Evidence map›Paper›PMID 17681352›Full record

ReviewMutation research2007

DNA topoisomerase II, genotoxicity, and cancer.

A Kathleen McClendon, Neil Osheroff

Open access · greenAbstract readReview
In one paragraph

Review in Mutation research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed
9.8field-weighted citation impact, top 1% 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

160 citing papers in PubMed, 399 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. DNA topological regulation in RNA polymerase II transcription.Cellular & molecular biology letters · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Structural Mechanisms of Topoisomerase-Targeting Drugs.Annual review of biochemistry · 2025
    Review
  12. Review
  13. Modulation of AAV transduction and integration targeting by topoisomerase poisons.Molecular therapy. Methods & clinical development · 2024
    Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

100 more citing papers are in PubMed but not listed here.

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.

A Kathleen McClendonDepartment of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232-0146, USA.
Neil Osheroff
Vanderbilt University · US

Funding

BIOCHEMICAL &CHEMICAL TRAINING FOR CANCER RESEARCHT32CA009582 · NCI · VANDERBILT UNIVERSITY · PI David K Cortez · 1987 to 2026
$8.8M
FUNCTION AND BIOLOGY OF EUKARYOTIC DNA TOPOISOMERASESR01GM033944 · NIGMS · VANDERBILT UNIVERSITY · PI OSHEROFF, NEIL · 1985 to 2015
$5.5M
DNA LESIONS AS ENDOGENOUS TOPOISOMERASE POISONSR01GM053960 · NIGMS · VANDERBILT UNIVERSITY · PI OSHEROFF, NEIL · 1996 to 2009
$2.2M
NCI NIH HHS 5 T32 CA09582NCI NIH HHS T32 CA009582NIGMS NIH HHS GM33944NIGMS NIH HHS GM53960NIGMS NIH HHS R01 GM033944NIGMS NIH HHS R01 GM053960
6 · The paper itself

Abstract

Type II topoisomerases are ubiquitous enzymes that play essential roles in a number of fundamental DNA processes. They regulate DNA under- and overwinding, and resolve knots and tangles in the genetic material by passing an intact double helix through a transient double-stranded break that they generate in a separate segment of DNA. Because type II topoisomerases generate DNA strand breaks as a requisite intermediate in their catalytic cycle, they have the potential to fragment the genome every time they function. Thus, while these enzymes are essential to the survival of proliferating cells, they also have significant genotoxic effects. This latter aspect of type II topoisomerase has been exploited for the development of several classes of anticancer drugs that are widely employed for the clinical treatment of human malignancies. However, considerable evidence indicates that these enzymes also trigger specific leukemic chromosomal translocations. In light of the impact, both positive and negative, of type II topoisomerases on human cells, it is important to understand how these enzymes function and how their actions can destabilize the genome. This article discusses both aspects of human type II topoisomerases.

Indexed as

MutationAntineoplastic AgentsDNA DamageDNA, SuperhelicalDNA Topoisomerases, Type IIHumansModels, MolecularNeoplasmsAntineoplastic AgentsDNA, SuperhelicalDNA Topoisomerases, Type II

Identifiers

PMID17681352
PMCPMC2679583
OpenAlexW2069151403

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.