Evidence map›Paper›PMID 33996894›Full record

ArticleFrontiers in molecular biosciences2021

Veliparib Is an Effective Radiosensitizing Agent in a Preclinical Model of Medulloblastoma.

Jessica Buck, Patrick J C Dyer, Hilary Hii, Brooke Carline, Mani Kuchibhotla, Jacob Byrne, Meegan Howlett, Jacqueline Whitehouse, Martin A Ebert, Kerrie L McDonald and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in molecular biosciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 14 citations in OpenAlex.

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  12. BRCA2 deficiency increases sensitivity of medulloblastoma to Olaparib by inhibiting RAD51-mediated DNA damage repair system.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    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

12 authors at 5 institutions in 1 country.

Jessica BuckBrain Tumour Research Program, Telethon Kids Cancer Centre, Telethon Kids Institute, Perth, WA, Australia.
Patrick J C DyerBrain Tumour Research Program, Telethon Kids Cancer Centre, Telethon Kids Institute, Perth, WA, Australia.
Hilary HiiBrain Tumour Research Program, Telethon Kids Cancer Centre, Telethon Kids Institute, Perth, WA, Australia.
Brooke CarlineBrain Tumour Research Program, Telethon Kids Cancer Centre, Telethon Kids Institute, Perth, WA, Australia.
Mani KuchibhotlaBrain Tumour Research Program, Telethon Kids Cancer Centre, Telethon Kids Institute, Perth, WA, Australia.
Jacob ByrneBrain Tumour Research Program, Telethon Kids Cancer Centre, Telethon Kids Institute, Perth, WA, Australia.
Meegan HowlettBrain Tumour Research Program, Telethon Kids Cancer Centre, Telethon Kids Institute, Perth, WA, Australia.
Jacqueline WhitehouseBrain Tumour Research Program, Telethon Kids Cancer Centre, Telethon Kids Institute, Perth, WA, Australia.
Martin A EbertSchool of Physics, Mathematics and Computing, University of Western Australia, Perth, WA, Australia.
Kerrie L McDonaldBrain Cancer Consultancy, Sydney, NSW, Australia.
Nicholas G GottardoBrain Tumour Research Program, Telethon Kids Cancer Centre, Telethon Kids Institute, Perth, WA, Australia.
Raelene EndersbyBrain Tumour Research Program, Telethon Kids Cancer Centre, Telethon Kids Institute, Perth, WA, Australia.
The Kids Research Institute Australia · AUCancer Australia · AUPrincess Margaret Hospital for Children · AUSir Charles Gairdner Hospital · AUUniversity of Western Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Medulloblastoma is the most common malignant childhood brain tumor, and 5-year overall survival rates are as low as 40% depending on molecular subtype, with new therapies critically important. As radiotherapy and chemotherapy act through the induction of DNA damage, the sensitization of cancer cells through the inhibition of DNA damage repair pathways is a potential therapeutic strategy. The poly-(ADP-ribose) polymerase (PARP) inhibitor veliparib was assessed for its ability to augment the cellular response to radiation-induced DNA damage in human medulloblastoma cells. DNA repair following irradiation was assessed using the alkaline comet assay, with veliparib inhibiting the rate of DNA repair. Veliparib treatment also increased the number of γH2AX foci in cells treated with radiation, and analysis of downstream pathways indicated persistent activation of the DNA damage response pathway. Clonogenicity assays demonstrated that veliparib effectively inhibited the colony-forming capacity of medulloblastoma cells, both as a single agent and in combination with irradiation. These data were then validated

Indexed as

DNA repairMedulloblastomapoly(ADP-ribose) polymeraseradiotherapyveliparib

Identifiers

PMID33996894
PMCPMC8116896
OpenAlexW3157912200

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.