Causes of genome instability: the effect of low dose chemical exposures in modern society

Sabine A S Langie; Gudrun Koppen; Daniel Desaulniers; Fahd Al-Mulla; Rabeah Al-Temaimi; Amedeo Amedei; Amaya Azqueta; William H Bisson; Dustin G 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 P 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

doi:10.1093/carcin/bgv031

Causes of genome instability: the effect of low dose chemical exposures in modern society

Sabine A S Langie, Gudrun Koppen, Daniel Desaulniers, Fahd Al-Mulla, Rabeah Al-Temaimi, Amedeo Amedei, Amaya Azqueta, William H Bisson, Dustin G 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 SalsamendiLorenzo Memeo, Chiara Mondello, Carmel Mothersill, Ann-Karin Olsen, Sofia Pavanello, Jayadev Raju, Emilio Rojas, Rabindra Roy, Elizabeth P 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

80 Citationer (Scopus)

Abstract

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, telomere length), acrylamide (DNA repair, chromosome segregation), bisphenol A (epigenetic modification, DNA damage signaling, mitochondrial function, chromosome segregation), benomyl (chromosome segregation), quinones (epigenetic modification) and nano-sized particles (epigenetic pathways, mitochondrial function, chromosome segregation, telomere length). The purpose of this review is to describe the crucial aspects of genome instability, to outline the ways in which environmental chemicals can affect this cancer hallmark and to identify candidate chemicals for further study. The overall aim is to make scientists aware of the increasing need to unravel the underlying mechanisms via which chemicals at low doses can induce genome instability and thus promote carcinogenesis.

Originalsprog	Engelsk
Tidsskrift	Carcinogenesis
Vol/bind	36
Udgave nummer	Supplement 1
Sider (fra-til)	S61-S88
Antal sider	28
ISSN	0143-3334
DOI	https://doi.org/10.1093/carcin/bgv031
Status	Udgivet - 1 jun. 2015

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Langie, S. A. S., Koppen, G., Desaulniers, D., Al-Mulla, F., Al-Temaimi, R., Amedei, A., Azqueta, A., Bisson, W. H., Brown, D. G., Brunborg, G., Charles, A. K., Chen, T., Colacci, A., Darroudi, F., Forte, S., Gonzalez, L., Hamid, R. A., Knudsen, L. E., Leyns, L., ... Collins, A. R. (2015). Causes of genome instability: the effect of low dose chemical exposures in modern society. Carcinogenesis, 36(Supplement 1), S61-S88. https://doi.org/10.1093/carcin/bgv031

Langie, SAS, Koppen, G, Desaulniers, D, Al-Mulla, F, Al-Temaimi, R, Amedei, A, Azqueta, A, Bisson, WH, Brown, DG, Brunborg, G, Charles, AK, Chen, T, Colacci, A, Darroudi, F, Forte, S, Gonzalez, L, Hamid, RA, Knudsen, LE, Leyns, L, Lopez de Cerain Salsamendi, A, Memeo, L, Mondello, C, Mothersill, C, Olsen, A-K, Pavanello, S, Raju, J, Rojas, E, Roy, R, Ryan, EP, Ostrosky-Wegman, P, Salem, HK, Scovassi, AI, Singh, N, Vaccari, M, Van Schooten, FJ, Valverde, M, Woodrick, J, Zhang, L, van Larebeke, N, Kirsch-Volders, M & Collins, AR 2015, 'Causes of genome instability: the effect of low dose chemical exposures in modern society', Carcinogenesis, bind 36, nr. Supplement 1, s. S61-S88. https://doi.org/10.1093/carcin/bgv031

@article{8582b1a7abbd4503861b4e531511ad44,

title = "Causes of genome instability: the effect of low dose chemical exposures in modern society",

abstract = "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, telomere length), acrylamide (DNA repair, chromosome segregation), bisphenol A (epigenetic modification, DNA damage signaling, mitochondrial function, chromosome segregation), benomyl (chromosome segregation), quinones (epigenetic modification) and nano-sized particles (epigenetic pathways, mitochondrial function, chromosome segregation, telomere length). The purpose of this review is to describe the crucial aspects of genome instability, to outline the ways in which environmental chemicals can affect this cancer hallmark and to identify candidate chemicals for further study. The overall aim is to make scientists aware of the increasing need to unravel the underlying mechanisms via which chemicals at low doses can induce genome instability and thus promote carcinogenesis.",

keywords = "Animals, Carcinogenesis, Carcinogens, Environmental, Environmental Exposure, Genomic Instability, Hazardous Substances, Humans, Neoplasms",

