Evidence map›Paper›PMID 21235428›Full record

ReviewExpert opinion on investigational drugs2011

Mechanisms of drug resistance in kinases.

Rina Barouch-Bentov, Karsten Sauer

Abstract readReview
In one paragraph

Review in Expert opinion on investigational drugs, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing 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

92 citing papers in PubMed.

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  13. Unraveling Extremely DamagingJournal of personalized medicine · 2023
    Article
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32 more citing papers are in PubMed but not listed here.

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.

Rina Barouch-BentovStanford University School of Medicine, Division of Infectious Disease and Geographic Medicine, Department of Medicine, Stanford, California 94305, USA.
Karsten Sauer

Funding

Inositol-Trisphosphate Kinase B (ItpkB) in T Cell Development and FunctionR01AI070845 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI SAUER, KARSTEN · 2008 to 2012
$3.0M
Mechanisms of Kinase Function and Drug Resistance in CancerR01GM100785 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI CHE, JIANWEI, SAUER, KARSTEN · 2011 to 2014
$1.4M
Integrated Functional Genomics Analysis of Druggable T Cell-Activating GenesR01GM088647 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI SAUER, KARSTEN · 2009 to 2010
$760k
NIAID NIH HHS R01 AI070845NIGMS NIH HHS R01 GM088647NIGMS NIH HHS R01 GM100785
6 · The paper itself

Abstract

introductionbecause of their important roles in disease and excellent 'druggability', kinases have become the second largest drug target family. The great success of the BCR-ABL inhibitor imatinib in treating chronic myelogenous leukemia illustrates the high potential of kinase inhibitor (KI) therapeutics, but also unveils a major limitation: the development of drug resistance. This is a significant concern as KIs reach large patient populations for an expanding array of indications. AREAS COVERED: we provide an up-to-date understanding of the mechanisms through which KIs function and through which cells can become KI-resistant. We review current and future approaches to overcome KI resistance, focusing on currently approved KIs and KIs in clinical trials. We then discuss approaches to improve KI efficacy and overcome drug resistance and novel approaches to develop less drug resistance-prone KI therapeutics. EXPERT OPINION: although drug resistance is a concern for current KI therapeutics, recent progress in our understanding of the underlying mechanisms and promising technological advances may overcome this limitation and provide powerful new therapeutics.

Indexed as

Drug Resistance, NeoplasmMolecular Targeted TherapyMutation, MissenseAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsClinical Trials as TopicFusion Proteins, bcr-ablHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveProtein Kinase InhibitorsProtein KinasesStereoisomerismAntineoplastic AgentsFusion Proteins, bcr-ablProtein Kinase InhibitorsProtein Kinases

Identifiers

PMID21235428
PMCPMC3095104

What OpenQuestion holds

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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.