Evidence map›Paper›PMID 23602475›Full record

ArticleCurrent biology : CB2013

Doxorubicin enhances nucleosome turnover around promoters.

Fan Yang, Christopher J Kemp, Steven Henikoff

Open access · bronzeAbstract read
In one paragraph

Article in Current biology : CB, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

71 citing papers in PubMed, 125 citations in OpenAlex.

  1. Reconstructing EBV reactivation and DNA damage response kinetics in morphologic pseudotime.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  10. Small Extracellular Vesicles from Breast Cancer Cells Induce Cardiotoxicity.International journal of molecular sciences · 2025
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11 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Fan YangBasic Science Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
Christopher J Kemp
Steven Henikoff
Fred Hutch Cancer Center · USHoward Hughes Medical Institute · US

Funding

Research Education About Cancer and Health (REACH) CoreU54CA132381 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI KAREN R PETERSON · 2007 to 2026
$25.3M
Trans-NetworkU54CA143862 · NCI · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · PI MELDRUM, DEIRDRE R. · 2009 to 2013
$8.4M
Epigenomic profiling of histone turnover kinetics in mammalian cellsR01ES020116 · NIEHS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HENIKOFF, STEVEN · 2010 to 2014
$2.4M
Howard Hughes Medical InstituteNCI NIH HHS U54 CA132381NCI NIH HHS U54 CA143862NIEHS NIH HHS R01 ES020116
6 · The paper itself

Abstract

Doxorubicin is an anthracycline DNA intercalator that is among the most commonly used anticancer drugs. Doxorubicin causes DNA double-strand breaks in rapidly dividing cells, although whether it also affects general chromatin properties is unknown. Here, we use a metabolic labeling strategy to directly measure nucleosome turnover to examine the effect of doxorubicin on chromatin dynamics in squamous cell carcinoma cell lines derived from genetically defined mice. We find that doxorubicin enhances nucleosome turnover around gene promoters and that turnover correlates with gene expression level. Consistent with a direct action of doxorubicin, enhancement of nucleosome turnover around promoters gradually increases with time of exposure to the drug. Interestingly, enhancement occurs both in wild-type cells and in cells lacking either the p53 tumor suppressor gene or the master regulator of the DNA damage response, ATM, suggesting that doxorubicin action on nucleosome dynamics is independent of the DNA damage checkpoint. In addition, another anthracycline drug, aclarubicin, shows similar effects on enhancing nucleosome turnover around promoters. Our results suggest that anthracycline intercalation promotes nucleosome turnover around promoters by its effect on DNA topology, with possible implications for mechanisms of cell killing during cancer chemotherapy.

Indexed as

AclarubicinAnimalsAntibiotics, AntineoplasticAtaxia Telangiectasia Mutated ProteinsDoxorubicinMiceMicroarray AnalysisNucleosomesPolymerase Chain ReactionPromoter Regions, GeneticTumor Cells, CulturedTumor Suppressor Protein p53AclarubicinAntibiotics, AntineoplasticAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseDoxorubicinNucleosomesTumor Suppressor Protein p53

Identifiers

PMID23602475
PMCPMC3678987
OpenAlexW1997634881

What OpenQuestion holds

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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.