Evidence map›Paper›PMID 11360198›Full record

ArticleOncogene2001

Mutant K-ras enhances apoptosis in embryonic stem cells in combination with DNA damage and is associated with increased levels of p19(ARF).

D G Brooks, R M James, C E Patek, J Williamson, M J Arends

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

16 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Inducible Intestine-Specific Expression of krasNeoplasia (New York, N.Y.) · 2018
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  10. Bmi1 is critical for lung tumorigenesis and bronchioalveolar stem cell expansion.Proceedings of the National Academy of Sciences of the United States of America · 2008
    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

5 authors at 2 institutions in 1 country.

D G BrooksSir Alastair Currie CRC Laboratories, Molecular Medicine Centre, University of Edinburgh, Crewe Road, Edinburgh, EH4 2XU, UK.
R M James
C E Patek
J Williamson
M J Arends
University of Edinburgh · GBAddenbrooke's Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The roles of K-ras in neoplasia are not entirely understood, although there is evidence that K-ras affects susceptibility to apoptosis, modulating survival of DNA damaged cells which would otherwise be eliminated. In this study, we investigated the effects of mutant K-ras on apoptosis in vitro following DNA damage. To avoid complications resulting from mutations in other cancer-related genes and from the presence of endogenous K-ras, we derived K-ras null embryonic stem cells. Expression of either wild-type or mutant K-ras was reconstructed by stable plasmid transfection. The cell lines were treated with etoposide, cisplatin and UV radiation and apoptosis measured flow cytometrically. Mutant K-ras potentiated the effect of etoposide-derived DNA damage by increasing apoptosis, whereas absence of K-ras had the opposite effect. This pattern was similar but less marked with cisplatin, whereas UV yielded no difference in apoptosis with regard to K-ras status, suggesting that the effect of K-ras on apoptosis is dependent on the nature of the DNA damage. To investigate possible mechanisms, we examined the expression of p19(ARF) mRNA by RT-PCR. Cells expressing mutant K-ras produced elevated levels of p19(ARF) mRNA, which could link K-ras status with p53 expression and hence susceptibility to DNA damage-induced apoptosis.

Indexed as

Protein BiosynthesisAnimalsAntineoplastic AgentsApoptosisCell LineCHO CellsCisplatinCricetinaeDNA DamageEmbryo, MammalianEtoposideGene Expression Regulation, DevelopmentalGenes, rasMiceMutationProteinsAntineoplastic AgentsCisplatinEtoposideProteinsRNA, MessengerTumor Suppressor Protein p14ARF

Identifiers

PMID11360198
OpenAlexW1991136519

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.