Journal
BLOOD
Volume 124, Issue 4, Pages 530-535Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2013-10-532085
Keywords
-
Categories
Funding
- 'Europe Against Cancer Programme' of the European Commission (SANCO)
- French League against Cancer (LNCC)
- National Institute for Health and Medical Research (INSERM), France
- Mutuelle Generale de l'Education Nationale (MGEN) (France)
- 3M Co (France)
- Gustave Roussy Institute (IGR) (France)
- General Councils of France (France)
- German Cancer Aid (Germany)
- German Cancer Research Centre (Germany)
- German Federal Ministry of Education and Research (Germany)
- Danish Cancer Society (Denmark)
- Health Research Fund (FIS) of the Spanish Ministry of Health [Exp P10710130]
- Regional Government of Andalucia
- Regional Government of Asturias
- Regional Government of Basque Country
- Regional Government of Murcia [6236]
- Regional Government of Navarra
- Catalan Institute of Oncology, La Caixa (Spain) [BM 06-130, RTICC-RD06/0020]
- Cancer Research UK
- Medical Research Council (UK)
- Hellenic Health Foundation (Greece)
- Italian Association for Research on Cancer (Italy)
- Italian National Research Council (Italy)
- Fondazione-Istituto Banco Napoli (Italy)
- Compagnia di San Paolo (Italy)
- Dutch Ministry of Public Health, Welfare and Sports (the Netherlands)
- Dutch Prevention Funds (the Netherlands)
- LK Research Funds (the Netherlands)
- Dutch ZON (Zorg Onderzoek Nederland) (the Netherlands)
- World Cancer Research Fund
- Swedish Cancer Society (Sweden)
- Swedish Scientific Council (Sweden)
- Regional Government of Skane (Sweden)
- European Research Council (Norway)
- Norwegian Research Council (Norway)
- Norwegian Cancer Society (Norway)
- Cancer Research UK [16491, 14136] Funding Source: researchfish
- Medical Research Council [G0401527, G1000143] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0512-10114] Funding Source: researchfish
Ask authors/readers for more resources
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 (odds ratio=1.34, 1.44, and 1.80 for quartiles 2-4, respectively; Ptrend=.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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available