HPV-positive oropharyngeal cancer
| HPV-positive oropharyngeal cancer | |
|---|---|
 |
|
| HPV positive HNSCC (in situ hybridization) | |
| Classification and external resources | |
| Specialty | oncology |
| ICD-10 |
C09.0-C10.9 C01,C02.4,C14.2 |
Human papillomavirus (HPV)-positive oropharyngeal cancer (OPC) also known as HPV16+ oropharyngeal cancer or HPV+ OPC is a recognized subtype of oropharyngeal squamous cell carcinomas (OSCC), associated with the HPV type 16 virus.
HPV oral infection precedes the development of HPV+ OPC. Slight injuries in the mucous membrane serve as an entry gate for HPV, which thus works into the basal layer of the epithelium. People testing positive for HPV16 oral infection have a 14 times increased risk of developing HPV+ OPC.
Immunosuppression seems to be an increased risk factor for HPV+ OPC. Individuals with TGF-β1 genetic variations, specially T869C, are more likely to have HPV16+ OPC. TGF-β1 plays an important role in controlling the immune system.
A 1993 study has found that patients with human papillomavirus (HPV)-associated anogenital cancers had a 4.3-fold increased risk of tonsillar squamous-cell carcinoma.
Although evidence suggests that HPV16 is the main cause of OPC between non-smokers and non-drinkers, the degree to which tobacco and/or alcohol use may contribute to increase the risk of HPV+ OPC is unclear.
Concomitant human herpesvirus-8 infection can potentiate the effects of HPV-16.
A prospective study has found that increased HPV+ OPC risk was observed more than 15 years after HPV exposure, pointing to a slow development of the disease, like in cervical cancer.
HPV associated cancers are caused by the expression of HPV's E6 and E7 proteins that bind to and inactivate tumor suppressor proteins p53 and retinoblastoma protein (pRB), respectively, leading to malignant transformation of HPV infected cells.
The biology of HPV+ OPC is distinct of HPV- OPC with P53 degradation (inactivated by E6 instead of by genetic mutation), pRB pathway inactivation (by E7 instead of Cyclin D1 amplification), and P16 upregulation (over-expression of p16 instead of inactivation due to reduced negative feedback from pRB).
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