Evidence map›Paper›PMID 25182801›Full record

ArticleCytometry. Part A : the journal of the International Society for Analytical Cytology2014

Effect of p53 activity on the sensitivity of human glioblastoma cells to PARP-1 inhibitor in combination with topoisomerase I inhibitor or radiation.

Francesco Sabbatino, Celeste Fusciello, Domenico Somma, Roberto Pacelli, Ravin Poudel, David Pepin, Antonio Leonardi, Chiara Carlomagno, Giuseppina Della Vittoria Scarpati, Soldano Ferrone and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cytometry. Part A : the journal of the International Society for Analytical Cytology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.0field-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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Evaluation of JC and Cytomegalo Viruses in Glioblastoma TissueAsian Pacific journal of cancer prevention : APJCP · 2016
    Article
  10. PARP1 is a novel independent prognostic factor for the poor prognosis of chordoma.Cancer biomarkers : section A of Disease markers · 2016
    Article
  11. 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

11 authors at 3 institutions in 2 countries.

Francesco SabbatinoDepartment of Clinical Medicine and Surgery, University of Naples "Federico II", Via Sergio Pansini 5, Naples, Italy, 80131; Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, 02114.
Celeste Fusciello
Domenico Somma
Roberto Pacelli
Ravin Poudel
David Pepin
Antonio Leonardi
Chiara Carlomagno
Giuseppina Della Vittoria Scarpati
Soldano Ferrone
Stefano Pepe
University of Naples Federico II · ITMassachusetts General Hospital · USUniversity of Salerno · IT

Funding

Combinatorial targeting of melanoma initiating cellsR01CA138188 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FERRONE, SOLDANO · 2008 to 2012
$1.5M
NCI NIH HHS R01 CA138188
6 · The paper itself

Abstract

Poly (ADP-Ribose) polymerase-1 (PARP-1) is involved in the DNA repairing system by sensing and signaling the presence of DNA damage. Inhibition of PARP-1 is tested in combination with DNA damaging agents such as topoisomerase I inhibitors or ionizing radiations (RT) for the treatment of glioblastoma (GBM). Disruption of p53, widely prevalent in GBMs, plays a major role in DNA repairing system. The current study investigates whether p53 activity has an effect on the sensitivity of human GBM cells to PARP-1 inhibitors in combination with topoisomerase I inhibitor topotecan (TPT) and/or RT. Human GBM cell lines carrying a different functional status of p53 were treated with PARP-1 inhibitor NU1025, in combination with TPT and/or RT. Cytotoxic effects were examined by analyzing the antiproliferative activity, the cell cycle perturbations, and the DNA damage induced by combined treatments. PARP inhibition enhanced the antiproliferative activity, the cell cycle perturbations and the DNA damage induced by both TPT or RT in GBM cells. These effects were influenced by the p53 activity: cells carrying an active p53 were more sensitive to the combination of PARP inhibitor and RT, while cells carrying an inactive p53 displayed a higher sensitivity to the combination of PARP inhibitor and TPT. Our study suggests that p53 activity influences the differential sensitivity of GBM cells to combined treatments of TPT, RT, and PARP inhibitors. © 2014 International Society for Advancement of Cytometry.

Indexed as

Poly(ADP-ribose) Polymerase InhibitorsAntineoplastic Combined Chemotherapy ProtocolsCell CycleCell Line, TumorCell ProliferationCombined Modality TherapyDNA DamageDNA RepairDNA Topoisomerases, Type IFlow CytometryGlioblastomaHumansPoly (ADP-Ribose) Polymerase-1QuinazolinesRadiation, IonizingTopoisomerase I InhibitorsDNA Topoisomerases, Type INU 1025PARP1 protein, humanPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase InhibitorsQuinazolinesTopoisomerase I InhibitorsTopotecanTumor Suppressor Protein p53combinatorial strategyglioblastomap53PARP inhibitorradiotherapytopotecan

Identifiers

PMID25182801
PMCPMC8728894
OpenAlexW2165171208

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.