Evidence map›Paper›PMID 14871939›Full record

ArticleEukaryotic cell2004

DNA repair functions that control sensitivity to topoisomerase-targeting drugs.

Mobeen Malik, John L Nitiss

Open access · diamondAbstract read
In one paragraph

Article in Eukaryotic cell, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. DNA- and DNA-Protein-Crosslink Repair in Plants.International journal of molecular sciences · 2019
    Review
  6. Site-Specific Cleavage by Topoisomerase 2: A Mark of the Core Centromere.International journal of molecular sciences · 2018
    Article
  7. Mechanisms of DNA-protein crosslink repair.Nature reviews. Molecular cell biology · 2017
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Neuroprotection and repair of 3'-blocking DNA ends by glaikit (gkt) encoding Drosophila tyrosyl-DNA phosphodiesterase 1 (TDP1).Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. 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

2 authors at 1 institution in 1 country.

Mobeen MalikDepartment of Molecular Pharmacology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
John L Nitiss
St. Jude Children's Research Hospital · US

Funding

XENOGRAFT STUDIESP01CA023099 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI HOUGHTON, PETER J · 1985 to 2011
$22.4M
DNA REPAIR AND ANTITOPOISOMERASE DRUG EFFECTSR01CA082313 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI NITISS, JOHN L · 1999 to 2010
$2.3M
NCI NIH HHS CA23099NCI NIH HHS CA82313NCI NIH HHS P01 CA023099NCI NIH HHS R01 CA082313
6 · The paper itself

Abstract

DNA topoisomerases play critical roles in a wide range of cellular processes by altering DNA topology to facilitate replication, transcription, and chromosome segregation. Topoisomerases alter DNA topology by introducing transient DNA strand breaks that involve a covalent protein DNA intermediate. Many agents have been found to prevent the religation of DNA strand breaks induced by the enzymes, thereby converting the enzymes into DNA-damaging agents. Repair of the DNA damage induced by topoisomerases is significant in understanding drug resistance arising following treatment with topoisomerase-targeting drugs. We have used the fission yeast Schizosaccharomyces pombe to identify DNA repair pathways that are important for cell survival following drug treatment. S. pombe strains carrying mutations in genes required for homologous recombination such as rad22A or rad32 (homologues of RAD52 and MRE11) are hypersensitive to drugs targeting either topoisomerase I or topoisomerase II. In contrast to results observed with Saccharomyces cerevisiae, S. pombe strains defective in nucleotide excision repair are also hypersensitive to topoisomerase-targeting agents. The loss of DNA replication or DNA damage checkpoints also sensitizes cells to both topoisomerase I and topoisomerase II inhibitors. Finally, repair genes (such as the S. pombe rad8+ gene) with no obvious homologs in other systems also play important roles in causing sensitivity to topoisomerase drugs. Since the pattern of sensitivity is distinct from that seen with other systems (such as the S. cerevisiae system), our results highlight the usefulness of S. pombe in understanding how cells deal with the unique DNA damage induced by topoisomerases.

Indexed as

DNA DamageDNA RepairTopoisomerase II InhibitorsTopoisomerase I InhibitorsCamptothecinCell CycleDose-Response Relationship, RadiationEnzyme InhibitorsEtoposideGenotypeMutationPlasmidsRecombination, GeneticSchizosaccharomycesSensitivity and SpecificityTemperatureCamptothecinEnzyme InhibitorsEtoposideTOP 53Topoisomerase II InhibitorsTopoisomerase I Inhibitors

Identifiers

PMID14871939
PMCPMC329506
OpenAlexW2105356590

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.