Restoring apoptosis as a strategy for cancer gene therapy: focus on p53 and mda-7.
Understanding the molecular and genetic determinants of cancer will provide unique opportunities for developing rational and effective therapies. Malignant cells are frequently resistant to chemotherapy and radiation induced programmed cell death (apoptosis). This resistance can occur by mutations in the tumor suppressor gene p53. Strategies designed to replace this defective tumor suppressor protein, as well as forced expression of a novel cancer specific apoptosis inducing gene, melanoma differentiation associated gene-7 (mda-7), offer promise for restoring apoptosis in tumor cells. Conditional-replicating viruses that selectively induce cytolysis in tumor cells provides an additional means of targeting cancer cells for destruction. Although these approaches represent works in progress, future refinements will in all likelihood result in the next generation of cancer therapies.
Lebedeva
Irina V
IV
Department of Pathology, Herbert Irving Comprehensive Cancer Center, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY 10032, USA.
Su
Zhao Zhong
ZZ
Sarkar
Devanand
D
Fisher
Paul B
PB
D000256:Adenoviridae; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D016147:Genes, Tumor Suppressor; D015316:Genetic Therapy / Q000379:methods*; D005822:Genetic Vectors; D006801:Humans; D007378:Interleukins / Q000235:genetics*; D009369:Neoplasms / Q000628:therapy*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*; D000099180:Interleukin-24
D007378:Interleukins; D016159:Tumor Suppressor Protein p53; D000099180:Interleukin-24