of oral squamous cell carcinoma patients and 11.1% (4/30) controls.”
Wang / Chin J Dent Res 1998 abstract
Human papilloma virus DNA detection in oral lesions in the Greek population. EP Aggelopoulou, D Skarlos, C Papadimitriou, C Kittas, C Troungos. Anticancer Res 1999 Mar-Apr;19(2B):1391-1395. 49% (50/102) samples including both carcinomas and papillomatous hyperplasias were HPV positive; “HPV-18 was detected only in carcinomas, while HPV-16 was more abundant in papillomatous hyperplasias and in a small percentage of carcinomas.”
Aggelopoulou / Anticancer Res 1999 abstract
Human papillomavirus in head and neck carcinomas: prevalence, physical status and relationship with clinical/pathological parameters. G Badaracco, A Venuti, R Morello, A Muller, ML Marcante. Anticancer Res 2000 Mar-Apr;20(2B):1301-1305. Of 66 tumors from various sites including 38 squamous cell carcinomas of the oral cavity, 24 were HPV-positive. “HPV 16 was integrated in 7/12 positive tumours without site-specificity. HPV infection was not related to age, gender, tumour stage, differentiation grade, and use of alcohol and/or tobacco.”
Badaracco / Anticancer Res 2000 abstract
“High risk” HPV types are frequently detected in potentially malignant and malignant oral lesions, but not in normal oral mucosa. M Bouda, VG Gorgoulis, NG Kastrinakis, A Giannoudis, E Tsoli, D Danassi-Afentaki, P Foukas, A Kyroudi, G Laskaris, CS Herrington, C Kittas. Mod Pathol 2000 Jun;13(6):644-653. “Nested PCR revealed the presence of HPV DNA in 48 of the 53 (91%) pathologic samples analyzed, whereas none (0%) of the normal specimens [derived from healthy individuals] was found to be infected. Positivity for HPV was independent of histology and the smoking habits of the analyzed group of patients.” The series included 19 oral squamous cell carcinomas.
Bouda / Mod Pathol 2000 abstract
Incidence of human papillomavirus 16 and 18 infection and p53 mutation in patients with oral squamous cell carcinoma in Japan. K Shima, I Kobayashi, I Saito, T Kiyoshima, K Matsuo, S Ozeki, M Ohishi, H Sakai. Br J Oral Maxillofac Surg 2000 Oct;38(5):445-450. “HPV16 and 18 E6/E7 DNA was detected in 9 (20%) and 25 (54%) of 36 samples.”
Shima / Br J Oral Maxillofac Surg 2000 abstract
Human papillomavirus infection and p53 alterations in oral squamous cell carcinoma. J Cao, ZY Zhang, Patima, YX Zhang, WT Chen. Chin J Dent Res 2000 Nov;3(3):44-49. 29/40 (72.5%) oral squamous cell carcinomas were positive for HPV.
Cao / Chin J Dent Res 2000 abstract
Detection of HPV in Japanese and Chinese oral carcinomas by in situ PCR. K Uobe, K Masuno, YR Fang, LJ Li, YM Wen, Y Ueda, A Tanaka. Oral Oncol 2001 Feb;37(2):146-152. “Analysis revealed the specific presence of HPV DNA in all cases of SCC in our Japanese (10/10) and Chinese (10/10) population samples.”
Uobe / Oral Oncol 2001 abstract
[Research on expression of human papillomavirus type 16 and telomerase in oral lesions.] Patiman, Z Zhang, J Cao. Zhonghua Kou Qiang Yi Xue Za Zhi 2001 Mar;36(2):119-121. “HPV16DNA was positive in 14.3% (1/7) of normal oral mucosa, 42.9% (3/7) of hyperplasia lesions, 66.6% (20/30) of dysplasia lesions and 81.6% (31/35) of OSCCs.”
Patiman / Zhonghua Kou Qiang Yi Xue Za Zhi 2001 abstract
Human papillomavirus as a risk factor for oral squamous cell carcinoma: A meta-analysis, 1982-1997. CS Miller, BM Johnstone. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001 Jun;91(6):622-635. In a meta-analysis of 94 reports, “The pooled odds ratio for the subset of studies directly comparing the prevalence of HPV in normal mucosa and OSCC was 5.37… The findings provide further quantitative evidence that oral infection with HPV, particularly with high-risk genotypes, is a significant independent risk factor for OSCC.” The authors also noted that differences in assay sensitivity indicate that these estimates may be conservative.
