Evidence map›Paper›PMID 29219147›Full record

ReviewCell research2018

Mitochondrial metabolism and cancer.

Paolo Ettore Porporato, Nicoletta Filigheddu, José Manuel Bravo-San Pedro, Guido Kroemer, Lorenzo Galluzzi

Open access · hybridAbstract readReview
In one paragraph

Review in Cell research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 735 papers.

0numbers the graph read from it
0cells of the map it votes in
735citing papers in PubMed
24.6field-weighted citation impact, top 1% 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

735 citing papers in PubMed, 1,266 citations in OpenAlex.

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675 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

5 authors at 4 institutions in 4 countries.

Paolo Ettore PorporatoDepartment of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, 10124 Torino, Italy.
Nicoletta FilighedduDepartment of Translational Medicine, University of Piemonte Orientale, 28100 Novara, Italy.
José Manuel Bravo-San PedroUniversité Paris Descartes/Paris V, Sorbonne Paris Cité, 75006 Paris, France.
Guido KroemerUniversité Paris Descartes/Paris V, Sorbonne Paris Cité, 75006 Paris, France.
Lorenzo GalluzziUniversité Paris Descartes/Paris V, Sorbonne Paris Cité, 75006 Paris, France.
Cornell University · USSorbonne Paris Cité · FRUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycolysis has long been considered as the major metabolic process for energy production and anabolic growth in cancer cells. Although such a view has been instrumental for the development of powerful imaging tools that are still used in the clinics, it is now clear that mitochondria play a key role in oncogenesis. Besides exerting central bioenergetic functions, mitochondria provide indeed building blocks for tumor anabolism, control redox and calcium homeostasis, participate in transcriptional regulation, and govern cell death. Thus, mitochondria constitute promising targets for the development of novel anticancer agents. However, tumors arise, progress, and respond to therapy in the context of an intimate crosstalk with the host immune system, and many immunological functions rely on intact mitochondrial metabolism. Here, we review the cancer cell-intrinsic and cell-extrinsic mechanisms through which mitochondria influence all steps of oncogenesis, with a focus on the therapeutic potential of targeting mitochondrial metabolism for cancer therapy.

Indexed as

CarcinogenesisCell Transformation, NeoplasticMitochondriaAnimalsAntineoplastic AgentsCalciumGlycolysisHumansMolecular Targeted TherapyNeoplasmsOxidation-ReductionAntineoplastic AgentsCalcium

Identifiers

PMID29219147
PMCPMC5835768
OpenAlexW2773927148

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.