Evidence map›Paper›PMID 21207372›Full record

ArticleInternational journal of cancer2011

Apurinic/apyrimidinic endonuclease is inversely associated with response to radiotherapy in pediatric ependymoma.

Michael S Bobola, Pawel P Jankowski, Mary E Gross, Jeffery Schwartz, Laura S Finn, A Blank, Richard G Ellenbogen, John R Silber

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
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  11. Article
  12. Review
  13. The Tumorigenic Roles of the Cellular REDOX Regulatory Systems.Oxidative medicine and cellular longevity · 2016
    Review
  14. Article
  15. Human apurinic/apyrimidinic endonuclease 1.Antioxidants & redox signaling · 2014
    Review
  16. Article
  17. Article
  18. Base excision repair targets for cancer therapy.American journal of cancer research · 2011
    Article
  19. 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 5 institutions in 1 country.

Michael S BobolaDepartment of Neurological Surgery, University of Washington, Seattle, WA 98195-6470, USA.
Pawel P Jankowski
Mary E Gross
Jeffery Schwartz
Laura S Finn
A Blank
Richard G Ellenbogen
John R Silber
Boston Children's Hospital · USNeurological Surgery · USUniversity of Washington · USIn-Q-Tel · USSeattle Children's Hospital · US

Funding

Ape1, oxidative stress and glioma alkylator resistanceR01CA104593 · NCI · UNIVERSITY OF WASHINGTON · PI SILBER, JOHN R · 2004 to 2008
$1.5M
COMBATING ALKYLATING AGENT RESISTANCE IN HUMAN GLIOMASR01CA082622 · NCI · UNIVERSITY OF WASHINGTON · PI SILBER, JOHN R · 2000 to 2002
$821k
DNA repair-based models of glioblastoma response to radiation and temozolomideR21CA131658 · NCI · UNIVERSITY OF WASHINGTON · PI SILBER, JOHN R · 2008 to 2009
$371k
NCI NIH HHS CA104593NCI NIH HHS CA82622NCI NIH HHS R01 CA104593NCI NIH HHS R21 CA131658
6 · The paper itself

Abstract

Apurinic/apyrimidinic endonuclease (Ap endo) is a key DNA repair activity that confers radiation resistance in human cells. Here we examined the association between Ap endo activity and response to radiotherapy in pediatric ependymomas, tumors for which treatment options are limited and survival rates are only about 50%. We assayed Ap endo activity in 36 ependymomas and expression of Ape1/Ref-1, the predominant Ap endo activity in humans, in 44 tumors by immunostaining. Cox proportional hazards regression models were used to analyze the association of activity or expression with progression-free survival or with overall survival. Activity varied 13-fold and was not associated with tumor or patient characteristics. In univariate models with Ap endo activity entered as a continuous variable, the hazard ratio for progression increased by a factor of 2.18 for every 0.01 unit increase in activity (p ≤ 0.003) in 24 grade II ependymomas. Risk for death increased by a factor of 1.89 (p ≤ 0.02) in the same population. The fraction of Ape1/Ref-1 immunopositive cells varied widely within individual tumors and was not associated with either progression-free or with overall survival. Suppressing Ap endo activity in pediatric ependymoma cells significantly increased radiation sensitivity, suggesting that the association of activity with radiation response reflected, at least in part, repair of radiation-induced DNA lesions. Our data indicate that Ap endo activity is predictive of outcome following radiotherapy, and suggest that Ape1/Ref-1 promotes radiation resistance in pediatric ependymomas. Our findings support the use of inhibitors of Ap endo activity to overcome resistance.

Indexed as

AdolescentBrain NeoplasmsChildDisease-Free SurvivalDNA-(Apurinic or Apyrimidinic Site) LyaseEpendymomaFemaleHumansInfantMaleRadiation ToleranceDNA-(Apurinic or Apyrimidinic Site) Lyase

Identifiers

PMID21207372
PMCPMC3285472
OpenAlexW1984743945

What OpenQuestion holds

Textmetadata
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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.