Analysis of human papillomavirus DNA in oral squamous cell carcinomas

Abstract

Evidence from several laboratories suggests that HPV plays a role in the etiology of squamous cell carcinomas of the oral cavity. A multifactorial risk factor profile for the development of oral cancer may include HPV in addition to well-established risk factors such as tobacco and alcohol use. The prevalence of oral carcinomas reported to be associated with HPV has varied widely due to differences in the sensitivity of the assay used for HPV detection. The aims of this study were: (1) to ascertain the prevalence of HPV DNA in oral squamous cell carcinomas using the most sensitive technique available, the polymerase chain reaction; (2) to determine the type of HPV in the tumors; and 3) to correlate the virologic data with other risk factor data obtained from patients' records. Fourteen (78%) of 18 primary tumors, 6 (67%) of 9 normal epithelial tissues from the patients and 5 (100%) of 5 neck metastases were HPV DNA-positive. Of the 14 HPV DNA-positive primary tumors, specific typing revealed HPV 16 in 2, HPV 18 in 2, HPV 16 and 18 in 5, HPV 6/11, 16 and 18 in 4, and HPV 6/11 in 1. HPV types in the normal or metastatic tissue were usually the same as those in the respective primary tumor. There was no significant association between HPV presence and any of 12 factors or patient characteristics studied.

“High Risk” HPV Types Are Frequently Detected in Potentially Malignant and Malignant Oral Lesions, But Not in Normal Oral Mucosa

“…None of the examined normal samples were found to be positive, which lies in accordance with some studies (18,23,26,29,32). However, other groups have observed a surprisingly high infection percentage in normal mucosa (3,11,16,41), possibly because they analyzed normal tissues that were adjacent to neoplastic lesions. In patients who had proliferative disorders, HPV positivity exceeded the percentage of smoking (71.7%), which is considered a major risk factor for oral carcinogenesis (3).…”

Tongue and tonsil carcinoma

“…Some investigators have found no evidence of HPV DNA by polymerase chain reaction technique in oral SCC, 25 whereas others found oral SCC lesions to be HPV DNA positive but found the same proportion of HPV DNA-positive normal oral mucosa biopsy specimens. 26 A large multicenter casecontrol study of 1415 cases with carcinoma of the oral cavity, 255 with carcinoma of the oropharynx, and 1732 controls was conducted across 9 countries in 5 continents by investigators from the International Agency for Research on Cancer. 27 In that study, the odds of detecting antibodies against HPV-16 L1 and/or E6 or E7 were significantly higher among cases with oral cavity carcinoma than among controls (for L1, the odds ratio [OR] was 1.5, 95% confidence interval [95% CI], 1.1-2.1; for HPV-E6 or HPV-E7, the OR was 2.9, 95% CI, 1.7-4.8).…”

Characterization of transformation related genes in oral cancer cells

“…Infection with high-risk human papilloma virus (HPV) and exposure to the chemical carcinogens in tobacco are associated with the development of oral cancers (Blot et al, 1988;Woods et al, 1993). Re¯ecting such epidemiological ®ndings, primary normal human oral keratinocyte (NHOK) can be converted to tumorigenic cells in a sequential twostep process utilizing transfection of HPV-16 or -18 DNA followed by exposure to chemical carcinogens (Kim et al, 1993;Shin et al, 1994;Park et al, 1995).…”