Evidence map›Paper›PMID 8761363›Full record

ArticleBritish journal of cancer1996

Variation in topoisomerase I gene copy number as a mechanism for intrinsic drug sensitivity.

H L McLeod, W N Keith

Abstract read
In one paragraph

Article in British journal of cancer, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Trial
  2. Trial
  3. Resistance to TOP-1 Inhibitors: Good Old Drugs Still Can Surprise Us.International journal of molecular sciences · 2023
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Pharmacologic resistance in colorectal cancer: a review.Therapeutic advances in medical oncology · 2016
    Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. DNA topoisomerase I in oncology: Dr Jekyll or Mr Hyde?Pathology oncology research : POR · 1999
    Review
  17. Article
  18. 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.

H L McLeodCRC Department of Medical Oncology, University of Glasgow, UK.
W N Keith

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA topoisomerase I (topo I) is the principle target for camptothecin and its derivatives such as SN38. Levels of topo I expression vary widely between and within tumour types and the basis for this is poorly understood. We have used fluorescence in situ hybridisation to detect the topo I locus in a panel of breast and colon cancer cell lines. This approach has identified a range of topo I gene copies from 1 to 6 between the cell lines as a result of DNA amplification, polysomy and isochromosome formation. Topo I gene copy number was highly correlated with topo I expression, (rs = 0.92), and inversely correlated to sensitivity to a 1 h exposure to SN38 (rs = -0.904). This illustrates the significant impact of altered topo I gene copy number on intrinsic drug sensitivity and influences potential mechanisms for acquisition of drug resistance.

Indexed as

Drug Resistance, NeoplasmGenetic VariationAntineoplastic Agents, PhytogenicBreast NeoplasmsCamptothecinCell LineCell SurvivalColonic NeoplasmsDNA Topoisomerases, Type IFemaleGene AmplificationGene ExpressionHumansIn Situ Hybridization, FluorescenceIrinotecanKaryotypingAntineoplastic Agents, PhytogenicCamptothecinDNA Topoisomerases, Type IIrinotecanNuclear Proteins

Identifiers

PMID8761363
PMCPMC2074660

What OpenQuestion holds

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Registered trials

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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.