Apoptin.
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.
Pietersen
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Department of Molecular Cell Biology, Leiden University Medical Center, The Netherlands.
Noteborn
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HM
D000818:Animals; D017209:Apoptosis; D002213:Capsid / Q000378:metabolism*; D036022:Capsid Proteins; D002471:Cell Transformation, Neoplastic; D017727:Chicken anemia virus; D006801:Humans; D051379:Mice; D009369:Neoplasms / Q000503:physiopathology / Q000628:therapy*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D014407:Tumor Cells, Cultured; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
D036022:Capsid Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; C091717:VP3 protein, Chicken anemia virus