Evidence map›Paper›PMID 26553138›Full record

ArticleRadiation oncology (London, England)2015

Combining carbon ion irradiation and non-homologous end-joining repair inhibitor NU7026 efficiently kills cancer cells.

Hongyu Ma, Akihisa Takahashi, Yukari Yoshida, Akiko Adachi, Tatsuaki Kanai, Tatsuya Ohno, Takashi Nakano

Open access · goldAbstract read
In one paragraph

Article in Radiation oncology (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
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  7. Review
  8. A perspective on tumor radiation resistance following high-LET radiation treatment.Journal of cancer research and clinical oncology · 2024
    Review
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  11. Basic and translational research on carbon-ion radiobiology.American journal of 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

7 authors at 1 institution in 1 country.

Hongyu MaDepartment of Radiation Oncology, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi, 371-8511, Gunma, Japan. gyoku0508@yahoo.co.jp.
Akihisa TakahashiGunma University Heavy Ion Medical Center, 3-39-22 Showa-machi, Maebashi, 371-8511, Gunma, Japan. a-takahashi@gunma-u.ac.jp.
Yukari YoshidaGunma University Heavy Ion Medical Center, 3-39-22 Showa-machi, Maebashi, 371-8511, Gunma, Japan. yyukari@gunma-u.ac.jp.
Akiko AdachiDepartment of Radiation Oncology, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi, 371-8511, Gunma, Japan. minami0127minaminami@yahoo.co.jp.
Tatsuaki KanaiGunma University Heavy Ion Medical Center, 3-39-22 Showa-machi, Maebashi, 371-8511, Gunma, Japan. Tkanai@gunma-u.ac.jp.
Tatsuya OhnoGunma University Heavy Ion Medical Center, 3-39-22 Showa-machi, Maebashi, 371-8511, Gunma, Japan. tohno@gunma-u.ac.jp.
Takashi NakanoDepartment of Radiation Oncology, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi, 371-8511, Gunma, Japan. tnakano@gunma-u.ac.jp.
Gunma University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOur previous data demonstrated that targeting non-homologous end-joining repair (NHEJR) yields a higher radiosensitivity than targeting homologous recombination repair (HRR) to heavy ions using DNA repair gene knockouts (KO) in mouse embryonic fibroblast (MEF). In this study, we determined if combining the use of an NHEJR inhibitor with carbon (C) ion irradiation was more efficient in killing human cancer cells compared with only targeting a HRR inhibitor.

methodsThe TP53-null human non-small cell lung cancer cell line H1299 was used for testing the radiosensitizing effect of NHEJR-related DNA-dependent protein kinase (DNA-PK) inhibitor NU7026, HRR-related Rad51 inhibitor B02, or both to C ion irradiation using colony forming assays. The mechanism underlying the inhibitor radiosensitization was determined by flow cytometry after H2AX phosphorylation staining. HRR-related Rad54-KO, NHEJR-related Lig4-KO, and wild-type TP53-KO MEF were also included to confirm the suppressing effect specificity of these inhibitors.

resultsNU7026 showed significant sensitizing effect to C ion irradiation in a concentration-dependent manner. In contrast, B02 showed a slight sensitizing effect to C ion irradiation. The addition of NU7026 significantly increased H2AX phosphorylation after C ion and x-ray irradiations in H1299 cells, but not B02. NU7026 had no effect on radiosensitivity to Lig4-KO MEF and B02 had no effect on radiosensitivity to Rad54-KO MEF in both irradiations.

conclusionThese results suggest that inhibitors targeting the NHEJR pathway could significantly enhance radiosensitivity of human cancer cells to C ion irradiation, rather than targeting the HRR pathway.

Indexed as

Carcinoma, Non-Small-Cell LungCell Line, TumorChromonesDNA End-Joining RepairHeavy Ion RadiotherapyHumansLung NeoplasmsMorpholinesRadiation-Sensitizing AgentsRadiation Tolerance2-(morpholin-4-yl)benzo(h)chromen-4-oneChromonesMorpholinesRadiation-Sensitizing Agents

Identifiers

PMID26553138
PMCPMC4638098
OpenAlexW2134446022

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.