Evidence map›Paper›PMID 36292921›Full record

ReviewInternational journal of molecular sciences2022

Evolutionary Origins of Metabolic Reprogramming in Cancer.

Natalia García-Sancha, Roberto Corchado-Cobos, Aurora Gómez-Vecino, Alejandro Jiménez-Navas, Manuel Jesús Pérez-Baena, Adrián Blanco-Gómez, Marina Holgado-Madruga, Jian-Hua Mao, Javier Cañueto, Sonia Castillo-Lluva and 2 more

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 59% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Review
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

12 authors at 3 institutions in 2 countries.

Natalia García-SanchaInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.ORCID 0000-0001-7731-7020
Roberto Corchado-CobosInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.ORCID 0000-0002-3452-2486
Aurora Gómez-VecinoInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.
Alejandro Jiménez-NavasInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.ORCID 0000-0001-7621-576X
Manuel Jesús Pérez-BaenaInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.ORCID 0000-0001-6820-215X
Adrián Blanco-GómezInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.
Marina Holgado-MadrugaInstituto de Investigación Biosanitaria de Salamanca (IBSAL), 37007 Salamanca, Spain.
Jian-Hua MaoLawrence Berkeley National Laboratory, Biological Systems and Engineering Division, Berkeley, CA 94720, USA.ORCID 0000-0001-9320-6021
Javier CañuetoInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.ORCID 0000-0003-0037-7353
Sonia Castillo-LluvaDepartamento de Bioquímica y Biología Molecular, Facultad de Ciencias Químicas, Universidad Complutense, 28040 Madrid, Spain.ORCID 0000-0001-5357-7178
Marina Mendiburu-EliçabeInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.ORCID 0000-0003-2573-8709
Jesús Pérez-LosadaInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.ORCID 0000-0003-2400-624X
Universidad de Salamanca · ESLawrence Berkeley National Laboratory · USUniversidad Complutense de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic changes that facilitate tumor growth are one of the hallmarks of cancer. These changes are not specific to tumors but also take place during the physiological growth of tissues. Indeed, the cellular and tissue mechanisms present in the tumor have their physiological counterpart in the repair of tissue lesions and wound healing. These molecular mechanisms have been acquired during metazoan evolution, first to eliminate the infection of the tissue injury, then to enter an effective regenerative phase. Cancer itself could be considered a phenomenon of antagonistic pleiotropy of the genes involved in effective tissue repair. Cancer and tissue repair are complex traits that share many intermediate phenotypes at the molecular, cellular, and tissue levels, and all of these are integrated within a Systems Biology structure. Complex traits are influenced by a multitude of common genes, each with a weak effect. This polygenic component of complex traits is mainly unknown and so makes up part of the missing heritability. Here, we try to integrate these different perspectives from the point of view of the metabolic changes observed in cancer.

Indexed as

NeoplasmsAnimalsPhenotypeSystems Biologycancerevolutionheritabilityinflammationintermediate phenotypesregenerative phasetissue repair

Identifiers

PMID36292921
PMCPMC9603151
OpenAlexW4304185084

What Socratic 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 Socratic graph.