Miller / Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001 abstract
High risk human papillomavirus in oral squamous carcinoma: evidence of risk factors in a Venezuelan rural population. Peliminary report. G Premoli-De-Percoco, JL Ramirez. J Oral Pathol Med 2001 Jul;30(6):355-361. 60% (30/50) oral squamous cell carcinomas were positive for HPV.
Premoli-De-Percoco / J Oral Pathol Med 2001 abstract
Human papillomavirus infection and survival in oral squamous cell cancer: a population-based study. SR Schwartz, B Yueh, JK McDougall, JR Daling, SM Schwartz. Otolaryngol Head Neck Surg 2001 Jul;125(1):1-9. 15.1% of 254 tumors were HPV positive.
Schwartz / Otolaryngol Head Neck Surg 2001 abstract
Prevalence of high-risk human papilloma virus types and its association with P53 codon 72 polymorphism in tobacco addicted oral squamous cell carcinoma (OSCC) patients of Eastern India. JK Nagpal, S Patnaik, BR Das. Int J Cancer 2002 Feb 10;97(5):649-653. 37/110 (33.6%) of oral squamous cell carcinomas were HPV positive.
Nagpal / Int J Cancer 2002 abstract
A possible role for EBV
More studies that observe interactions are needed, rather than studying each virus separately. In comparison, see how much effort has been expended in dead-end investigations of p53 mutations.
Prevalence of Epstein-Barr virus in oral squamous cell carcinomas, premalignant lesions and normal mucosa — a study using the polymerase chain reaction. I Cruz, AJ Van den Brule, RD Steenbergen, PJ Snijders, CJ Meijer, JM Walboomers, GB Snow, I Van der Waal. Oral Oncol 1997 May;33(3):182-188. “EBV was found in 100% of OSCCs, in 77.8% of premalignant lesions and in 8.3% of clinically normal oral mucosa (P=0.0001).”
Cruz / Oral Oncol 1997 abstract
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. K Tsuhako, I Nakazato, J Miyagi, T Iwamasa, A Arasaki, H Hiratsuka, H Sunakawa, G Kohama, T Abo. J Oral Pathol Med 2000 Feb;29(2):70-79. In 60 OSCCs from Okinawa, 78% were positive for HPV and 76.6% for EBV; in 42 from Sapporo (a lower incidence area), 26.2% and 38.1% were positive respectively.
Tsuhako / J Oral Pathol Med 2000 abstract
No direct role for Epstein-Barr virus in oral carcinogenesis: a study at the DNA, RNA and protein levels. I Cruz, AJ Van Den Brule, AA Brink, PJ Snijders, JM Walboomers, I Van Der Waal, CJ Meijer. Int J Cancer 2000 May 1;86(3):356-361. Study established that transciption was not occurring.
Cruz / Int J Cancer 2000 abstract
Demonstration of Epstein-Barr virus in odontogenic and nonodontogenic tumors by the polymerase chain reaction (PCR). HS Jang, JO Cho, CY Yoon, HJ Kim, JC Park. J Oral Pathol Med 2001 Nov;30(10):603-610. “[T]he appearance of EBV genes seems to suggest the complicated roles that the EBV genes play.”
Jang / J Oral Pathol Med 2001 abstract
HPV: Review of Existing Research and Recommendations for Patient Education
Rebecca Anhang, MS, Annekathryn Goodman, MD and Sue J. Goldie, MD, MPH
The potential for human papillomavirus (HPV) DNA testing in cervical cancer prevention programs has been a topic at the forefront of cervical cancer policy discussions in recent years. To prevent some of the anxiety and psychological distress often experienced on HPV diagnosis and during the period of management, mass patient education must accompany the incorporation of HPV DNA testing into screening protocols. To contribute to a growing body of work that provides an empiric basis for development of effective counseling messages about HPV and HPV testing, this paper highlights women’s most common information gaps and psychosocial concerns and describes the different perspectives offered by women’s usual sources of information about HPV, including the crucial role of the clinical community in creating a shared decision making environment in which screening decisions and results can be discussed.