1. Academic Validation
  2. [Cell cycle, mitosis and therapeutic applications]

[Cell cycle, mitosis and therapeutic applications]

  • Bull Cancer. 2011 Oct;98(9):1037-45. doi: 10.1684/bdc.2011.1382.
Antonin Levy 1 Laurence Albiges-Sauvin Christophe Massard Jean-Charles Soria Eric Deutsch
Affiliations

Affiliation

  • 1 Institut Gustave-Roussy, service de radiothérapie oncologie, université Paris-XI, Villejuif, France. [email protected]
Abstract

Genomic DNA is constantly under stress of endogenous and exogenous DNA damaging agents. Without proper care, the DNA damage causes an alteration of the genomic structure and can lead to cell death or the occurrence of mutations involved in tumorigenesis. During the process of evolution, organisms have acquired a series of response mechanisms and repair of DNA damage, thereby ensuring the maintenance of genome stability and faithful transmission of genetic information. The checkpoints are the major mechanisms by which a cell can respond to DNA damage, either by actively stopping the cell cycle or by induction of Apoptosis. Two parallel signalling pathways, ATM and ATR respond to genotoxic stress by activating their downstream target proteins including the two effectors kinases Chk1 and Chk2. Promising preliminary data render these proteins potential targets for therapeutic development against Cancer.

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