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Telomere length, ATM mutation status and cancer risk in Ataxia-Telangiectasia families.
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- Open access
- 5.19 M
Renault, Anne-Laure
Mebirouk, Noura
Cavaciuti, Eve
Le Gal, Dorothée
Lecarpentier, Julie
d'Enghien, Catherine Dubois
Laugé, Anthony
Dondon, Marie-Gabrielle
Labbé, Martine
Lesca, Gaetan
Leroux, Dominique
Gladieff, Laurence
Adenis, Claude
Faivre, Laurence
Gilbert-Dussardier, Brigitte
Lortholary, Alain
Fricker, Jean-Pierre
Dahan, Karin
[UCL]
Bay, Jacques-Olivier
Longy, Michel
Buecher, Bruno
Janin, Nicolas
[UCL]
Zattara, Hélène
Berthet, Pascaline
Combès, Audrey
Coupier, Isabelle
CoF-AT study collaborators
Hall, Janet
Stoppa-Lyonnet, Dominique
Andrieu, Nadine
Lesueur, Fabienne
Recent studies have linked constitutive telomere length (TL) to aging-related diseases including cancer at different sites. ATM participates in the signaling of telomere erosion, and inherited mutations in ATM have been associated with increased risk of cancer, particularly breast cancer. The goal of this study was to investigate whether carriage of an ATM mutation and TL interplay to modify cancer risk in ataxia-telangiectasia (A-T) families.The study population consisted of 284 heterozygous ATM mutation carriers (HetAT) and 174 non-carriers (non-HetAT) from 103 A-T families. Forty-eight HetAT and 14 non-HetAT individuals had cancer, among them 25 HetAT and 6 non-HetAT were diagnosed after blood sample collection. We measured mean TL using a quantitative PCR assay and genotyped seven single-nucleotide polymorphisms (SNPs) recurrently associated with TL in large population-based studies.HetAT individuals were at increased risk of cancer (OR = 2.3, 95%CI = 1.2-4.4, P = 0.01), and particularly of breast cancer for women (OR = 2.9, 95%CI = 1.2-7.1, P = 0.02), in comparison to their non-HetAT relatives. HetAT individuals had longer telomeres than non-HetAT individuals (P = 0.0008) but TL was not associated with cancer risk, and no significant interaction was observed between ATM mutation status and TL. Furthermore, rs9257445 (ZNF311) was associated with TL in HetAT subjects and rs6060627 (BCL2L1) modified cancer risk in HetAT and non-HetAT women.Our findings suggest that carriage of an ATM mutation impacts on the age-related TL shortening and that TL per se is not related to cancer risk in ATM carriers. TL measurement alone is not a good marker for predicting cancer risk in A-T families.
| Document type | Article de périodique (Journal article) – Article de recherche |
|---|---|
| Access type | Accès libre |
| Publication date | 2017 |
| Language | Anglais |
| Journal information | "Carcinogenesis : integrative cancer research" - Vol. 38, no.10, p. 994-1003 (2017) |
| Peer reviewed | yes |
| Publisher | Oxford University Press ((United Kingdom) Oxford) |
| issn | 0143-3334 |
| e-issn | 1460-2180 |
| Publication status | Publié |
| Affiliations |
UCL
- (SLuc) Service de néphrologie UCL - (SLuc) Centre de génétique médicale UCL |
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| Bibliographic reference | Renault, Anne-Laure ; Mebirouk, Noura ; Cavaciuti, Eve ; Le Gal, Dorothée ; Lecarpentier, Julie ; et. al. Telomere length, ATM mutation status and cancer risk in Ataxia-Telangiectasia families.. In: Carcinogenesis : integrative cancer research, Vol. 38, no.10, p. 994-1003 (2017) |
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| Permanent URL | http://hdl.handle.net/2078.1/201660 |