Evidence map›Paper›PMID 31969449›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

Requirement for epithelial p38α in KRAS-driven lung tumor progression.

Jessica Vitos-Faleato, Sebastián M Real, Nuria Gutierrez-Prat, Alberto Villanueva, Elisabet Llonch, Matthias Drosten, Mariano Barbacid, Angel R Nebreda

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  5. KDM5D histone demethylase mediates p38α inactivation via its enzymatic activity to inhibit cancer progression.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Article
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  9. Article
  10. Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. CDK4/6 and MAPK-Crosstalk as Opportunity for Cancer Treatment.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  17. p38β and Cancer: The Beginning of the Road.International journal of molecular sciences · 2020
    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

8 authors at 4 institutions in 1 country.

Jessica Vitos-FaleatoInstitute for Research in Biomedicine, The Barcelona Institute of Science and Technology, 08028 Barcelona, Spain.ORCID 0000-0002-9016-4695
Sebastián M RealInstitute for Research in Biomedicine, The Barcelona Institute of Science and Technology, 08028 Barcelona, Spain.ORCID 0000-0001-7286-2724
Nuria Gutierrez-PratInstitute for Research in Biomedicine, The Barcelona Institute of Science and Technology, 08028 Barcelona, Spain.ORCID 0000-0001-6717-8434
Alberto VillanuevaProgram Against Cancer Therapeutic Resistance, Catalan Institute of Oncology, Bellvitge Institute for Biomedical Research, 08907 L'Hospitalet de Llobregat, Spain.
Elisabet LlonchInstitute for Research in Biomedicine, The Barcelona Institute of Science and Technology, 08028 Barcelona, Spain.ORCID 0000-0003-3979-2597
Matthias DrostenMolecular Oncology Program, Centro Nacional de Investigaciones Oncológicas, 28029 Madrid, Spain.ORCID 0000-0002-3205-456X
Mariano BarbacidMolecular Oncology Program, Centro Nacional de Investigaciones Oncológicas, 28029 Madrid, Spain.ORCID 0000-0002-1480-2624
Angel R NebredaInstitute for Research in Biomedicine, The Barcelona Institute of Science and Technology, 08028 Barcelona, Spain; angel.nebreda@irbbarcelona.org.ORCID 0000-0002-7631-4060
Institute for Research in Biomedicine · ESSpanish National Cancer Research Centre · ESBellvitge University Hospital · ESInstitució Catalana de Recerca i Estudis Avançats · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant transformation entails important changes in the control of cell proliferation through the rewiring of selected signaling pathways. Cancer cells then become very dependent on the proper function of those pathways, and their inhibition offers therapeutic opportunities. Here we identify the stress kinase p38α as a nononcogenic signaling molecule that enables the progression of Kras

Indexed as

Adenocarcinoma of LungAnimalsCell Line, TumorCell ProliferationDisease Models, AnimalDisease ProgressionHumansLungLung NeoplasmsMiceMice, Inbred C57BLMitogen-Activated Protein Kinase 14Neoplastic ProcessesProto-Oncogene Proteins p21(ras)Hras protein, mouseMitogen-Activated Protein Kinase 14Proto-Oncogene Proteins p21(ras)KRASlung adenocarcinomanononcogene addictionp38αTIMP-1

Identifiers

PMID31969449
PMCPMC7007552
OpenAlexW3001531511

What OpenQuestion holds

Textmetadata
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.