Apoptin

Adv Exp Med Biol. 2000;465:153-61.

Abstract

Tumor cells are often characterized by the traithey are more resistant to apoptosis induced by e.g. cytotoxic agents than normal cells. Resistance to apoptosis induction can be a direct consequence of mutations in certain tumor-suppressor genes (p53) or of certain proto-oncogenes (Bcl-2). Therefore, new cancer therapies are under development to bypass the resistance to chemo- and radio-therapy of tumors. Apoptin acts independently of p53, is stimulated by Bcl-2 and is insensitive to BCR-ABL, which means that Apoptin can induce apoptosis in cases where present (chemo)-therapeutic agents, unfortunately, will fail. The fact that Apoptin induces apoptosis in human tumorigenic cells but not in normal diploid cells, implies that side-effects of Apoptin treatment are expected to be minor. In-vivo results with a first prototype of anti-tumor therapy based on expression of Apoptin indicate that Apoptin has low acute toxicity and is effective as an anti-tumor agent.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis*
  • Capsid / metabolism*
  • Capsid Proteins*
  • Cell Transformation, Neoplastic
  • Chicken anemia virus*
  • Humans
  • Mice
  • Neoplasms / physiopathology
  • Neoplasms / therapy*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Tumor Cells, Cultured
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Capsid Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Suppressor Protein p53
  • VP3 protein, Chicken anemia virus