Evidence map›Paper›PMID 31678118›Full record

ReviewBiochimica et biophysica acta. Molecular cell research2020

Therapeutic targeting of RAS: New hope for drugging the "undruggable".

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

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta. Molecular cell research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
–field-weighted citation impact
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

55 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. CRIF counteracts oncogenic Ras and regulates heterochromatin.Molecular genetics and genomics : MGG · 2025
    Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Molecules (Basel, Switzerland) · 2023
    Article
  14. Review
  15. Article
  16. Review
  17. Targeting PI3Kα overcomes resistance to KRasActa pharmacologica Sinica · 2023
    Article
  18. Covalent inhibitor targets KRasGenes & diseases · 2023
    Review
  19. Article
  20. Article
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.

Imran KhanDepartment of Cell and Molecular Pharmacology and Experimental Therapeutics, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, United States of America; Ralph H. Johnson VA Medical Center, Charleston, SC 29401, United States of America.
J Matthew RhettDepartment of Cell and Molecular Pharmacology and Experimental Therapeutics, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, United States of America; Ralph H. Johnson VA Medical Center, Charleston, SC 29401, United States of America.
John P O'BryanDepartment of Cell and Molecular Pharmacology and Experimental Therapeutics, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, United States of America; Ralph H. Johnson VA Medical Center, Charleston, SC 29401, United States of America. Electronic address: obryanjo@musc.edu.

Funding

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 R01 CA212608
6 · The paper itself

Abstract

RAS is the most frequently mutated oncogene in cancer and a critical driver of oncogenesis. Therapeutic targeting of RAS has been a goal of cancer research for more than 30 years due to its essential role in tumor formation and maintenance. Yet the quest to inhibit this challenging foe has been elusive. Although once considered "undruggable", the struggle to directly inhibit RAS has seen recent success with the development of pharmacological agents that specifically target the KRAS(G12C) mutant protein, which include the first direct RAS inhibitor to gain entry to clinical trials. However, the limited applicability of these inhibitors to G12C-mutant tumors demands further efforts to identify more broadly efficacious RAS inhibitors. Understanding allosteric influences on RAS may open new avenues to inhibit RAS. Here, we provide a brief overview of RAS biology and biochemistry, discuss the allosteric regulation of RAS, and summarize the various approaches to develop RAS inhibitors.

Indexed as

Allosteric RegulationAlternative SplicingAntibodies, MonoclonalHumansMutationNeoplasmsProtein Processing, Post-Translationalras ProteinsSmall Molecule LibrariesAntibodies, Monoclonalras ProteinsSmall Molecule LibrariesCancerDrug discoveryGTPaseMonobodyRAS inhibitorSignal transduction

Identifiers

PMID31678118
PMCPMC6937383

What OpenQuestion 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 OpenQuestion graph.