Introduction: HPV is the most common sexually transmitted disease worldwide. The risk of contracting it at least once in a lifetime among men and women is estimated at 50%.
Although HPV infections are asymptomatic and resolve within 2 years, approximately 10% of people develop persistent infection, and their risk of developing head and neck cancer increases.
The most common types of HPV are 16 and 18 in cancers of the genital tract and cancers of the mouth, throat, and digestive tract.
Genotypes 6 and 11 cause more anogenital warts and respiratory papillomatosis but are rarely associated with cancer.
The purpose of this review is to organize the evidence of the association between HPV infection and oral and pharyngeal cancers.
Methods: Oropharyngeal squamous cell carcinoma (OPSCC) Human papillomavirus HPV+ is one of the fastest growing cancers among young people. HPV 16 accounts for approximately 95% of oral and pharyngeal cancers with HPV+.
HPV-related head and neck tumors have different characteristics from HPV HNSCC. Patients are younger and often non-smokers and do not consume alcohol. Meanwhile, alcohol and tobacco consumption are the most important factors for head and neck cancer. In addition, HPV-related OPC in Populations with higher social and economic class are seen.
OPSCC is detected in the advanced stages of the disease due to the lack of early symptoms.
Unlike tobacco- and alcohol-related squamous cell carcinomas of the head and neck (HNSCC), patients with HPV-related OPSCC have shown significantly higher cure rates.
Results: Identification of PMHC:HPV16/18 complexes with high avidity may be a way to expand antitumor therapies for different patient populations.
Effective immunotherapy for HPV HNSCC requires a combination of therapeutic approaches to overcome adaptive immune resistance as the tumor continuously evolves with exposure to different therapies.
Elucidating the details of the immune evasion mechanism of HPV is important to control its persistent infection.
During the oncogenic process, the extrachromosomal HPV genome often integrates into the host genome.
HPV genome integration is the most important factor associated with stable and high expression of E6 and E7 oncoproteins. However, many of these integrations may be silent integrations due to increased overall genetic instability.
Conclusion: Integration includes induction and high expression of E6 and E7 in the host, which leads to cell cycle activation and increased genomic stability. This integration leads to disruption of E2 expression.
By binding to ubiquitin ligase, E6 protein breaks down P53 protein and by increasing cell telomerase activity, immortalizes cells and inhibits apoptosis.
E7 protein activates E2F by binding to pRb (retinoplasma), which leads to cell cycle activation and increased genomic instability of the host.
The different characteristics of HPV-related oropharyngeal cancer have led to clinical trials to test new treatment strategies.
Today, simultaneous chemotherapy has established its role as a definitive adjuvant treatment option after surgery for patients with advanced regional disease. In untreatable recurrent or metastatic conditions, the emergence of immunotherapy and biological drugs, both alone and It has been added to our armamentarium in combination with chemotherapy to relieve patients' symptoms, optimize disease control and prolong survival.