The environmental pollutant and tobacco smoke constituent dibenzo[def,p]chrysene is a co-factor for malignant progression of mouse oral papillomavirus infections.

摘要: Abstract HPV infections in the oral cavity that progress to cancer are on increase USA. Model systems study co-factors for progression of these lacking as HPVs species-restricted and cannot grow preclinical animal models. We have recently developed a mouse papillomavirus (MmuPV1) mucosal infection model provides opportunities test, first time, hypothesis tobacco carcinogens can impact papillomas squamous cell carcinoma (SCC). Four cohorts mice per sex were included: (1) infected with MmuPV1 treated orally DMSO-saline; (2) carcinogen, dibenzo[def,p]chrysene (DBP); (3) uninfected DMSO-saline, (4) DBP. Oral swabs collected monthly subsequent assessment viral load. tissues situ DNA/RNA detection, protein staining, pathological hyperplasia, SCC at termination. observed increased rates tissue DBP when compared or virus individually, each which showed minimal disease. Virally-infected epithelium strong levels E4/L1 staining. In contrast, areas reduced DNA staining indicative lower copy nucleus but RNA signals. Several host markers (p120 ctn, p53, S100A9) also examined tissues; particular significance, p120 ctn discriminated normal un-infected from papilloma epithelium. summary, we confirmed our is an excellent platform assess including PV cancerous progression. Our findings assist design novel prevention/treatment strategies positive vs. negative