Abstract
Head and neck carcinomas (HNCs) collectively are the sixth most common cancer with an annual incidence of about 400,000 cases in the US. The most well-established risk factors for HNCs are tobacco and alcohol abuse. With the increasing public awareness, the incidence of HNCs is decreasing. But there is an increasing incidence of oropharyngeal squamous cell carcinoma (OPSCC) has been observed during the last decade. This phenomena is associated with persistent infection with high-risk HPV. HPV associated OPSCC patients tend to be younger males of high socioeconomic status. The increasing incidence causes a significant loss to social resources, given that it’s reported that HPV associated OPSCC represents about 60% of OPSCC cases. There is a growing amount of data supporting the hypothesis that HPV-associated OPSCC has a better survival rate due to a higher sensitivity to chemotherapy and radiotherapy as compared to HPV-unrelated OPSCC. Although the HPV positivity is associated with increased radio-sensitivity, the underlying mechanisms are not yet fully understood. This review summarizes the current knowledge on the effects of HPV infection and its carcinogenesis on the radiosensitivity of OPSCC, from the molecular to histologic level, providing a comprehensive insight of this special tumor entity.
Highlights
Head and neck carcinomas (HNCs) collectively are the sixth most common cancer with an annual incidence of ~ 400,000 cases [1], and represent about 3.5% of all malignant tumors in western societies [2, 3] and other parts of the world
DNA damage in human papillomavirus (HPV)-related and HPV-unrelated Head and neck squamous cell carcinomas (HNSCC) cell lines occurs by different mechanisms, which illustrate the reasons for the increased sensitivity of HPV-related oropharyngeal squamous cell carcinoma (OPSCC) [14]
HPV-positive OPSCC tends to respond favorably to radiotherapy when compared to HPV-negative OPSCC
Summary
Head and neck carcinomas (HNCs) collectively are the sixth most common cancer with an annual incidence of ~ 400,000 cases [1], and represent about 3.5% of all malignant tumors in western societies [2, 3] and other parts of the world. DNA damage in HPV-related and HPV-unrelated HNSCC cell lines occurs by different mechanisms, which illustrate the reasons for the increased sensitivity of HPV-related OPSCC [14]. This review summarizes the current literature on the effects of radiation therapy on OPSCC cell lines and how HPV infection alters these mechanisms to create a higher sensitivity to treatment.
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