Evidence map›Paper›PMID 26794465›Full record

ArticleMolecular oncology2016

Enhanced efficacy of combined HDAC and PARP targeting in glioblastoma.

Rikke D Rasmussen, Madhavsai K Gajjar, Kamilla E Jensen, Petra Hamerlik

Open access · bronzeAbstract read
In one paragraph

Article in Molecular oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

52 citing papers in PubMed, 75 citations in OpenAlex.

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  10. Histone ADP-ribosylation promotes resistance to PARP inhibitors by facilitating PARP1 release from DNA lesions.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  13. A Bifunctional PARP-HDAC Inhibitor with Activity in Ewing Sarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
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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 2 institutions in 1 country.

Rikke D RasmussenBrain Tumor Biology Group, Danish Cancer Society Research Center, Strandboulevarden 49, 2100-DK, Copenhagen, Denmark.
Madhavsai K GajjarBrain Tumor Biology Group, Danish Cancer Society Research Center, Strandboulevarden 49, 2100-DK, Copenhagen, Denmark.
Kamilla E JensenBrain Tumor Biology Group, Danish Cancer Society Research Center, Strandboulevarden 49, 2100-DK, Copenhagen, Denmark.
Petra HamerlikBrain Tumor Biology Group, Danish Cancer Society Research Center, Strandboulevarden 49, 2100-DK, Copenhagen, Denmark; Department of Radiation Biology, The Finsen Center, Copenhagen University Hospital, Blegdamsvej 9, 2100-DK, Copenhagen, Denmark. Electronic address: pkn@cancer.dk.
Danish Cancer Society · DKCopenhagen University Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent clinical trials have demonstrated that targeting chromatin remodeling factors is as a promising strategy for the treatment of glioblastoma (GBM). We and others have shown constitutive activation of DNA damage response (DDR) pathways in gliomas and suggested that targeting the DDR may improve the currently grim prognosis for patients. Based on our previous findings that inhibition of poly(ADP-ribose) polymerase (PARP) increases radio-sensitivity of the notoriously radio-resistant GBM cells, we hypothesized that epigenetic down-regulation of the DDR responses and induction of oxidative stress via HDAC inhibition would contribute to more efficient targeting of this deadly disease. Our data show that SAHA, an HDAC class I + II inhibitor, in combination with olaparib (PARP inhibitor): i) enhanced inhibition of GBM cell survival, ii) induced apoptosis, and iii) impaired cell cycle progression. These results provide a pre-clinical rationale for combined administration of SAHA and olaparib, which are already individually in clinical trials.

Indexed as

AnimalsApoptosisBrainBrain NeoplasmsCell Line, TumorCell SurvivalDNA RepairDrug SynergismDrug Therapy, CombinationGlioblastomaHistone Deacetylase 1Histone Deacetylase InhibitorsHumansMice, Inbred BALB CMice, NudePhthalazinesHistone Deacetylase 1Histone Deacetylase InhibitorsolaparibPhthalazinesPiperazinesPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesDNA repairGenotoxic stressGlioblastomaOlaparibSAHA

Identifiers

PMID26794465
PMCPMC5423160
OpenAlexW2234974003

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.