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Autoantibody to p185erbB2/neu oncoprotein by vaccination with xenogenic DNA

A Concetti1, A Amici, C Petrelli

  • 1Department of Biology M. C. A., Camerino (MC), Italy. Concetti@cambio.unicam.it

Cancer Immunology, Immunotherapy : CII
|December 1, 1996
PubMed

Insights

DNA vaccination using the erbB2/neu gene generates antibodies against the erbB2/neu oncoprotein. This approach shows potential for treating human breast cancer without causing harmful autoimmunity.

Area of Science:

  • Oncology
  • Immunology
  • Gene Therapy

Background:

  • Current breast cancer treatments explore antibody therapies and vaccination against the erbB2/neu oncoprotein (p185).
  • The erbB2/neu gene's potential as an immunogen for cancer therapy is under investigation.

Purpose of the Study:

  • To investigate the efficacy of using the erbB2/neu gene as an immunogen for generating anti-cancer autoantibodies.
  • To assess the safety and potential autoimmune effects of this DNA vaccination strategy.

Main Methods:

  • Intramuscular and intradermal injections of full-length rat neuNT DNA into mice.
  • Analysis of generated autoantibodies for binding to p185 and human ErbB2.
  • In vitro assays using SKBR3 tumor cells and natural killer cells.
  • Long-term observation of mice for toxic effects.

Main Results:

  • DNA vaccination successfully generated anti-p185 autoantibodies in mice.
  • These autoantibodies recognized both mouse p185 and human ErbB2, staining human breast adenocarcinoma samples.
  • Anti-p185 IgG mediated inhibition of human SKBR3 tumor cell growth and natural killer cell-mediated lysis.
  • No discernible toxic effects were observed in mice even after one year of continuous antibody presence.

Conclusions:

  • DNA vaccination with the erbB2/neu gene is a viable strategy for inducing anti-cancer autoantibodies.
  • This approach holds promise for breast cancer treatment, potentially without inducing harmful autoimmunity.
  • Further research into boosting anti-ErbB2 immunity via DNA vaccination is warranted.

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