Dataset Information

Mitochondrial DNA copy number and future risk of B-cell lymphoma in a nested case-control study in the prospective EPIC cohort.

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 (odds ratio = 1.34, 1.44, and 1.80 for quartiles 2-4, respectively; P trend = .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.

SUBMITTER: Hosnijeh FS

PROVIDER: S-EPMC4110659 | biostudies-other | 2014 Jul

REPOSITORIES: biostudies-other

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Mitochondrial DNA copy number and future risk of B-cell lymphoma in a nested case-control study in the prospective EPIC cohort.

Hosnijeh Fatemeh Saberi FS Lan Qing Q Rothman Nathaniel N San Liu Chin C Cheng Wen-Ling WL Nieters Alexandra A Guldberg Per P Tjønneland Anne A Campa Daniele D Martino Alessandro A Boeing Heiner H Trichopoulou Antonia A Lagiou Pagona P Trichopoulos Dimitrios D Krogh Vittorio V Tumino Rosario R Panico Salvatore S Masala Giovanna G Weiderpass Elisabete E Huerta Castaño José María JM Ardanaz Eva E Sala Núria N Dorronsoro Miren M Quirós J Ramón JR Sánchez María-José MJ Melin Beatrice B Johansson Ann Sofie AS Malm Johan J Borgquist Signe S Peeters Petra H PH Bueno-de-Mesquita H Bas HB Wareham Nick N Khaw Kay-Tee KT Travis Ruth C RC Brennan Paul P Siddiq Afshan A Riboli Elio E Vineis Paolo P Vermeulen Roel R

Blood 20140604 4

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 analys ...[more]

PMID: 24899624

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Project description:ObjectiveTo determine whether infection with human enterovirus or adenovirus, both common intestinal viruses, predicts development of coeliac disease.DesignCase-control study nested within Norwegian birth cohort recruited between 2001 and 2007 and followed to September 2016.SettingNorwegian population.ParticipantsChildren carrying the HLA genotype DR4-DQ8/DR3-DQ2 conferring increased risk of coeliac disease.ExposuresEnterovirus and adenovirus detected using real time polymerase chain reaction in monthly stool samples from age 3 to 36 months.Main outcome measureCoeliac disease diagnosed according to standard criteria. Coeliac disease antibodies were tested in blood samples taken at age 3, 6, 9, and 12 months and then annually. Adjusted odds ratios from mixed effects logistic regression model were used to assess the relation between viral infections before development of coeliac disease antibodies and coeliac disease.ResultsAmong 220 children, and after a mean of 9.9 (SD 1.6) years, 25 children were diagnosed as having coeliac disease after screening and were matched to two controls each. Enterovirus was found in 370 (17%) of 2135 samples and was significantly more frequent in samples collected before development of coeliac disease antibodies in cases than in controls (adjusted odds ratio 1.49, 95% confidence interval 1.07 to 2.06; P=0.02). The association was restricted to infections after introduction of gluten. High quantity samples (>100 000 copies/μL) (adjusted odds ratio 2.11, 1.24 to 3.60; P=0.01) and long lasting infections (>2 months) (2.16, 1.16 to 4.04; P=0.02) gave higher risk estimates. Both the commonly detected enterovirus species Enterovirus A and Enterovirus B were significantly associated with coeliac disease. The association was not found for infections during or after development of coeliac disease antibodies. Adenovirus was not associated with coeliac disease.ConclusionsIn this longitudinal study, a higher frequency of enterovirus, but not adenovirus, during early childhood was associated with later coeliac disease. The finding adds new information on the role of viral infections in the aetiology of coeliac disease.

Dataset Information

Mitochondrial DNA copy number and future risk of B-cell lymphoma in a nested case-control study in the prospective EPIC cohort.

Publications

Mitochondrial DNA copy number and future risk of B-cell lymphoma in a nested case-control study in the prospective EPIC cohort.

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