Human Papillomavirus and Oral Cancer: The International Agency for Research on Cancer Multicenter Study

Abstract

HPV appears to play an etiologic role in many cancers of the oropharynx and possibly a small subgroup of cancers of the oral cavity. The most common HPV type in genital cancers (HPV16) was also the most common in these tumors. The mechanism of transmission of HPV to the oral cavity warrants further investigation.

Prevalence of types 16 and 33 is increased in high‐risk human papillomavirus positive women with cervical intraepithelial neoplasia grade 2 or worse

“…HPV 16 accounts for 95% or more of the hrHPV positive tumors in the oral cavity and oropharynx. [23][24][25][26] Our data on the distribution of hrHPV types may have implications for hrHPV test cocktails, not only for cervical screening but also for the triage policy of women with BMD or normal cytology. By distinguishing the hrHPV types with an increased progression risk to CIN3/cervical carcinoma, the specificity of hrHPV testing could be increased, resulting in follow-up algorithms with different time intervals for certain hrHPV types, which may improve the screening efficiency for CIN3 and cervical cancer and consequently the cost-effectiveness.…”

Café Discussions on Oral Sex, Oral Cancer, and HPV Infection: Summative Report

“…Oral cancer significantly impacts quality of life, physically and psychosocially, and the genetic links between some types of oral-pharyngeal carcinomas and ano-genital malignancies have been established via the human papillomavirus (HPV), particularly the strains 16 and 18 as found by Herrero et al (2003) and others (Anhang, Goodman, & Goldie, 2004;Cox, 2000;D'Souza et al, 2007;Ha & Califano, 2004). Since HPV 16 is the most predominant strain in ano-genital carcinomas, its transmission to the oropharyngeal region can occur through the mouth, especially during oral sex in sexually active individuals (Scully, 2005).…”

HPV16 semiquantitative viral load and serologic biomarkers in oral and oropharyngeal squamous cell carcinomas

“…[1][2][3][4] Among HPV DNA-positive oropharyngeal SCCs, 90% are positive for HPV16. [1][2][3][4] Nonetheless, HPV DNA detection in tumor biopsies may not be sufficient evidence of causation.…”

“…[1][2][3][4] Among HPV DNA-positive oropharyngeal SCCs, 90% are positive for HPV16. [1][2][3][4] Nonetheless, HPV DNA detection in tumor biopsies may not be sufficient evidence of causation. HPV16 DNA from tumor specimens analyzed jointly with markers of expression of the viral oncogene E6, mutational patterns of the cancer suppressor gene TP53 and levels of allelic loss, have helped identify a subset of these cancers that may be the consequence of HPV infection.…”

“…HPV16 DNA from tumor specimens analyzed jointly with markers of expression of the viral oncogene E6, mutational patterns of the cancer suppressor gene TP53 and levels of allelic loss, have helped identify a subset of these cancers that may be the consequence of HPV infection. 1,2,[5][6][7][8] HPV viral load, a measure of the amount of viral DNA in biopsy specimens, alone or in conjunction with well-characterized HPV serologic assays, may clarify the role of HPV among oral and oropharyngeal cases. Antibodies against HPV E6 and E7 are markers of an invasive HPV-associated malignancy 9,10 and are rarely present among individuals with HPV DNA-negative oral and oropharyngeal tumors.…”