Evidence map›Paper›PMID 32723567›Full record

ReviewAdvances in cancer research2020

Biology, pathology, and therapeutic targeting of RAS.

J Matthew Rhett, Imran Khan, John P O'Bryan

Open access · greenAbstract readReview
In one paragraph

Review in Advances in cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
8.7field-weighted citation impact, top 2% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. [Advances in Diagnosis and Targeted Therapy of KRASG12C Mutant 
Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Regulation of Ras Signaling by S-Nitrosylation.Antioxidants (Basel, Switzerland) · 2023
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. The Ras dimer structure.Chemical science · 2021
    Article
  16. Molecular assemblies of the catalytic domain of SOS with KRas and oncogenic mutants.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  17. Review
  18. Article
  19. Inhibition of RAS: proven and potential vulnerabilities.Biochemical Society transactions · 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

3 authors at 2 institutions in 1 country.

J Matthew RhettDepartment of Cell and Molecular Pharmacology and Experimental Therapeutics, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, United States; Ralph H. Johnson VA Medical Center, Charleston, SC, United States.
Imran KhanDepartment of Cell and Molecular Pharmacology and Experimental Therapeutics, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, United States; Ralph H. Johnson VA Medical Center, Charleston, SC, United States.
John P O'BryanDepartment of Cell and Molecular Pharmacology and Experimental Therapeutics, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, United States; Ralph H. Johnson VA Medical Center, Charleston, SC, United States. Electronic address: obryanjo@musc.edu.
Medical University of South Carolina · USMUSC Hollings Cancer Center · US

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI John J Lemasters · 2009 to 2026
$42.7M
Probing RAS-mediated Signaling with Monobody InhibitorsR01CA212608 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SHOHEI KOIDE, John P O'Bryan · 2017 to 2026
$5.8M
Novel Functions for Ras Family GTPasesI01BX002095 · VA · RALPH H JOHNSON VA MEDICAL CENTER · PI O'BRYAN, JOHN P · 2014 to 2024
–
BLRD VA I01 BX002095NCI NIH HHS P30 CA138313NCI NIH HHS R01 CA212608
6 · The paper itself

Abstract

RAS was identified as a human oncogene in the early 1980s and subsequently found to be mutated in nearly 30% of all human cancers. More importantly, RAS plays a central role in driving tumor development and maintenance. Despite decades of effort, there remain no FDA approved drugs that directly inhibit RAS. The prevalence of RAS mutations in cancer and the lack of effective anti-RAS therapies stem from RAS' core role in growth factor signaling, unique structural features, and biochemistry. However, recent advances have brought promising new drugs to clinical trials and shone a ray of hope in the field. Here, we will exposit the details of RAS biology that illustrate its key role in cell signaling and shed light on the difficulties in therapeutically targeting RAS. Furthermore, past and current efforts to develop RAS inhibitors will be discussed in depth.

Indexed as

AnimalsAntineoplastic AgentsHumansMolecular Targeted TherapyMutationNeoplasmsOncogenesras ProteinsSignal TransductionAntineoplastic Agentsras ProteinsAutophagyCancerGrowth factor signalingGTPaseMAPKMonobodyRASSmall molecule inhibitor

Identifiers

PMID32723567
PMCPMC7393484
OpenAlexW3041728664

What Socratic holds

Textmetadata
LicenceTDM
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.