Evidence map›Paper›PMID 11021755›Full record

ArticleLeukemia2000

The effects of dose, route of administration, drug scheduling and MDR-1 gene transfer on the genotoxicity of etoposide in bone marrow.

S D Turner, J A Rafferty, L J Fairbairn, J Ashby, H Tinwell, H G Eckert, C Baum, L S Lashford

Abstract read
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In one paragraph

Article in Leukemia, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 44% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. 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

8 authors at 4 institutions in 2 countries.

S D TurnerDepartment of Experimental Haematology, Paterson Institute for Cancer Research, Manchester, UK.
J A Rafferty
L J Fairbairn
J Ashby
H Tinwell
H G Eckert
C Baum
L S Lashford
Cancer Research UK Manchester Institute · GBAstraZeneca (United Kingdom) · GBLeibniz Institute of Virology (LIV) · DEThe Christie Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have used the bone marrow micronucleus assay (BMMN) as a measure of clastogenicity, in response to etoposide exposure in murine bone marrow. Oral delivery of etoposide resulted in a reduced number of micronucleated polychromatic erythrocytes (MPE) relative to the same dose delivered intraperitoneally (P < 0.001). Daily fractionation of the oral schedule of etoposide led to a more than six-fold increase in cumulative MPE frequency over that observed with the same total, unfractionated dose, with the potency of the response increasing with serial exposure (r = 0.79). Retrovirally-mediated expression of MDR1 in murine bone marrow resulted in partial protection against the clastogenic activity of etoposide relative to mock transduced control mice. The model system developed has indicated a variety of factors able to influence the genotoxicity of etoposide. It should now be possible to further exploit this model in order to define other factors governing haemopoietic sensitivity to etoposide.

Indexed as

Gene Transfer, HorizontalAnimalsAntineoplastic Agents, PhytogenicATP Binding Cassette Transporter, Subfamily B, Member 1Bone MarrowDrug Administration RoutesDrug Administration ScheduleEtoposideFemaleMaleMiceMicronucleus TestsAntineoplastic Agents, PhytogenicATP Binding Cassette Transporter, Subfamily B, Member 1Etoposide

Identifiers

PMID11021755
OpenAlexW2314715458

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.