ONYX-015, an E1B gene-attenuated adenovirus, causes tumor-specific cytolysis and antitumoral efficacy that can be augmented by standard chemotherapeutic agents.
Nat Med
; 3(6): 639-45, 1997 Jun.
Article
en En
| MEDLINE
| ID: mdl-9176490
ABSTRACT
The 55-kilodalton (kDa) protein from the E1B-region of adenovirus binds to and inactivates the p53 gene, which is mutated in half of human cancers. We have previously shown that the replication and cytopathogenicity of an E1B, 55-kDa gene-attenuated adenovirus, ONYX-015, is blocked by functional p53 in RKO and U20S carcinoma lines. We now report that normal human cells were highly resistant to ONYX-015-mediated, replication-dependent cytolysis. In contrast, a wide range of human tumor cells, including numerous carcinoma lines with either mutant or normal p53 gene sequences (exons 5-9), were efficiently destroyed. Antitumoral efficacy was documented following intratumoral or intravenous administration of ONYX-015 to nude mouse-human tumor xenografts; efficacy with ONYX-015 plus chemotherapy (cisplatin, 5-fluorouracil) was significantly greater than with either agent alone.
Search on Google
Banco de datos:
MEDLINE
Asunto principal:
Endotelio Vascular
/
Proteínas E1B de Adenovirus
/
Proteínas de la Cápside
/
Neoplasias Experimentales
Tipo de estudio:
Etiology_studies
Límite:
Female
/
Humans
Idioma:
En
Año:
1997
Tipo del documento:
Article