
Relationship between HPV and biomarkers annexin A1 and P53 in oropharyngeal cancer
2014; Elsevier BV; Volume: 46; Linguagem: Inglês
10.1097/01.pat.0000454431.15263.c4
ISSN1465-3931
AutoresCleberson Jean dos Santos Queiroz, Cíntia Mara de Amorim Gomes Nakata, Egle Solito, Amílcar Sabino Damazo,
Tópico(s)Neonatal Respiratory Health Research
ResumoBackground Human papillomavirus (HPV) is often present in oropharyngeal cancers. Here, we investigated the prevalence of HPV and its relationship with p53, p16 and ANXA1 (ANXA1). Methods We have analyzed tumor and adjacent mucosa from 22 patients with squamous cell carcinoma of the oropharynx and morphologically normal epithelium. We evaluated the presence of HPV (subtypes 16/18 and 31/33) by chromogenic in situ hybridization and expression of p16, p53, ANXA1 and phosphoryl-ation of ANXA1 residues Ser27 (ANXA1-SER) and Tyr21 (ANXA1-TYR) by immunofluorescence. Results We have detected the presence of HPV genome in 59% of tumors and 92% were also positive for p16 immunostaining. We demonstrated reduction in expression of ANXA1 and ANXA1-TYR in tumors compared to negative controls and lower levels of p53 in HPV+ tumors. However, we observed increased level of ANXA1 and ANXA1-SER beside neoplasia. Conclusions Our results confirm high prevalence of HPV in oropharyngeal cancer and reduction in p53 expression in HPV + tumors. Further, we observed tumoral hypoexpression of ANXA1 and ANXA1-TYR. Increase in ANXA1-SER beyond HPV+ neoplasia sugests that epithelium had been activated by infectious agent. Therefore, ANXA1 and its phosphorylated forms can play important roles in response to HPV infection and carcinogenesis. Human papillomavirus (HPV) is often present in oropharyngeal cancers. Here, we investigated the prevalence of HPV and its relationship with p53, p16 and ANXA1 (ANXA1). We have analyzed tumor and adjacent mucosa from 22 patients with squamous cell carcinoma of the oropharynx and morphologically normal epithelium. We evaluated the presence of HPV (subtypes 16/18 and 31/33) by chromogenic in situ hybridization and expression of p16, p53, ANXA1 and phosphoryl-ation of ANXA1 residues Ser27 (ANXA1-SER) and Tyr21 (ANXA1-TYR) by immunofluorescence. We have detected the presence of HPV genome in 59% of tumors and 92% were also positive for p16 immunostaining. We demonstrated reduction in expression of ANXA1 and ANXA1-TYR in tumors compared to negative controls and lower levels of p53 in HPV+ tumors. However, we observed increased level of ANXA1 and ANXA1-SER beside neoplasia. Our results confirm high prevalence of HPV in oropharyngeal cancer and reduction in p53 expression in HPV + tumors. Further, we observed tumoral hypoexpression of ANXA1 and ANXA1-TYR. Increase in ANXA1-SER beyond HPV+ neoplasia sugests that epithelium had been activated by infectious agent. Therefore, ANXA1 and its phosphorylated forms can play important roles in response to HPV infection and carcinogenesis.
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