Evidence map›Paper›PMID 32168915›Full record

ReviewInternational journal of molecular sciences2020

The p38 Pathway: From Biology to Cancer Therapy.

Adrián Martínez-Limón, Manel Joaquin, María Caballero, Francesc Posas, Eulàlia de Nadal

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 240 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
240citing papers in PubMed, 2 pooled it
18.4field-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

240 citing papers in PubMed, 2 syntheses or guidelines pooled it, 391 citations in OpenAlex.

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180 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 1 institution in 1 country.

Adrián Martínez-LimónInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Baldiri Reixac, 10, 08028 Barcelona, Spain.
Manel JoaquinInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Baldiri Reixac, 10, 08028 Barcelona, Spain.
María CaballeroInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Baldiri Reixac, 10, 08028 Barcelona, Spain.ORCID 0000-0003-1198-9697
Francesc PosasInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Baldiri Reixac, 10, 08028 Barcelona, Spain.ORCID 0000-0002-4164-7076
Eulàlia de NadalInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Baldiri Reixac, 10, 08028 Barcelona, Spain.ORCID 0000-0003-0039-5607
Universitat Pompeu Fabra · ES

Funding

Fundación Científica Asociación Española Contra el Cáncer PROYE18010POSAMinisterio de Ciencia e Innovación BFU2017-85152-P and FEDERMinisterio de Ciencia e Innovación PGC2018-094136-B-I00 and FEDER
6 · The paper itself

Abstract

The p38 MAPK pathway is well known for its role in transducing stress signals from the environment. Many key players and regulatory mechanisms of this signaling cascade have been described to some extent. Nevertheless, p38 participates in a broad range of cellular activities, for many of which detailed molecular pictures are still lacking. Originally described as a tumor-suppressor kinase for its inhibitory role in RAS-dependent transformation, p38 can also function as a tumor promoter, as demonstrated by extensive experimental data. This finding has prompted the development of specific inhibitors that have been used in clinical trials to treat several human malignancies, although without much success to date. However, elucidating critical aspects of p38 biology, such as isoform-specific functions or its apparent dual nature during tumorigenesis, might open up new possibilities for therapy with unexpected potential. In this review, we provide an extensive description of the main biological functions of p38 and focus on recent studies that have addressed its role in cancer. Furthermore, we provide an updated overview of therapeutic strategies targeting p38 in cancer and promising alternatives currently being explored.

Indexed as

AnimalsAntineoplastic AgentsClinical Studies as TopicGene Expression Regulation, NeoplasticHumansMAP Kinase Signaling SystemNeoplasmsp38 Mitogen-Activated Protein KinasesPhosphorylationAntineoplastic Agentsp38 Mitogen-Activated Protein Kinasescancer treatmentoncogenicityp38 MAPKphosphorylationSAPKtumor suppressor

Identifiers

PMID32168915
PMCPMC7139330
OpenAlexW3010908253

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.