Evidence map›Paper›PMID 28499833›Full record

ReviewSeminars in cancer biology2017

Mitochondrial dysfunction in cancer: Potential roles of ATF5 and the mitochondrial UPR.

Pan Deng, Cole M Haynes

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

73 citing papers in PubMed, 119 citations in OpenAlex.

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13 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

2 authors at 1 institution in 1 country.

Pan DengDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 10605, USA; BCMB Allied Program, Weill Cornell Medical College, 1300 York Avenue, New York, New York 10065, USA.
Cole M HaynesDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 10605, USA; BCMB Allied Program, Weill Cornell Medical College, 1300 York Avenue, New York, New York 10065, USA. Electronic address: cole.haynes@umassmed.edu.
Cornell University · US

Funding

MAINTENANCE OF MITOCHONDRIAL PROTEIN FOLDING AS AN AGING EFFECTORR01AG040061 · NIA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HAYNES, COLE M · 2011 to 2020
$3.6M
Coordinated Repair and Regeneration of Defective MitochondriaR37AG047182 · NIA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Cole M Haynes · 2020 to 2026
$3.2M
The Role of the Mitochondrial UPR in Ischemic ProtectionR01HL127891 · NHLBI · UNIVERSITY OF ROCHESTER · PI BROOKES, PAUL S, NEHRKE, KEITH · 2015 to 2018
$2.5M
Coordinated Repair and Regeneration of Defective MitochondriaR01AG047182 · NIA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HAYNES, COLE M · 2015 to 2019
$2.1M
NHLBI NIH HHS R01 HL127891NIA NIH HHS R01 AG040061NIA NIH HHS R01 AG047182NIA NIH HHS R37 AG047182
6 · The paper itself

Abstract

Mitochondria form a cellular network of organelles, or cellular compartments, that efficiently couple nutrients to energy production in the form of ATP. As cancer cells rely heavily on glycolysis, historically mitochondria and the cellular pathways in place to maintain mitochondrial activities were thought to be more relevant to diseases observed in non-dividing cells such as muscles and neurons. However, more recently it has become clear that cancers rely heavily on mitochondrial activities including lipid, nucleotide and amino acid synthesis, suppression of mitochondria-mediated apoptosis as well as oxidative phosphorylation (OXPHOS) for growth and survival. Considering the variety of conditions and stresses that cancer cell mitochondria may incur such as hypoxia, reactive oxygen species and mitochondrial genome mutagenesis, we examine potential roles for a mitochondrial-protective transcriptional response known as the mitochondrial unfolded protein response (UPR

Indexed as

Unfolded Protein ResponseActivating Transcription FactorsAnimalsGene Expression Regulation, NeoplasticHumansMitochondriaNeoplasmsSignal TransductionStress, PhysiologicalActivating Transcription FactorsATF5 protein, humanATF5CancerMitochondriaUPR(mt)

Identifiers

PMID28499833
PMCPMC5681445
OpenAlexW2614010945

What OpenQuestion holds

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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.