Antitumor Effect of E1B Defective Adenoviruses in Human Malignant Cells View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

1998

AUTHORS

P. Martín Duque , C. Alonso , R. Sánchez-Prieto , M. Lleonart , Santiago Ramón y Cajal

ABSTRACT

It has previously been reported that expression of the adenoviral gene E1A dramatically increases sensitivity to DNA damaging agents and decreases the tumorigenicity of murine and human malignant cells by both p53 dependent and independent pathways (1–3, for a review see reference 4). Given the fact that the E1a protein is expressed at high levels during adenovirus 5 infection and due to its highly cytotoxic potential 5, we decided to study the effects of an adenovirus lacking the E1B gene. 19K E1B has been reported to overcome the cytotoxicity of E1A by blocking apoptosis, and the 55K-E1B inactivates the p53 protein (5, 6). Consequently, we hypothesized that deletions in both E1B ORFs could result in enhanced antitumor cytotoxicity and induction of sensitivity to DNA-damaging agents. More... »

PAGES

87-89

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-1-4615-5357-1_14

DOI

http://dx.doi.org/10.1007/978-1-4615-5357-1_14

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1009617941

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/10026855


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