ONYX-015, an E1B gene-attenuated adenovirus, causes tumor-specific cytolysis and antitumoral efficacy that can be augmented by standard chemotherapeutic agents View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1997-06

AUTHORS

C Heise, A Sampson-Johannes, A Williams, F McCormick, D D Von Hoff, D H Kirn

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. More... »

PAGES

639-645

Journal

TITLE

Nature Medicine

ISSUE

6

VOLUME

3

Author Affiliations

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nm0697-639

    DOI

    http://dx.doi.org/10.1038/nm0697-639

    DIMENSIONS

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    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/9176490


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