Evidence map›Paper›PMID 10970695›Full record

ArticleBritish journal of cancer2000

Drug resistance features and S-phase fraction as possible determinants for drug response in a panel of human ovarian cancer xenografts.

G M Kolfschoten, T M Hulscher, H M Pinedo, E Boven

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 28 citations in OpenAlex.

  1. Observational
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  5. GSTP1 arrests bladder cancer T24 cells in G0/G1 phase and up-regulates p21 expression.International journal of clinical and experimental medicine · 2014
    Article
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  7. Integrated genome-wide DNA copy number and expression analysis identifies distinct mechanisms of primary chemoresistance in ovarian carcinomas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009
    Article
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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

4 authors at 1 institution in 1 country.

G M KolfschotenDepartment of Medical Oncology, University Hospital Vrije Universiteit, De Boelelaan 1117, Amsterdam, HV, 1081, The Netherlands.
T M Hulscher
H M Pinedo
E Boven
Vrije Universiteit Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multidrug resistance (MDR) and more specifically the expression of P-glycoprotein (Pgp) have been studied extensively in vitro. Unfortunately, it appears that the predictive value of MDR recognized in vitro is mostly an incorrect measure to determine the responsiveness of a particular tumour in the clinic. This misunderstood or overvalued role of MDR might explain the failure of strategies to reverse Pgp function by the use of modulators in solid tumours. To obtain more insight in in vivo drug resistance we investigated a panel of 15 human ovarian cancer xenografts consisting of the most common histological subtypes known in ovarian cancer patients. The response rate to cisplatin, cyclophosphamide and doxorubicin in the xenografts resembled the results of phase II trials with these agents in ovarian cancer patients. This resemblance justifies drug resistance studies in this experimental in vivo human tumour system. We determined the expression levels of MDR 1, MRP 1, LRP and topoisomerase IIalpha mRNA by the RNase protection assay and the presence of MRP1 and LRP proteins by immunohistochemistry. The S-phase fraction was investigated as a separate parameter by flow cytometry. In none of the 15 ovarian cancer xenografts was MDR 1 expression detectable. The expression levels of MRP 1 and LRP were low to moderate and resembled the presence of the MRP1 and LRP proteins. There was a weak, inverse relationship between the expression levels of LRP and sensitivity to cisplatin and cyclophosphamide (r = -0.44 and -0.45), but not to doxorubicin. The levels of topoisomerase IIalpha varied among the xenografts (0.73-2.66) and failed to correlate with doxorubicin resistance (r = 0.14). The S-phase fraction, however, showed a relation with the sensitivity to cisplatin (r = 0.66). Among the determinants studied in ovarian cancer in vivo, LRP mRNA and the S-phase fraction were the best predictive factors for drug response and most specifically for the activity of cisplatin.

Indexed as

DNA Topoisomerases, Type IIAnimalsAntigens, NeoplasmATP-Binding Cassette, Sub-Family C ProteinsATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily B, Member 1Cell CycleCisplatinCyclophosphamideDNA-Binding ProteinsDoxorubicinDrug Resistance, NeoplasmDrug Screening Assays, AntitumorFemaleFlow CytometryGenes, MDRAntigens, NeoplasmATP-Binding Cassette, Sub-Family C ProteinsATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily B, Member 1CisplatinCyclophosphamideDNA-Binding ProteinsDNA Topoisomerases, Type IIDoxorubicinIsoenzymesMajor Vault ProteinNeoplasm ProteinsRNA, MessengerVault Ribonucleoprotein Particles

Identifiers

PMID10970695
PMCPMC2374672
OpenAlexW2104241850

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.