Abstract
Oropharyngeal squamous cell carcinoma (OPSCC) has been known to be a highly aggressive disease associated with human papilloma virus (HPV) infection. To investigate the relationship between HPV and chronic inflammation in oropharyngeal carcinogenesis, we collected 140 oral mucous fresh specimens including 50 OPSCC patients, 50 cancer in situ, 30 precancerous lesions, and 10 normal oral mucous. Our data demonstrated that there was a significantly higher proportion of severe chronic inflammation in dysplastic epithelia in comparison with that in normal tissues (P<0.001). The positive rate of HPV 16 was parallel with the chronic inflammation degrees from mild to severe inflammation (P<0.05). The positive rate of HPV 16 was progressively improved with the malignant progression of oral mucous (P<0.05). In addition, CD11b+ LIN- HLA-DR-CD33+ MDSCs were a critical cell population that mediates inflammation response and immune suppression in HPV-positive OPSCC. These indicated that persistent chronic inflammation-related HPV infection might drive oropharyngeal carcinogenesis and MDSCs might pay an important role during this process. Thus, a combination of HPV infection and inflammation expression might become a helpful biomedical marker to predict oropharyngeal carcinogenesis.
Highlights
Head and neck squamous cell carcinoma (HNSCC) includes cancers arising from the lining epithelium of the oral cavity, larynx, pharynx, and nasopharynx
Chronic inflammation correlates with the progression of oropharyngeal carcinogenesis To clarify the possible role of chronic inflammation in oropharyngeal carcinogenesis, we observed the morphology of neutrophils and lymphocytes and counted their number in microscope fields on smear slides from 140 samples including the specimens of 10 normal oral mucous, 30 dysplasia, 50 caner in situ and 50 oropharyngeal cancer (Fig 1A)
The results showed that the percentage of moderate-severe inflammation in the specimens of dysplasia, cancer in situ and cancer was much higher than that in normal oral mucous (P0.05, Fig 1B), indicating that there might be some relationship between chronic inflammation and oropharyngeal squamous cell carcinomas (OPSCC) carcinogenesis
Summary
Head and neck squamous cell carcinoma (HNSCC) includes cancers arising from the lining epithelium of the oral cavity, larynx, pharynx, and nasopharynx. High-risk human papilloma virus (HPV) has been recognized as an important risk factor in a subset of oropharyngeal squamous cell carcinomas (OPSCC) and HPV-positive OPSCC has a more favorable prognosis compared to HPV-negative OPSCC[1,2,3,4]. The incidence of HPV-positive OPSCC in the United States enhanced at approximately 7.5% per year while the incidence of HPV-negative reduced in parallel with smoking, so the percentage of HPV-positive OPSCC enhanced from less than 20% to more than 70% from 1988 to 2004[5]. Ang et al [6] showed that the death risk of HPV-positive OPSCC significantly improved with each additional pack-year of tobacco smoking, indicating that HPV state is not a sufficient etiology of carcinogenesis and demands the accumulation of additional factors
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