Evidence map›Paper›PMID 32936431›Full record

ReviewCancer metastasis reviews2020

Novel regulation of Ras proteins by direct tyrosine phosphorylation and dephosphorylation.

László Buday, Virág Vas

Open access · hybridAbstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Targeting KRAS in pancreatic cancer.Oncology research · 2024
    Review
  5. Regulation of Ras Signaling by S-Nitrosylation.Antioxidants (Basel, Switzerland) · 2023
    Review
  6. Article
  7. Review
  8. Targeting KRAS in Pancreatic Cancer.Journal of personalized medicine · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Post-translational modification of RAS proteins.Current opinion in structural biology · 2021
    Review
  15. Review
  16. Review
  17. Review
  18. 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

2 authors at 2 institutions in 1 country.

László BudayInstitute of Enzymology, Research Centre for Natural Sciences, Budapest, 1117, Hungary. buday.laszlo@ttk.hu.
Virág VasInstitute of Enzymology, Research Centre for Natural Sciences, Budapest, 1117, Hungary.
HUN-REN Research Centre for Natural Sciences · HUInstitute of Molecular Life Sciences · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Somatic mutations in the RAS genes are frequent in human tumors, especially in pancreatic, colorectal, and non-small-cell lung cancers. Such mutations generally decrease the ability of Ras to hydrolyze GTP, maintaining the protein in a constitutively active GTP-bound form that drives uncontrolled cell proliferation. Efforts to develop drugs that target Ras oncoproteins have been unsuccessful. Recent emerging data suggest that Ras regulation is more complex than the scientific community has believed for decades. In this review, we summarize advances in the "textbook" view of Ras activation. We also discuss a novel type of Ras regulation that involves direct phosphorylation and dephosphorylation of Ras tyrosine residues. The discovery that pharmacological inhibition of the tyrosine phosphoprotein phosphatase SHP2 maintains mutant Ras in an inactive state suggests that SHP2 could be a novel drug target for the treatment of Ras-driven human cancers.

Indexed as

AnimalsGenes, rasHumansNeoplasmsPhosphorylationProto-Oncogene Proteins p21(ras)TyrosineProto-Oncogene Proteins p21(ras)TyrosineCancer therapyRasRas signalingSHP2SOSTyrosine phosphorylation

Identifiers

PMID32936431
PMCPMC7680326
OpenAlexW3087735389

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.