Authors
Sabine AS Langie, Gudrun Koppen, Daniel Desaulniers, Fahd Al-Mulla, Rabeah Al-Temaimi, Amedeo Amedei, Amaya Azqueta, William H Bisson, Dustin Brown, Gunnar Brunborg, Amelia K Charles, Tao Chen, Annamaria Colacci, Firouz Darroudi, Stefano Forte, Laetitia Gonzalez, Roslida A Hamid, Lisbeth E Knudsen, Luc Leyns, Adela Lopez de Cerain Salsamendi, Lorenzo Memeo, Chiara Mondello, Carmel Mothersill, Ann-Karin Olsen, Sofia Pavanello, Jayadev Raju, Emilio Rojas, Rabindra Roy, Elizabeth Ryan, Patricia Ostrosky-Wegman, Hosni K Salem, A Ivana Scovassi, Neetu Singh, Monica Vaccari, Frederik J Van Schooten, Mahara Valverde, Jordan Woodrick, Luoping Zhang, Nik van Larebeke, Micheline Kirsch-Volders, Andrew R Collins
Publication date
2015/6/1
Source
Carcinogenesis
Volume
36
Issue
Suppl_1
Pages
S61-S88
Publisher
Oxford University Press
Description
Genome instability is a prerequisite for the development of cancer. It occurs when genome maintenance systems fail to safeguard the genome’s integrity, whether as a consequence of inherited defects or induced via exposure to environmental agents (chemicals, biological agents and radiation). Thus, genome instability can be defined as an enhanced tendency for the genome to acquire mutations; ranging from changes to the nucleotide sequence to chromosomal gain, rearrangements or loss. This review raises the hypothesis that in addition to known human carcinogens, exposure to low dose of other chemicals present in our modern society could contribute to carcinogenesis by indirectly affecting genome stability. The selected chemicals with their mechanisms of action proposed to indirectly contribute to genome instability are: heavy metals (DNA repair, epigenetic modification, DNA damage signaling …
Scholar articles
SAS Langie, G Koppen, D Desaulniers, F Al-Mulla… - Carcinogenesis, 2015