Evidence map›Paper›PMID 26901439›Full record

ArticleeLife2016

Mitochondrial DNA copy number variation across human cancers.

Ed Reznik, Martin L Miller, Yasin Şenbabaoğlu, Nadeem Riaz, Judy Sarungbam, Satish K Tickoo, Hikmat A Al-Ahmadie, William Lee, Venkatraman E Seshan, A Ari Hakimi and 1 more

Abstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 317 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
317citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

317 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
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  17. Mitochondrial function meets oncology: the multifaceted role of TFAM across cancer types.Apoptosis : an international journal on programmed cell death · 2026
    Review
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257 more citing papers are in PubMed but not listed here.

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

11 authors.

Ed ReznikComputational Biology Program, Memorial Sloan Kettering Cancer Center, New York, United States.ORCID http://orcid.org/0000-0002-6511-5947
Martin L MillerCancer Research UK, Cambridge Institute, Cambridge, United Kingdom.
Yasin ŞenbabaoğluComputational Biology Program, Memorial Sloan Kettering Cancer Center, New York, United States.ORCID http://orcid.org/0000-0003-0958-958X
Nadeem RiazDepartment of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, United States.
Judy SarungbamDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, United States.
Satish K TickooDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, United States.
Hikmat A Al-AhmadieDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, United States.
William LeeComputational Biology Program, Memorial Sloan Kettering Cancer Center, New York, United States.
Venkatraman E SeshanDepartment of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, United States.
A Ari HakimiComputational Biology Program, Memorial Sloan Kettering Cancer Center, New York, United States.
Chris SanderComputational Biology Program, Memorial Sloan Kettering Cancer Center, New York, United States.

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Cancer Research UK 21141NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

Mutations, deletions, and changes in copy number of mitochondrial DNA (mtDNA), are observed throughout cancers. Here, we survey mtDNA copy number variation across 22 tumor types profiled by The Cancer Genome Atlas project. We observe a tendency for some cancers, especially of the bladder, breast, and kidney, to be depleted of mtDNA, relative to matched normal tissue. Analysis of genetic context reveals an association between incidence of several somatic alterations, including IDH1 mutations in gliomas, and mtDNA content. In some but not all cancer types, mtDNA content is correlated with the expression of respiratory genes, and anti-correlated to the expression of immune response and cell-cycle genes. In tandem with immunohistochemical evidence, we find that some tumors may compensate for mtDNA depletion to sustain levels of respiratory proteins. Our results highlight the extent of mtDNA copy number variation in tumors and point to related therapeutic opportunities.

Indexed as

DNA Copy Number VariationsDNA, MitochondrialHumansImmunohistochemistryNeoplasmsPathology, MolecularDNA, Mitochondrialcancercomputational biologycopy numberhumanhuman biologymedicinemetabolismmitochondriamtDNAsequencingsystems biology

Identifiers

PMID26901439
PMCPMC4775221

What OpenQuestion holds

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LicenceCC BY
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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.