Evidence map›Paper›PMID 11713279›Full record

ArticleMolecular and cellular biology2001

Transcriptional consequences of topoisomerase inhibition.

I Collins, A Weber, D Levens

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

58 citing papers in PubMed, 117 citations in OpenAlex.

  1. Article
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  13. Ribosomal DNA and the nucleolus in the context of genome organization.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. Oncogenic fusion protein EWS-FLI1 is a network hub that regulates alternative splicing.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  18. Transcription-generated torsional stress destabilizes nucleosomes.Nature structural & molecular biology · 2014
    Article
  19. Article
  20. Article
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

3 authors at 2 institutions in 1 country.

I CollinsLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892-1500, USA.
A Weber
D Levens
National Cancer Institute · USCenter for Cancer Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In principle, the generation, transmission, and dissipation of supercoiling forces are determined by the arrangement of the physical barriers defining topological boundaries and the disposition of enzymes creating (polymerases and helicases, etc.) or releasing (topoisomerases) torsional strain in DNA. These features are likely to be characteristic for individual genes. By using topoisomerase inhibitors to alter the balance between supercoiling forces in vivo, we monitored changes in the basal transcriptional activity and DNA conformation for several genes. Every gene examined displayed an individualized profile in response to inhibition of topoisomerase I or II. The expression changes elicited by camptothecin (topoisomerase I inhibitor) or adriamycin (topoisomerase II inhibitor) were not equivalent. Camptothecin generally caused transcription complexes to stall in the midst of transcription units, while provoking little response at promoters. Adriamycin, in contrast, caused dramatic changes at or near promoters and prevented transcription. The response to topoisomerase inhibition was also context dependent, differing between chromosomal or episomal c-myc promoters. In addition to being well-characterized DNA-damaging agents, topoisomerase inhibitors may evoke a biological response determined in part from transcriptional effects. The results have ramifications for the use of these drugs as antineoplastic agents.

Indexed as

Topoisomerase II InhibitorsTopoisomerase I InhibitorsTranscription, GeneticAntineoplastic AgentsBase SequenceBlotting, SouthernCamptothecinCell LineCell NucleusDNA DamageDoxorubicinEnzyme InhibitorsGenes, mycHumansMolecular Sequence DataPlasmidsAntineoplastic AgentsCamptothecinDoxorubicinEnzyme InhibitorsRNA, MessengerTopoisomerase II InhibitorsTopoisomerase I Inhibitors

Identifiers

PMID11713279
PMCPMC100007
OpenAlexW2122317160

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.