Mitochondrial DNA copy number and future risk of B-cell lymphoma in a nested case-control study in the prospective EPIC cohort.
(2014) In Blood 124(4). p.530-535- Abstract
- It has been suggested that mitochondrial dysfunction and DNA damage are involved in lymphomagenesis. Increased copy number of mitochondrial DNA (mtDNA) as a compensatory mechanism of mitochondrial dysfunction previously has been associated with B-cell lymphomas, in particular chronic lymphocytic leukemia (CLL). However, current evidence is limited and based on a relatively small number of cases. Using a nested case-control study, we extended these findings with a focus on subtype specific analyses. Relative mtDNA copy number was measured in the buffy coat of prospectively collected blood of 469 lymphoma cases and 469 matched controls. The association between mtDNA copy number and the risk of developing lymphoma and histologic subtypes was... (More)
- It has been suggested that mitochondrial dysfunction and DNA damage are involved in lymphomagenesis. Increased copy number of mitochondrial DNA (mtDNA) as a compensatory mechanism of mitochondrial dysfunction previously has been associated with B-cell lymphomas, in particular chronic lymphocytic leukemia (CLL). However, current evidence is limited and based on a relatively small number of cases. Using a nested case-control study, we extended these findings with a focus on subtype specific analyses. Relative mtDNA copy number was measured in the buffy coat of prospectively collected blood of 469 lymphoma cases and 469 matched controls. The association between mtDNA copy number and the risk of developing lymphoma and histologic subtypes was examined using logistic regression models. We found no overall association between mtDNA and risk of lymphoma. Subtype analyses revealed, significant increased risks of CLL (n=102) with increasing mtDNA copy number (OR=1.34, 1.44 and 1.80 for quartiles 2-4, respectively P-trend=0.001). mtDNA copy number was not associated with follow-up time suggesting that this observation is not strongly influenced by indolent disease status. This study substantially strengthens the evidence that mtDNA copy number is related to risk of CLL and supports the importance of mitochondrial dysfunction as a possible mechanistic pathway in CLL ontogenesis. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4529164
- author
- organization
- publishing date
- 2014
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Blood
- volume
- 124
- issue
- 4
- pages
- 530 - 535
- publisher
- American Society of Hematology
- external identifiers
-
- pmid:24899624
- wos:000342619600016
- scopus:84904892128
- pmid:24899624
- ISSN
- 1528-0020
- DOI
- 10.1182/blood-2013-10-532085
- language
- English
- LU publication?
- yes
- id
- 39c3420c-566c-4f24-879b-c3929d10ccd7 (old id 4529164)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/24899624?dopt=Abstract
- date added to LUP
- 2016-04-01 10:17:38
- date last changed
- 2022-04-27 20:39:12
@article{39c3420c-566c-4f24-879b-c3929d10ccd7,
abstract = {{It has been suggested that mitochondrial dysfunction and DNA damage are involved in lymphomagenesis. Increased copy number of mitochondrial DNA (mtDNA) as a compensatory mechanism of mitochondrial dysfunction previously has been associated with B-cell lymphomas, in particular chronic lymphocytic leukemia (CLL). However, current evidence is limited and based on a relatively small number of cases. Using a nested case-control study, we extended these findings with a focus on subtype specific analyses. Relative mtDNA copy number was measured in the buffy coat of prospectively collected blood of 469 lymphoma cases and 469 matched controls. The association between mtDNA copy number and the risk of developing lymphoma and histologic subtypes was examined using logistic regression models. We found no overall association between mtDNA and risk of lymphoma. Subtype analyses revealed, significant increased risks of CLL (n=102) with increasing mtDNA copy number (OR=1.34, 1.44 and 1.80 for quartiles 2-4, respectively P-trend=0.001). mtDNA copy number was not associated with follow-up time suggesting that this observation is not strongly influenced by indolent disease status. This study substantially strengthens the evidence that mtDNA copy number is related to risk of CLL and supports the importance of mitochondrial dysfunction as a possible mechanistic pathway in CLL ontogenesis.}},
author = {{Saberi Hosnijeh, Fatemeh and Lan, Qing and Rothman, Nathaniel and Liu, Chin San and Cheng, Wen-Ling and Nieters, Alexandra and Guldberg, Per and Tjønneland, Anne and Campa, Daniele and Martino, Alessandro and Boeing, Heiner and Trichopoulou, Antonia and Lagiou, Pagona and Trichopoulos, Dimitrios and Krogh, Vittorio and Tumino, Rosario and Panico, Salvatore and Masala, Giovanna and Weiderpass, Elisabete and Huerta Castaño, José María and Ardanaz, Eva and Sala, Núria and Dorronsoro, Miren and Quirós, J Ramón and Sánchez, María-José and Melin, Beatrice and Johansson, Ann Sofie and Malm, Johan and Borgquist, Signe and Peeters, Petra H and Bueno-de-Mesquita, H Bas and Wareham, Nick and Khaw, Kay-Tee and Travis, Ruth C and Brennan, Paul and Siddiq, Afshan and Riboli, Elio and Vineis, Paolo and Vermeulen, Roel}},
issn = {{1528-0020}},
language = {{eng}},
number = {{4}},
pages = {{530--535}},
publisher = {{American Society of Hematology}},
series = {{Blood}},
title = {{Mitochondrial DNA copy number and future risk of B-cell lymphoma in a nested case-control study in the prospective EPIC cohort.}},
url = {{http://dx.doi.org/10.1182/blood-2013-10-532085}},
doi = {{10.1182/blood-2013-10-532085}},
volume = {{124}},
year = {{2014}},
}