Evidence map›Paper›PMID 28357528›Full record

Trial reportCancer causes & control : CCC2017

A prospective study of mitochondrial DNA copy number and the risk of prostate cancer.

Amy Moore, Qing Lan, Jonathan N Hofmann, Chin-San Liu, Wen-Ling Cheng, Ta-Tsung Lin, Sonja I Berndt

Open access · greenAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Cancer causes & control : CCC, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Cancer epithelia-derived mitochondrial DNA is a targetable initiator of a paracrine signaling loop that confers taxane resistance.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  9. Article
  10. Mitochondrial DNA Copy-Number Variation and Pancreatic Cancer Risk in the Prospective EPIC Cohort.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2020
    Article
  11. Review
  12. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Amy MooreDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA. amy.moore@nih.gov.
Qing LanDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Jonathan N HofmannDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Chin-San LiuVascular and Genomic Research Center, Changhua Christian Hospital, 7F No. 235, Syuguang Rd., Changhua, 500, Taiwan.
Wen-Ling ChengVascular and Genomic Research Center, Changhua Christian Hospital, 7F No. 235, Syuguang Rd., Changhua, 500, Taiwan.
Ta-Tsung LinVascular and Genomic Research Center, Changhua Christian Hospital, 7F No. 235, Syuguang Rd., Changhua, 500, Taiwan.
Sonja I BerndtDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Changhua Christian Hospital · TWNational Cancer Institute · USNational Institutes of Health · US

Funding

Etiologic Studies of Prostate CancerZIACP010221 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI ALBANES, DEMETRIUS · 2011 to 2019
$4.1M
Intramural NIH HHS ZIA CP010221
6 · The paper itself

Abstract

purposeEvidence suggests that mitochondrial DNA (mtDNA) copy number increases in response to DNA damage. Increased mtDNA copy number has been observed in prostate cancer (PCa) cells, suggesting a role in PCa development, but this association has not yet been investigated prospectively.

methodsWe conducted a nested case-control study (793 cases and 790 controls) of men randomized to the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) to evaluate the association between pre-diagnosis mtDNA copy number, measured in peripheral blood leukocytes, and the risk of PCa. We used logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) and polytomous logistic regression to analyze differences in associations by non-aggressive (Stage I/II AND Gleason grade < 8) or aggressive (Stage III/IV OR Gleason grade ≥ 8) PCa.

resultsAlthough mtDNA copy number was not significantly associated with PCa risk overall (OR 1.23, 95% CI 0.97-1.55, p = 0.089), increasing mtDNA copy number was associated with an increased risk of non-aggressive PCa (OR 1.29, 95% CI 1.01-1.65, p = 0.044) compared to controls. No association was observed with aggressive PCa (OR 1.02, 95% CI 0.64-1.63, p = 0.933). Higher mtDNA copy number was also associated with increased PSA levels among controls (p = 0.014).

conclusionsThese results suggest that alterations in mtDNA copy number may reflect disruption of the normal prostate glandular architecture seen in early-stage disease, as opposed to reflecting the large number of tumor cells seen with advanced PCa.

Indexed as

DNA Copy Number VariationsDNA, MitochondrialAgedCase-Control StudiesDNA DamageHumansMaleMiddle AgedNeoplasm GradingProspective StudiesProstatic NeoplasmsRisk FactorsDNA, MitochondrialCopy numberGeneticsMitochondrial DNAProspectiveProstate cancerRisk factors

Identifiers

PMID28357528
PMCPMC10353756
OpenAlexW2603312965

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.