Revue: | Electronic journal of biotechnology |
Base de datos: | PERIÓDICA |
Número de sistema: | 000267140 |
ISSN: | 0717-3458 |
Autores: | Park, No-Hee1 Kang, Mo K |
Instituciones: | 1University of California, School of Dentistry, Los Angeles, California. Estados Unidos de América |
Año: | 2000 |
Periodo: | Abr |
Volumen: | 3 |
Número: | 1 |
País: | Chile |
Idioma: | Inglés |
Tipo de documento: | Artículo |
Enfoque: | Experimental, aplicado |
Resumen en inglés | Development of oral cancer proceeds through discrete molecular genetic changes that are acquired from the loss of genomic integrity after continued exposure to environmental risk factors. Of particular importance in oral cancer development are tobacco-related chemical carcinogens and human papillomavirus (HPV) infection. To understand the mechanisms by which these risk factors contribute to tumorigenesis, we developed an in vitro model of sequential, multistep oral carcinogenesis model of normal human oral keratinocytes (NHOK) by immortalizing these cells with cloned "high risk" HPV genome. HPV viral genome alone failed to give rise to a tumorigenic cell population, which required further exposure to chemical carcinogens. HPV-immortalized cells exhibited impaired cell cycle control and DNA repair activity upon exposure to DNA damaging agents, and accumulated elevated frequency of spontaneous and mutagen-induced mutation. Furthermore, expression of E6 and E7 oncoproteins of "high risk" HPV were found to be sufficient for the enhanced mutation frequency in NHOK. These findings suggest that viral infection in combination with existing chemical carcinogens may be the paramount causative agents for the induction of genetic instability and development of oral cancer |
Disciplinas: | Medicina, Biología |
Palabras clave: | Odontología, Oncología, Virus, Cáncer, Boca, Papiloma, Queratinocitos, Factores de riesgo, Genoma |
Keyword: | Medicine, Biology, Dentistry, Oncology, Virus, Cancer, Mouth, Papillomavirus, Keratinocytes, Risk factors, Genome |
Texte intégral: | Texto completo (Ver HTML) |