Abstract |
Maintaining the genetic integrity is a key process in cell viability and is enabled by a wide network of repair pathways. When this system is defective, it generates genomic instability and results in an accumulation of chromosomal aberrations and mutations that may be responsible for various clinical phenotypes, including susceptibility to develop cancer. Indeed, these defects can promote not only the initiation of cancer, but also allow the tumor cells to rapidly acquire mutations during their evolution. Several genes are involved in these damage repair systems and particular polymorphisms are predictive of the onset of cancer, the best described of them being BRCA. In addition to its impact on carcinogenesis, the DNA damage repair system is now considered as a therapeutic target of choice for cancer treatment, as monotherapy or in combination with other cytotoxic therapies, such as chemotherapies or radiotherapy. PARP inhibitors are nowadays the best known, but other agents are emerging in the field of clinical research. The enthusiasm in this area is coupled with promising results and a successful collaboration between clinicians and biologists would allow to optimize treatment plans in order to take full advantage of the DNA repair system modulation.
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Authors | Chloé Rancoule, Alexis Vallard, Jean-Baptiste Guy, Sophie Espenel, Sylvie Sauvaigo, Claire Rodriguez-Lafrasse, Nicolas Magné |
Journal | Bulletin du cancer
(Bull Cancer)
Vol. 104
Issue 11
Pg. 962-970
(Nov 2017)
ISSN: 1769-6917 [Electronic] France |
Vernacular Title | Altération de la réparation de l’ADN et cancer. |
PMID | 29132683
(Publication Type: Journal Article, Review)
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Copyright | Copyright © 2017 Société Française du Cancer. Published by Elsevier Masson SAS. All rights reserved. |
Chemical References |
- Antineoplastic Agents
- DNA, Neoplasm
- Neoplasm Proteins
- Poly(ADP-ribose) Polymerase Inhibitors
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Topics |
- Antineoplastic Agents
(pharmacology, therapeutic use)
- Cell Transformation, Neoplastic
(genetics)
- Clinical Trials, Phase III as Topic
- Combined Modality Therapy
- DNA Damage
- DNA Repair
(drug effects)
- DNA, Neoplasm
(drug effects, genetics)
- Humans
- Molecular Targeted Therapy
- Mutation
- Neoplasm Proteins
(antagonists & inhibitors, physiology)
- Neoplasms
(drug therapy, etiology, genetics, therapy)
- Poly(ADP-ribose) Polymerase Inhibitors
(pharmacology, therapeutic use)
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