Evidence map›Paper›PMID 42165669›Full record

ArticleCancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology2026

Mitochondrial DNA Breaks and Copy Number and the Risk of Lung Cancer in the Shanghai Women's Health Study.

Batel Blechter, Xiao-Ou Shu, Wei Hu, Elizabeth R Francis, Wei Zheng, Qiuyin Cai, Hui Cai, Gong Yang, H Dean Hosgood, Richard M Cawthon and 1 more

Abstract read
In one paragraph

Article in Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Batel BlechterDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland.ORCID 0000-0001-7610-2554
Xiao-Ou ShuDivision of Epidemiology, Department of Medicine, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee.ORCID 0000-0002-0711-8314
Wei HuDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland.ORCID 0000-0002-4138-7905
Elizabeth R FrancisDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland.ORCID 0009-0003-7851-4175
Wei ZhengDivision of Epidemiology, Department of Medicine, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee.ORCID 0000-0003-1226-070X
Qiuyin CaiDivision of Epidemiology, Department of Medicine, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee.ORCID 0000-0002-9384-5648
Hui CaiDivision of Epidemiology, Department of Medicine, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee.ORCID 0000-0002-2388-1694
Gong YangDivision of Epidemiology, Department of Medicine, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee.ORCID 0000-0002-7006-5825
H Dean HosgoodDepartment of Epidemiology and Population Health, Albert Einstein College of Medicine, New York, New York.ORCID 0000-0003-4151-1133
Richard M CawthonHuman Genetics, University of Utah, Salt Lake City, Utah.ORCID 0000-0001-6073-9112
Qing LanDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland.ORCID 0000-0002-0888-8839

Funding

Intramural NIH HHS Z99 CA999999Intramural Research Program (IRP)
6 · The paper itself

Abstract

backgroundLung cancer remains the leading cause of cancer mortality worldwide, and approximately one quarter of cases occur among individuals who never smoke. Mitochondria are highly susceptible to oxidative damage from environmental stressors, which can alter mitochondrial DNA (mtDNA) copy number (mtDNAcn) and induce mtDNA fragmentation. Although prior studies of mtDNAcn and lung cancer have yielded inconsistent results, the role of mtDNA fragmentation has not been examined.

methodsWe conducted a nested case-control study within the prospective Shanghai Women's Health Study, including 789 incident lung cancer cases among never-smoking women and 789 individually matched controls. Prediagnostic whole-blood samples were analyzed for mtDNA fraction with breaks (mtDNAfb) and mtDNAcn using high-throughput quantitative PCR assays. Conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) for lung cancer risk associated with mtDNAfb and mtDNAcn, adjusting for age, body mass index, and plate. We further assessed an interaction between mtDNAfb and mtDNAcn.

resultsHigher mtDNAfb was inversely associated with lung cancer risk, with 34% lower odds among participants with high mtDNAfb compared with those with low mtDNAfb (OR = 0.66; 95% CI, 0.51-0.85). Notably, a significant interaction was observed between mtDNAfb and mtDNAcn (P interaction = 8.3 × 10-6), with a stronger inverse association between mtDNAfb and lung cancer among women with low mtDNAcn.

conclusionsLower mtDNA fragmentation is associated with increased lung cancer risk among never-smoking women, particularly among those with low mtDNAcn. IMPACT: mtDNA fragmentation may represent a novel biomarker of impaired mitochondrial response to oxidative stress relevant to lung carcinogenesis.

Indexed as

DNA Copy Number VariationsDNA, MitochondrialLung NeoplasmsAgedCase-Control StudiesChinaFemaleHumansMiddle AgedProspective StudiesRisk FactorsWomen's HealthDNA, Mitochondrial

Identifiers

PMID42165669
PMCPMC13274563

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.