Evidence map›Paper›PMID 23422001›Full record

ArticleCell cycle (Georgetown, Tex.)2013

Single-cell microarray enables high-throughput evaluation of DNA double-strand breaks and DNA repair inhibitors.

David M Weingeist, Jing Ge, David K Wood, James T Mutamba, Qiuying Huang, Elizabeth A Rowland, Michael B Yaffe, Scott Floyd, Bevin P Engelward

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 64 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

David M WeingeistDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Jing Ge
David K Wood
James T Mutamba
Qiuying Huang
Elizabeth A Rowland
Michael B Yaffe
Scott Floyd
Bevin P Engelward
Massachusetts Institute of Technology · USHarvard University · US

Funding

Tumor Cell Networks CenterU54CA112967 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LAUFFENBURGER, DOUGLAS A · 2004 to 2015
$26.2M
TOXICOLOGY CORE UNITP30ES002109 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LEVINE, STUART S · 1985 to 2020
$25.6M
TRAINING GRANTS IN ENVIROMENTAL TOXICOLOGYT32ES007020 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI ESSIGMANN, JOHN M · 1985 to 2024
$13.1M
Protein Kinase Signaling and Cell Cycle ControlR01ES015339 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI YAFFE, MICHAEL B · 2007 to 2017
$4.3M
Comet-Chip: A High-Throughput DNA Damage Sensor for Enviornmental Health StudiesU01ES016045 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI ENGELWARD, BEVIN P. · 2007 to 2010
$1.8M
CometChip: Enabling Translation of DNA Damage and Repair AssaysR21ES019498 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI ENGELWARD, BEVIN P., SOBOL, ROBERT W · 2011 to 2012
$434k
NCI NIH HHS CA112967NCI NIH HHS U54 CA112967NIEHS NIH HHS ES015339NIEHS NIH HHS P30 ES002109NIEHS NIH HHS P30-ES002109NIEHS NIH HHS R01 ES015339NIEHS NIH HHS R21 ES019498NIEHS NIH HHS R21-ES019498NIEHS NIH HHS T32 ES007020NIEHS NIH HHS T32-ES007020NIEHS NIH HHS U01 ES016045NIEHS NIH HHS U01-ES016045
6 · The paper itself

Abstract

A key modality of non-surgical cancer management is DNA damaging therapy that causes DNA double-strand breaks that are preferentially toxic to rapidly dividing cancer cells. Double-strand break repair capacity is recognized as an important mechanism in drug resistance and is therefore a potential target for adjuvant chemotherapy. Additionally, spontaneous and environmentally induced DSBs are known to promote cancer, making DSB evaluation important as a tool in epidemiology, clinical evaluation and in the development of novel pharmaceuticals. Currently available assays to detect double-strand breaks are limited in throughput and specificity and offer minimal information concerning the kinetics of repair. Here, we present the CometChip, a 96-well platform that enables assessment of double-strand break levels and repair capacity of multiple cell types and conditions in parallel and integrates with standard high-throughput screening and analysis technologies. We demonstrate the ability to detect multiple genetic deficiencies in double-strand break repair and evaluate a set of clinically relevant chemical inhibitors of one of the major double-strand break repair pathways, non-homologous end-joining. While other high-throughput repair assays measure residual damage or indirect markers of damage, the CometChip detects physical double-strand breaks, providing direct measurement of damage induction and repair capacity, which may be useful in developing and implementing treatment strategies with reduced side effects.

Indexed as

AnimalsCell LineCHO CellsChromonesCricetinaeDNA-Activated Protein KinaseDNA Breaks, Double-StrandedDNA DamageDNA RepairDrug Resistance, NeoplasmEnzyme InhibitorsHigh-Throughput Screening AssaysHumansMorpholinesNeoplasms2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one2-(morpholin-4-yl)benzo(h)chromen-4-one8-dibenzothiophen-4-yl-2-morpholin-4-yl-chromen-4-oneChromonesDNA-Activated Protein KinaseEnzyme InhibitorsMorpholinesDNA double-strand breaksDNA-PK inhibitorsDNA repairhigh throughputmicroarrayneutral comet assayneutral single-cell electrophoresis assaynon-homologous end-joining

Identifiers

PMID23422001
PMCPMC3637349
OpenAlexW2086210951

What OpenQuestion holds

Textmetadata
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.