Evidence map›Paper›PMID 24194914›Full record

ArticlePloS one2013

Genome-wide transcriptional effects of the anti-cancer agent camptothecin.

Artur Veloso, Benjamin Biewen, Michelle T Paulsen, Nathan Berg, Leonardo Carmo de Andrade Lima, Jayendra Prasad, Karan Bedi, Brian Magnuson, Thomas E Wilson, Mats Ljungman

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.7field-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

30 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Dynamic Supercoiling Sponsors Transcription Amplification by MYC.bioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. The DNA damage response to transcription stress.Nature reviews. Molecular cell biology · 2019
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

10 authors at 3 institutions in 2 countries.

Artur VelosoDepartment of Radiation Oncology, University of Michigan Comprehensive Cancer Center and Translational Oncology Program, University of Michigan, Ann Arbor, Michigan, United States of America ; Bioinformatics Program and Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan, United States of America.
Benjamin Biewen
Michelle T Paulsen
Nathan Berg
Leonardo Carmo de Andrade Lima
Jayendra Prasad
Karan Bedi
Brian Magnuson
Thomas E Wilson
Mats Ljungman
University of Michigan–Ann Arbor · USMichigan Center for Translational Pathology · USMichigan United · US

Funding

Development and Validation of BruChase-Seq and BrUV-SeqR01HG006786 · NHGRI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LJUNGMAN, MATS · 2012 to 2014
$1.1M
Mechanisms of Genotoxic Stress-regulated Gene Expression in Human CellsR21ES020946 · NIEHS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LJUNGMAN, MATS · 2012 to 2013
$424k
NHGRI NIH HHS 1R01HG006786NHGRI NIH HHS R01 HG006786NIEHS NIH HHS 1R21ES020946NIEHS NIH HHS R21 ES020946
6 · The paper itself

Abstract

The anti-cancer drug camptothecin inhibits replication and transcription by trapping DNA topoisomerase I (Top1) covalently to DNA in a "cleavable complex". To examine the effects of camptothecin on RNA synthesis genome-wide we used Bru-Seq and show that camptothecin treatment primarily affected transcription elongation. We also observed that camptothecin increased RNA reads past transcription termination sites as well as at enhancer elements. Following removal of camptothecin, transcription spread as a wave from the 5'-end of genes with no recovery of transcription apparent from RNA polymerases stalled in the body of genes. As a result, camptothecin preferentially inhibited the expression of large genes such as proto-oncogenes, and anti-apoptotic genes while smaller ribosomal protein genes, pro-apoptotic genes and p53 target genes showed relative higher expression. Cockayne syndrome group B fibroblasts (CS-B), which are defective in transcription-coupled repair (TCR), showed an RNA synthesis recovery profile similar to normal fibroblasts suggesting that TCR is not involved in the repair of or RNA synthesis recovery from transcription-blocking Top1 lesions. These findings of the effects of camptothecin on transcription have important implications for its anti-cancer activities and may aid in the design of improved combinatorial treatments involving Top1 poisons.

Indexed as

Antineoplastic Agents, PhytogenicBase SequenceCamptothecinDNA HelicasesDNA Repair EnzymesDNA Topoisomerases, Type IFibroblastsGene LibraryGenomeHumansMolecular Sequence DataPoly-ADP-Ribose Binding ProteinsSequence Analysis, DNATranscription Elongation, GeneticAntineoplastic Agents, PhytogenicCamptothecinDNA HelicasesDNA Repair EnzymesDNA Topoisomerases, Type IERCC6 protein, humanPoly-ADP-Ribose Binding ProteinsTOP1 protein, human

Identifiers

PMID24194914
PMCPMC3806802
OpenAlexW2130225953

What OpenQuestion holds

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LicenceCC BY
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.