author = "Langie, {Sabine A S} and Gudrun Koppen and Daniel Desaulniers and Fahd Al-Mulla and Rabeah Al-Temaimi and Amedeo Amedei and Amaya Azqueta and Bisson, {William H} and Brown, {Dustin G} and Gunnar Brunborg and Charles, {Amelia K} and Tao Chen and Annamaria Colacci and Firouz Darroudi and Stefano Forte and Laetitia Gonzalez and Hamid, {Roslida A} and Knudsen, {Lisbeth E} and Luc Leyns and {Lopez de Cerain Salsamendi}, Adela and Lorenzo Memeo and Chiara Mondello and Carmel Mothersill and Ann-Karin Olsen and Sofia Pavanello and Jayadev Raju and Emilio Rojas and Rabindra Roy and Ryan, {Elizabeth P} and Patricia Ostrosky-Wegman and Salem, {Hosni K} and Scovassi, {A Ivana} and Neetu Singh and Monica Vaccari and {Van Schooten}, {Frederik J} and Mahara Valverde and Jordan Woodrick and Luoping Zhang and {van Larebeke}, Nik and Micheline Kirsch-Volders and Collins, {Andrew R}",

year = "2015",

month = jun,

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doi = "10.1093/carcin/bgv031",

language = "English",

volume = "36",

pages = "S61--S88",

journal = "Carcinogenesis",

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T1 - Causes of genome instability

T2 - the effect of low dose chemical exposures in modern society

AU - Langie, Sabine A S

AU - Koppen, Gudrun

AU - Desaulniers, Daniel

AU - Al-Mulla, Fahd

AU - Al-Temaimi, Rabeah

AU - Amedei, Amedeo

AU - Azqueta, Amaya

AU - Bisson, William H

AU - Brown, Dustin G

AU - Brunborg, Gunnar

AU - Charles, Amelia K

AU - Chen, Tao

AU - Colacci, Annamaria

AU - Darroudi, Firouz

AU - Forte, Stefano

AU - Gonzalez, Laetitia

AU - Hamid, Roslida A

AU - Knudsen, Lisbeth E

AU - Leyns, Luc

AU - Lopez de Cerain Salsamendi, Adela

AU - Memeo, Lorenzo

AU - Mondello, Chiara

AU - Mothersill, Carmel

AU - Olsen, Ann-Karin

AU - Pavanello, Sofia

AU - Raju, Jayadev

AU - Rojas, Emilio

AU - Roy, Rabindra

AU - Ryan, Elizabeth P

AU - Ostrosky-Wegman, Patricia

AU - Salem, Hosni K

AU - Scovassi, A Ivana

AU - Singh, Neetu

AU - Vaccari, Monica

AU - Van Schooten, Frederik J

AU - Valverde, Mahara

AU - Woodrick, Jordan

AU - Zhang, Luoping

AU - van Larebeke, Nik

AU - Kirsch-Volders, Micheline

AU - Collins, Andrew R

PY - 2015/6/1

Y1 - 2015/6/1

N2 - 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, telomere length), acrylamide (DNA repair, chromosome segregation), bisphenol A (epigenetic modification, DNA damage signaling, mitochondrial function, chromosome segregation), benomyl (chromosome segregation), quinones (epigenetic modification) and nano-sized particles (epigenetic pathways, mitochondrial function, chromosome segregation, telomere length). The purpose of this review is to describe the crucial aspects of genome instability, to outline the ways in which environmental chemicals can affect this cancer hallmark and to identify candidate chemicals for further study. The overall aim is to make scientists aware of the increasing need to unravel the underlying mechanisms via which chemicals at low doses can induce genome instability and thus promote carcinogenesis.

AB - 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, telomere length), acrylamide (DNA repair, chromosome segregation), bisphenol A (epigenetic modification, DNA damage signaling, mitochondrial function, chromosome segregation), benomyl (chromosome segregation), quinones (epigenetic modification) and nano-sized particles (epigenetic pathways, mitochondrial function, chromosome segregation, telomere length). The purpose of this review is to describe the crucial aspects of genome instability, to outline the ways in which environmental chemicals can affect this cancer hallmark and to identify candidate chemicals for further study. The overall aim is to make scientists aware of the increasing need to unravel the underlying mechanisms via which chemicals at low doses can induce genome instability and thus promote carcinogenesis.

KW - Animals

KW - Carcinogenesis

KW - Carcinogens, Environmental

KW - Environmental Exposure

KW - Genomic Instability

KW - Hazardous Substances

KW - Humans

KW - Neoplasms

U2 - 10.1093/carcin/bgv031

DO - 10.1093/carcin/bgv031

M3 - Review

C2 - 26106144

SN - 0143-3334

VL - 36

SP - S61-S88

JO - Carcinogenesis

JF - Carcinogenesis

IS - Supplement 1

ER -

Causes of genome instability: the effect of low dose chemical exposures in modern society

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