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01.12.2018 | Research article | Ausgabe 1/2018 Open Access

Breast Cancer Research 1/2018

Mitochondrial DNA copy number variation, leukocyte telomere length, and breast cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) study

Zeitschrift:
Breast Cancer Research > Ausgabe 1/2018
Autoren:
Daniele Campa, Myrto Barrdahl, Aurelia Santoro, Gianluca Severi, Laura Baglietto, Hanane Omichessan, Rosario Tumino, H. B(as). Bueno-de-Mesquita, Petra H. Peeters, Elisabete Weiderpass, Maria-Dolores Chirlaque, Miguel Rodríguez-Barranco, Antonio Agudo, Marc Gunter, Laure Dossus, Vittorio Krogh, Giuseppe Matullo, Antonia Trichopoulou, Ruth C. Travis, Federico Canzian, Rudolf Kaaks
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Electronic supplementary material

The online version of this article (https://​doi.​org/​10.​1186/​s13058-018-0955-5) contains supplementary material, which is available to authorized users.

Abstract

Background

Leukocyte telomere length (LTL) and mitochondrial genome (mtDNA) copy number and deletions have been proposed as risk markers for various cancer types, including breast cancer (BC).

Methods

To gain a more comprehensive picture on how these markers can modulate BC risk, alone or in conjunction, we performed simultaneous measurements of LTL and mtDNA copy number in up to 570 BC cases and 538 controls from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. As a first step, we measured LTL and mtDNA copy number in 96 individuals for which a blood sample had been collected twice with an interval of 15 years.

Results

According to the intraclass correlation (ICC), we found very good stability over the time period for both measurements, with ICCs of 0.63 for LTL and 0.60 for mtDNA copy number. In the analysis of the entire study sample, we observed that longer LTL was strongly associated with increased risk of BC (OR 2.71, 95% CI 1.58–4.65, p = 3.07 × 10− 4 for highest vs. lowest quartile; OR 3.20, 95% CI 1.57–6.55, p = 1.41 × 10− 3 as a continuous variable). We did not find any association between mtDNA copy number and BC risk; however, when considering only the functional copies, we observed an increased risk of developing estrogen receptor-positive BC (OR 2.47, 95% CI 1.05–5.80, p = 0.04 for highest vs. lowest quartile).

Conclusions

We observed a very good correlation between the markers over a period of 15 years. We confirm a role of LTL in BC carcinogenesis and suggest an effect of mtDNA copy number on BC risk.
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