Evidence map›Paper›PMID 18594537›Full record

ArticleBritish journal of cancer2008

Attenuated p53 activation in tumour-associated stromal cells accompanies decreased sensitivity to etoposide and vincristine.

A C Dudley, S-C Shih, A R Cliffe, K Hida, M Klagsbrun

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. P53: A Guardian of Immunity Becomes Its Saboteur through Mutation.International journal of molecular sciences · 2020
    Review
  6. P53 Mutant p53OncoTargets and therapy · 2020
    Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Interleukin-6 receptor in spindle-shaped stromal cells, a prognostic determinant of early breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  14. Review
  15. Article
  16. Gene-modified embryonic stem cell test to characterize chemical risks.Environmental science and pollution research international · 2015
    Article
  17. Review
  18. Review
  19. Article
  20. 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

5 authors at 2 institutions in 2 countries.

A C DudleyVascular Biology Program, Department of Surgery, Children's Hospital and Harvard Medical School, Boston, MA 02115, USA.
S-C Shih
A R Cliffe
K Hida
M Klagsbrun
Harvard University · USHokkaido University · JP

Funding

TUMOR DORMANCY INDUCED BY BLOCKED ANGIOGENESISP01CA045548 · NCI · CHILDREN'S HOSPITAL BOSTON · PI KLAGSBRUN, MICHAEL · 1987 to 2011
$22.6M
CHARACTERIZATION OF NEUROPILIN, A NOVEL VEGF RECEPTORR37CA037392 · NCI · CHILDREN'S HOSPITAL BOSTON · PI KLAGSBRUN, MICHAEL · 1987 to 2008
$5.6M
Targeting the vasculature to enhance anti-tumor immunityR01CA177875 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Andrew Carl Dudley · 2014 to 2026
$4.5M
Neuropilin and semaphorin, anti-angiogenesis activities and mechanismsR56CA037392 · NCI · BOSTON CHILDREN'S HOSPITAL · PI KLAGSBRUN, MICHAEL · 2009 to 2009
$384k
HEPARIN BINDING ANGIOGENIC GROWTH FACTORSR01CA037392 · NCI · CHILDREN'S HOSPITAL BOSTON · PI KLAGSBRUN, MICHAEL · 1985 to 1999
–
NCI NIH HHS CA37392NCI NIH HHS CA45548NCI NIH HHS L30 CA117002NCI NIH HHS P01 CA045548NCI NIH HHS R01 CA037392NCI NIH HHS R01 CA177875NCI NIH HHS R37 CA037392NCI NIH HHS R56 CA037392
6 · The paper itself

Abstract

Alterations in the tumour suppressor p53 have been reported in tumour-associated stromal cells; however, the consequence of these alterations has not been elucidated. We investigated p53 status and responses to p53-activating drugs using tumour-associated stromal cells from A375 melanoma and PC3 prostate carcinoma xenografts, and a spontaneous prostate tumour model (TRAMP). p53 accumulation after treatment with different p53-activating drugs was diminished in tumour-associated stromal cells compared to normal stromal cells. Tumour-associated stromal cells were also less sensitive to p53-activating drugs - this effect could be reproduced in normal stromal cells by p53 knockdown. Unlike normal stromal cells, tumour stromal cells failed to arrest in G(2) after etoposide treatment, failed to upregulate p53-inducible genes, and failed to undergo apoptosis after treatment with vincristine. The lower levels of p53 in tumour stromal cells accompanied abnormal karyotypes and multiple centrosomes. Impaired p53 function in tumour stroma might be related to genomic instability and could enable stromal cell survival in the destabilising tumour microenvironment.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell CycleCell Line, TumorDisease Models, AnimalDrug Resistance, NeoplasmEtoposideGene ExpressionGenes, p53HumansMiceStromal CellsVincristineXenograft Model Antitumor AssaysAntineoplastic AgentsEtoposideVincristine

Identifiers

PMID18594537
PMCPMC2453010
OpenAlexW2094519728

What OpenQuestion holds

Textmetadata
LicenceTDM
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.