Mutant Adenoviruses Selectively Replication-Competent in Tumor Cells

  • Makoto Sunamura
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 465)

Keywords

Destroy Tumor Cell Human Adenovirus Type Induce Cell Cycle Progression Growth Arrest Gene 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Adams P.D., and Kaelin W.G. Transcriptional control by E2F. Semin Cancer Biol 6, 99–108, 1995.PubMedCrossRefGoogle Scholar
  2. Baker S.J., Markowitz E.R., Fearon J.K., Willson K.V., and Vogelstein B. Suppression of human colorectal carcinoma cell growth by wild-type p53. Science 249, 912–915, 1990.PubMedGoogle Scholar
  3. Barker D.D., and Berk A.J. Adenovirus proteins from both E1B reading frames are required for transformation of rodent cells by viral infection and DNA transfection. Virology 156, 107–121, 1987.PubMedCrossRefGoogle Scholar
  4. Beck G.R., Zerler B.R., and Moran E. Introduction to DNA tumor viruses: adenovirus, simian virus 40, and polyomavirus. In: McCance D.J. ed. Human Tumor Viruses. Washington DC: Am Soc Microbiol, 1998.Google Scholar
  5. Bischoff J.R., et al. An adenovirus mutant that replicates selectively in p53-deficient human tumor cells. Science 274, 373–376, 1996.PubMedCrossRefGoogle Scholar
  6. Chinnadurai G. Control of apoptosis by human adenoviruses. Semin in Virol 8, 399–408, 1998.Google Scholar
  7. Chrivia J.C., Kwok R.P., Lamb N., Hagiwara M., Montminy MR., and Goodman R.H. Phosphorylated CREB binds specifically to the nuclear protein CBP. Nature 365:855–859, 1993.PubMedCrossRefGoogle Scholar
  8. Donehower L.A., et al. Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumors. Nature 353, 215–221, 1992.Google Scholar
  9. Egan C., Jelsma T.N., Howe J.A., Bayley S.T., Ferguson B., and Branton P.E. Mapping of cellular proteinbinding sites on the products of early-region 1A of human adenovirus type 5. Mol Cell Biol 8, 3955–3959, 1988.PubMedGoogle Scholar
  10. Greenblatt M.S., Bennet W.P., Hollstein M., and Harris C.C. Mutations in the p53 tumor suppressor gene: Clues to cancer etiology and molecular pathogenesis. Cancer Res 54, 4855–4878, 1994.PubMedGoogle Scholar
  11. Harlow E., Whyte P., Franza B.R. Jr, and Schley C. Association of adenovirus early-region 1A proteins with cellular polypeptides. Mol Cell Biol 6, 1579–1589, 1986.PubMedGoogle Scholar
  12. Heise C., et al. 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, 639–645, 1997.PubMedCrossRefGoogle Scholar
  13. Jelsma T.N., Howe J.A., Mymryk J.S., Evelegh C.M., Cunniff N.F., and Bayley S.T. Sequences in E1A proteins of human adenovirus 5 required for cell transformation, repression of a transcriptional enhancer, and induction of proliferating cell nuclear antigen. Virology 171, 120–130, 1989.PubMedCrossRefGoogle Scholar
  14. Kirn D., Hermiston T., and McCormick F. ONYX-105: Clinical data are encouraging. Nat Med 4, 1341–1342, 1998.PubMedCrossRefGoogle Scholar
  15. Kwok R.P., Lundblad J.R., Chrivia J.C., Richards J.P., Bachinger H.P., Brennan R.G., Roberts S.G., Green M.R., and Goodman R.H. Nuclear protein CBP is a coactivator for the transcription factor CREB. Nature 370(6486):223–226, 1994.PubMedCrossRefGoogle Scholar
  16. Lowe S.W., and Ruley H.E. Stabilization of the p53 tumor suppressor is induced by adenovirus E1A and accompanied apoptosis. Genes Dev 7, 535–545, 1993.PubMedGoogle Scholar
  17. Malkin D., et al. Germ line p53 mutations in a familial syndrome of breast cancer, sarcomas, and other neoplasias. Science 250, 1233–1238, 1990.PubMedGoogle Scholar
  18. Motoi F., Sunamura M., Sadata A., Yoshida Y., Matsuno S., and Hamada H. Effective gene therapy for pancreatic cancer by cytokines mediated by restricted replication-competent adenovirus. (submitted for publication).Google Scholar
  19. Mymryk J.S. Tumor suppressive properties of the adenovirus 5 E1A oncogene. Oncogene 13, 1581–1589, 1996.PubMedGoogle Scholar
  20. Ricciardi R.P. Transformation and tumorigenesis mediated by the adenovirus E1A and E1B oncogenes. In: Barbanti-Brodano G., Bendienelli M., Friedman H., eds. DNA Tumor Viruses: Oncogenic Mechanisms. New York: Plenum Press, 195–225, 1995.Google Scholar
  21. Teodoro J.G., and Branton P.E. Regulation of p53-dependent apoptosis, transcriptional repression, and cell transformation by phosphorylation of the 55-kilodalton E1B protein of human adenovirus type 5. Virol 71, 3620–3627, 1997.Google Scholar
  22. Weinberg R.A. The retinoblastoma protein and cell cycle control. Cell 81, 323–330, 1995.PubMedCrossRefGoogle Scholar
  23. Whyte P., et al. Association between an oncogene and an anti-oncogene: the adenovirus E1A proteins bind to the retinoblastoma gene product. Nature 334, 124–129, 1988.PubMedCrossRefGoogle Scholar
  24. Whyte P., Williamson N.M., and Harlow E. Cellular targets for transformation by the adenovirus E1A proteins. Cell 56, 67–75, 1989.PubMedCrossRefGoogle Scholar
  25. Yee S.P., and Branton so. Detection of cellular proteins associated with human adenovirus type 5 early region 1A polypeptides. Virology 147, 142–153, 1985.PubMedCrossRefGoogle Scholar
  26. Yonish-Rouach E., et al. Wild type p53 induces apoptosis of myeloid leulemic cells that is inhibited by interleukin-6. Nature 353, 345–347, 1991.Google Scholar

Copyright information

© Kluwer Academic Publishers 2002

Authors and Affiliations

  • Makoto Sunamura
    • 1
  1. 1.First Department of SurgeryTohoku University School of Medicine SendaiJapan

Personalised recommendations