This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Andreú, T. Articles by von Melchner, H. Search for Related Content PubMed PubMed Citation Articles by Andreú, T. Articles by von Melchner, H.

Self-deleting Suicide Vectors (SDSV)

Selective Killing of p53-deficient Cancer Cells¹

Laboratory for Molecular Hematology, Department of Hematology, University of Frankfurt Medical School, 60596 Frankfurt [T. A., C. E., E-M. W., H. v. M.]; Department for Cancer Research, Asta-Medica AG, 60314, Frankfurt [T. K., A. W., P. M.]; Gene Expression Program, European Molecular Biology Laboratory, 69117 Heidelberg [A. F. S.]; and MainGen Biotechnologie GmbH, 60314 Frankfurt [R. K.], Germany

A self-deleting retrovirus vector carrying a herpes simplex virus (HSV)-thymidine kinase suicide gene has been developed to selectively kill cancer cells expressing a dysfunctional p53 tumor suppressor protein. When cells containing functional p53 are infected with the virus, the integrated provirus and the HSV-thymidine kinase gene are deleted from the genome by site-specific recombination (Cre/loxP). In contrast, cells without p53 or cells expressing a DNA-binding mutant of p53 retain the provirus and become susceptible to killing by ganciclovir. This strategy provides a new concept for the selective killing of cancer cells that can be adapted to any other dysfunctional transcription factor expressed by different tumors.

This article has been cited by other articles:

				V. Dixit and R. L. Juliano Selective Killing of Smad4-Negative Tumor Cells via a Designed Repressor Strategy Mol. Pharmacol., July 1, 2008; 74(1): 289 - 297. [Abstract] [Full Text] [PDF]