Evidence map›Paper›PMID 25594021›Full record

ArticleOncoscience2014

Damaged mitochondria in Fanconi anemia - an isolated event or a general phenomenon?

Giovanni Pagano, Pavithra Shyamsunder, Rama S Verma, Alex Lyakhovich

Open access · bronzeAbstract read
In one paragraph

Article in Oncoscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
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  4. FANCL supports Parkin-mediated mitophagy in a ubiquitin ligase-independent manner.Biochimica et biophysica acta. Molecular basis of disease · 2022
    Article
  5. Mitochondrial DNA Instability in Mammalian Cells.Antioxidants & redox signaling · 2022
    Review
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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

4 authors at 2 institutions in 4 countries.

Giovanni PaganoItalian National Cancer Institute, G Pascale Foundation, CROM, Mercogliano, AV, Italy.
Pavithra ShyamsunderStem Cell and Molecular Biology laboratory, Department of Biotechnology, Indian Institute of Technology Madras, Chennai.
Rama S VermaStem Cell and Molecular Biology laboratory, Department of Biotechnology, Indian Institute of Technology Madras, Chennai.
Alex LyakhovichDuke-NUS Graduate Medical School, Singapore ; Novosibirsk Institute of Molecular Biology and Biophysics, Russian Federation ; Queen's University Belfast, UK.
Indian Institute of Technology Madras · INInstitute of Molecular Biology and Biophysics · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fanconi anemia (FA) is known as an inherited bone marrow failure syndrome associated with cancer predisposition and susceptibility to a number of DNA damaging stimuli, along with a number of clinical features such as upper limb malformations, increased diabetes incidence and typical anomalies in skin pigmentation. The proteins encoded by FA-defective genes (FANC proteins) display well-established roles in DNA damage and repair pathways. Moreover, some independent studies have revealed that mitochondrial dysfunction (MDF) is also involved in FA phenotype. Unconfined to FA, we have shown that other syndromes featuring DNA damage and repair (such as ataxia-telangiectasia, AT, and Werner syndrome, WS) display MDF-related phenotypes, along with oxidative stress (OS) that, altogether, may play major roles in these diseases. Experimental and clinical studies are warranted in the prospect of future therapies to be focused on compounds scavenging reactive oxygen species (ROS) as well as protecting mitochondrial functions.

Indexed as

DNA damage and repairFanconi anemiamitochondrial dysfunctionoxidative stressreactive oxygen species

Identifiers

PMID25594021
PMCPMC4278298
OpenAlexW2145239383

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Registered trials

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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.