Evidence map›Paper›PMID 20423990›Full record

ArticleMolecular cancer therapeutics2010

A bead-based activity screen for small-molecule inhibitors of signal transduction in chronic myelogenous leukemia cells.

Juliesta E Sylvester, Stephen J Kron

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

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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 1 institution in 1 country.

Juliesta E SylvesterDepartment of Biochemistry and Molecular Biology, The University of Chicago, Chicago, Illinois, USA.
Stephen J Kron
University of Chicago · US

Funding

Molecular screening: MALDI-TOF scanning of peptides(RMI)R01HG003864 · NHGRI · UNIVERSITY OF CHICAGO · PI KRON, STEPHEN J. · 2005 to 2008
$2.3M
BCR-ABL Kinase Assays for STI571 Sensitivity of ResponseR33CA103235 · NCI · UNIVERSITY OF CHICAGO · PI KRON, STEPHEN J. · 2004 to 2006
$1.6M
Solid-state analysis of kinase activity in cell extractsR01GM074691 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI PALECEK, SEAN P · 2006 to 2010
$1.3M
BCR-ABL Kinase Assays for STI571 Sensitivity of ResponseR21CA103235 · NCI · UNIVERSITY OF CHICAGO · PI KRON, STEPHEN J. · 2003 to 2003
$153k
NCI NIH HHS CA103235NCI NIH HHS R21 CA103235NCI NIH HHS R33 CA103235NHGRI NIH HHS HG003864NHGRI NIH HHS R01 HG003864NIGMS NIH HHS GM074691NIGMS NIH HHS R01 GM074691
6 · The paper itself

Abstract

Chronic myelogenous leukemia is characterized by the presence of the chimeric BCR-ABL gene, which is expressed as the constitutively active Bcr-Abl kinase. Although kinase activity is directly responsible for the clinical phenotype, current diagnostic and prognostic methods focus on a genetic classification system in which molecularly distinct subcategories are used to predict patient responses to small-molecule inhibitors of the Bcr-Abl kinase. Point mutations in the kinase domain are a central factor regulating inhibitor resistance; however, compensatory signaling caused by the activation of unrelated kinases can influence inhibitor efficacy. Kinase activity profiling can be used as a complementary approach to genetic screening and allows direct screening of small-molecule inhibitors. We developed a quantitative assay to monitor tyrosine kinase activities and inhibitor sensitivities in a model of chronic myelogenous leukemia using peptide reporters covalently immobilized on Luminex beads. Kinase activity is quantified by nonlinear regression from well-specific internal standard curves. Using optimized synthetic substrates and peptides derived from native substrates as probes, we measured kinase inhibition in cell lysates by the signal transduction inhibitors imatinib and dasatinib. Taking advantage of a convenient 96-well plate format, this assay also allows a straightforward and quantitative analysis of the differential effects of ATP and inhibitors on kinase activity. This method for analyzing a focused signaling network benefits from rigorous statistical analysis and short processing times, thereby offering a powerful tool for drug discovery and clinical testing.

Indexed as

MicrospheresAntineoplastic AgentsCalibrationDose-Response Relationship, DrugDrug Screening Assays, AntitumorFusion Proteins, bcr-ablHumansK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveModels, BiologicalPhosphorylationProtein Kinase InhibitorsPyridinesPyridonesPyrimidinesSignal TransductionAntineoplastic AgentsFusion Proteins, bcr-ablPD 166326PD 173955Protein Kinase InhibitorsPyridinesPyridonesPyrimidinesSmall Molecule Libraries

Identifiers

PMID20423990
PMCPMC2868067
OpenAlexW2151327379

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.