Evidence map›Paper›PMID 29248537›Full record

ReviewSeminars in cancer biology2019

Direct inhibition of RAS: Quest for the Holy Grail?

Russell Spencer-Smith, John P O'Bryan

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
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  10. Molecular Dynamics as a Tool for Virtual Ligand Screening.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
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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.

Russell Spencer-SmithDepartment of Pharmacology, University of Illinois at Chicago, Chicago, IL, USA; University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL, USA; Jesse Brown VA Medical Center, Chicago, IL, USA.
John P O'BryanDepartment of Pharmacology, University of Illinois at Chicago, Chicago, IL, USA; University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL, USA; Jesse Brown VA Medical Center, Chicago, IL, USA. Electronic address: obryanj@uic.edu.
University of Chicago Medical Center · USUniversity of Illinois Chicago · US

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
Development of novel RAS inhibitory agents for cancer therapyR21CA201717 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI O'BRYAN, JOHN P · 2016 to 2017
$492k
Differential Regulation of PI3KC2beta by Ras Protooncogenes In Acute Myeloid LeukemiaF31CA192822 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SMITH, RUSSELL SPENCER · 2015 to 2017
$111k
BIOLOGIC CHARACTERIZATION OF A NOVEL SHC-LIKE GENEF32CA068733 · NCI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI O'BRYAN, JOHN P · 1995 to 1996
–
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 F31 CA192822NCI NIH HHS F32 CA068733NCI NIH HHS R01 CA212608NCI NIH HHS R21 CA201717
6 · The paper itself

Abstract

RAS GTPases (H-, K-, and N-RAS) are the most frequently mutated oncoprotein family in human cancer. However, the relatively smooth surface architecture of RAS and its picomolar affinity for nucleotide have given rise to the assumption that RAS is an "undruggable" target. Recent advancements in drug screening, molecular modeling, and a greater understanding of RAS function have led to a resurgence in efforts to pharmacologically target this challenging foe. This review focuses on the state of the art of RAS inhibition, the approaches taken to achieve this goal, and the challenges of translating these discoveries into viable therapeutics.

Indexed as

AnimalsAntineoplastic AgentsDrug DiscoveryGene Expression Regulation, NeoplasticHigh-Throughput Screening AssaysHumansModels, MolecularMolecular Targeted TherapyMultigene FamilyNeoplasmsProtein MultimerizationProtein Transportras ProteinsSignal TransductionStructure-Activity RelationshipAntineoplastic Agentsras ProteinsCancerHigh-throughput screeningRAS biologicsRAS inhibitorRAS monobody

Identifiers

PMID29248537
PMCPMC6258355
OpenAlexW2775445984

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.