NDLI: Etoposide (VP-16-213)-induced gene alterations: potential contribution to cell death.

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Etoposide (VP-16-213)-induced gene alterations: potential contribution to cell death.

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Etoposide (VP-16-213)-induced gene alterations: potential contribution to cell death.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Berger, N. A. Schmotzer, J. A. Helms, S. R. Chatterjee, S.
Description	Author Affiliation: Berger NA ( Department of Medicine, University Hospitals of Cleveland, Case Western Reserve University, OH 44106.);
Abstract	We have shown previously a good correlation between etoposide-induced sister chromatid exchanges (SCE) and cytotoxicity. A semisynthetic derivative of podophyllotoxin, etoposide is also called Vepesid (Bristol; code designation VP-16-213, abbreviated VP-16). Since SCE represent DNA recombinational events, we hypothesized that VP-16-induced SCE might result in nonhomologous recombination in which segments of DNA were either deleted or added, leading to an alteration of gene sequences responsible for essential cell proteins. Alterations of such essential genes and consequent interference with formation of their products could consequently lead to cell death. To evaluate whether VP-16 treatment caused sufficient levels of DNA sequence alterations to interfere with gene product formation, we isolated hypoxanthine (guanine) phosphoribosyltransferase (HPRT)-deficient mutants from Chinese hamster V79 cells grown in the presence or absence of VP-16. DNA from 3 spontaneous mutants and 10 VP-16-induced mutants was analyzed by Southern blot hybridization to a full-length hamster HPRT cDNA probe. Most of the VP-16-induced mutants showed partial deletions and/or rearrangements of the HPRT gene. In contrast, spontaneous mutants showed negligible deletions or rearrangements. These results provide strong support for our hypothesis that deletion of genetic sequences may constitute an important component of the mechanism of VP-16-induced cell death.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	19
Volume Number	88
Language	English
Publisher	National Academy of Sciences
Publisher Date	1991-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	DNA Damage Etoposide Toxicity Hypoxanthine Phosphoribosyltransferase Genetics Animals Cell Line Cell Survival Drug Effects Chromosome Deletion Cricetinae Cricetulus DNA Mutational Analysis Polymorphism, Restriction Fragment Length Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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