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DNA-damage-induced checkpoint pathways in the nematode Caenorhabditis elegans.


Hofmann, E R; Milstein, S; Hengartner, M O (2000). DNA-damage-induced checkpoint pathways in the nematode Caenorhabditis elegans. Cold Spring Harbor Symposia on Quantitative Biology, 64:467-473.

Abstract

Genomic instability is believed to be an enabling characteristic of cancer (Hanahan and Weinberg 2000).Therefore, it is not surprising that sophisticated mechanisms exist to maintain the integrity of the genome. Damage to DNA triggers checkpoint controls that result in cellcycle arrest and repair of the lesion (Nurse 1997, 2000;Weinert 1998). In multicellular organisms, when DNAdamage is extensive, these potentially harmful cells areeliminated by apoptosis (Enoch and Norbury 1995; Evanand Littlewood 1998). Defects in communications between DNA damage and the apoptotic program leads tothe survival of cells with unstable genomes vulnerable tooncogene activation, ultimately leading to tumor development (Morgan and Kastan 1997; Orr-Weaver andWeinberg 1998; Hanahan and Weinberg 2000). Geneticwork in yeast has greatly improved our understanding ofthe molecular mechanisms of DNA-damage-inducedcheckpoint arrest and repair. On the other hand, DNAdamage-induced apoptosis cannot be studied in yeasts, asthe apoptotic program is missing in both Saccharomycescerevisiae and Schizosaccharomyces pombe (Fraser andJames 1998)...

Genomic instability is believed to be an enabling characteristic of cancer (Hanahan and Weinberg 2000).Therefore, it is not surprising that sophisticated mechanisms exist to maintain the integrity of the genome. Damage to DNA triggers checkpoint controls that result in cellcycle arrest and repair of the lesion (Nurse 1997, 2000;Weinert 1998). In multicellular organisms, when DNAdamage is extensive, these potentially harmful cells areeliminated by apoptosis (Enoch and Norbury 1995; Evanand Littlewood 1998). Defects in communications between DNA damage and the apoptotic program leads tothe survival of cells with unstable genomes vulnerable tooncogene activation, ultimately leading to tumor development (Morgan and Kastan 1997; Orr-Weaver andWeinberg 1998; Hanahan and Weinberg 2000). Geneticwork in yeast has greatly improved our understanding ofthe molecular mechanisms of DNA-damage-inducedcheckpoint arrest and repair. On the other hand, DNAdamage-induced apoptosis cannot be studied in yeasts, asthe apoptotic program is missing in both Saccharomycescerevisiae and Schizosaccharomyces pombe (Fraser andJames 1998)...

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:07 Faculty of Science > Institute of Molecular Life Sciences
Dewey Decimal Classification:570 Life sciences; biology
Language:English
Date:2000
Deposited On:11 Feb 2008 12:19
Last Modified:05 Apr 2016 12:16
Publisher:Cold Spring Harbor Laboratory Press
ISSN:0091-7451
Publisher DOI:10.1101/sqb.2000.65.467
PubMed ID:12760063

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