Distinct distribution of HPV types among cancer-free Afro-Caribbean women from Tobago.

Human papillomavirus (HPV), a sexually transmitted virus causes cervical carcinomas, and is associated with approximately 36% of oropharyngeal tumours where HPV16 is the predominant genotype. The cervical cancer incidence rate in Trinidad and Tobago is about two times higher than the worldwide rate. We have for the first time determined the prevalence and type distribution of cervical HPV infections among cancer-free Afro-Caribbean women from Tobago, and compared it with the HPV subtypes observed in their oral cavity. Thirty-five per cent of the women were cervical HPV positive. The most common high-risk type detected in the cervix was HPV45 rather than HPV16 and 18. The prevalence of HPV infection in the oral mucosa was 6.6%. The distribution of HPV genotypes in healthy Tobagonian women is different from that reported in studies conducted in European and North American populations. This may have important implications for vaccine introduction in this and other Afro-Caribbean countries.

The epidemiology and risk factors of head and neck cancer: a focus on human papillomavirus.

Head and neck cancer was the eighth leading cause of cancer death worldwide in 2000. Although the incidence of head and neck squamous cell carcinoma (HNSCC) in the United States is relatively low, survival is poor and has not improved for several decades. While tobacco and alcohol are the primary risk factors for HNSCC development, epidemiological studies report a strong association with human papillomavirus (HPV) in a subset of HNSCC. More than 95% of cervical squamous cell carcinomas are linked to persistent HPV infection; evidence demonstrates that HPV is a necessary carcinogen. Not all HPV-positive HNSCC express the viral oncogenes (E6 and E7), which suggests that HPV may function as a carcinogen in a smaller proportion of HNSCC. This review presents our current understanding of the relationship between HPV and HNSCC, and describes future research directions that may lead to a better understanding of the involvement of HPV in head and neck cancer.

11q13 amplification status and human papillomavirus in relation to p16 expression defines two distinct etiologies of head and neck tumours.

Two distinct etiologies of head and neck squamous cell carcinoma (HNSCC) have been proposed, DNA damage owing to tobacco and alcohol exposure and human papillomavirus (HPV) oncogene-mediated transformation. Common genetic alterations in HNSCC include TP53 mutations, 11q13 amplification (amp) and CDKN2A/p16 mutations or promoter methlyation. However, in HPV+ HNSCC it is frequent to observe wild-type TP53 and expression of p16. The relationship of this unusual pattern with 11q13 amp has not been tested. In a retrospective study on 125 HNSCC patients, only 17% (five out of 30) of HPV+ vs 44% (39 out of 89) of HPV - tumours expressed 11q13 amp (adjusted odds ratio (OR)=0.2, 95% confidence interval (CI)=0.1-0.6). A subpopulation of tumours (n=69) were classified according to the three molecular markers, TP53, p16 and 11q13 amp. In addition to wild-type TP53, and p16 expression, HPV+ tumours were more likely not to be amplified at 11q13 (OR=6.5, 95% CI=1.8-23.9). As HPV+ HNSCC lack the genetic alterations which are common in other tumours, we hypothesise that HPV infection may represent an early event in the HNSCC carcinogenic process, thus suggesting a distinct molecular pathway.