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IMR Press / FBL / Volume 10 / Issue 2 / DOI: 10.2741/1628

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Article
Adenovirus E1A gene-induced tumor cell rejection through cellular sensitization to immune and nonimmune apoptotic injuries
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Affiliation
1 Section of Infectious Diseases, Department of Medicine, University of Illinois at Chicago, College of Medicine, Chicago, IL 60612, USA
2 Depts of Medicine and Immunology, National Jewish Medical and Research Center and University of Colorado Health Sciences Center (UCHSC) and the UCHSC Cancer Center, Denver, CO 80206
Front. Biosci. (Landmark Ed) 2005, 10(2), 1396–1414; https://doi.org/10.2741/1628
Published: 1 May 2005
Abstract

The E1A gene of human adenovirus (Ad) serotypes 2 and 5 induces susceptibility of cells from several species, including human, to lysis by natural killer cells, activated macrophages and a variety of other immunologic and nonimmune cellular injuries. This E1A activity is the rationale behind some treatment strategies using combined adenoviral vector infection and chemotherapy for cancer. This review will consider the evolution of the studies that have resulted in the current understanding of the cellular mechanisms of E1A-induced tumor cell cytolytic susceptibility and sensitization to apoptotic injury. The translation of in vitro observations to experimental models testing E1A-induced tumor rejection in the context of the cellular immune response and E1A-induced sensitization of human tumor cells to therapeutic injuries will be discussed. Review of available information on the molecular mechanisms of E1A-induced cellular sensitivity to immune and nonimmune injuries will be used as a basis for consideration of possible future directions of this research.

Keywords
E1A oncogene
NK cell
Macrophage
Activated Macrophage
Cytotoxicity
Apoptosis
Tumor
Tumorigenicity
Immunity
Innate Immunity
Adaptive Immunity
NF-Kappa B Activation
Chemotherapy
Review
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