Evidence map›Paper›PMID 25531293›Full record

ArticlePloS one2014

Carbon-ion beam irradiation kills X-ray-resistant p53-null cancer cells by inducing mitotic catastrophe.

Napapat Amornwichet, Takahiro Oike, Atsushi Shibata, Hideaki Ogiwara, Naoto Tsuchiya, Motohiro Yamauchi, Yuka Saitoh, Ryota Sekine, Mayu Isono, Yukari Yoshida and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 44 citations in OpenAlex.

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  4. 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

13 authors at 3 institutions in 2 countries.

Napapat AmornwichetDepartment of Radiation Oncology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan; Department of Radiology, Chulalongkorn University, Pathumwan, Bangkok, Thailand.
Takahiro OikeDepartment of Radiation Oncology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan; Division of Genome Biology, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
Atsushi ShibataAdvanced Scientific Research Leaders Development Unit, Gunma University, Maebashi, Gunma, Japan.
Hideaki OgiwaraDivision of Genome Biology, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
Naoto TsuchiyaDivision of Genome Biology, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
Motohiro YamauchiDivision of Radiation Biology and Protection, Atomic Bomb Disease Institute, Nagasaki University, Sakamoto, Nagasaki, Japan.
Yuka SaitohDepartment of Radiation Oncology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Ryota SekineAdvanced Scientific Research Leaders Development Unit, Gunma University, Maebashi, Gunma, Japan.
Mayu IsonoGunma University Heavy Ion Medical Center, Maebashi, Gunma, Japan.
Yukari YoshidaGunma University Heavy Ion Medical Center, Maebashi, Gunma, Japan.
Tatsuya OhnoGunma University Heavy Ion Medical Center, Maebashi, Gunma, Japan.
Takashi KohnoDivision of Genome Biology, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
Takashi NakanoDepartment of Radiation Oncology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Gunma University · JPGunma University Hospital · JPNagasaki University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeTo understand the mechanisms involved in the strong killing effect of carbon-ion beam irradiation on cancer cells with TP53 tumor suppressor gene deficiencies. MATERIALS AND

methodsDNA damage responses after carbon-ion beam or X-ray irradiation in isogenic HCT116 colorectal cancer cell lines with and without TP53 (p53+/+ and p53-/-, respectively) were analyzed as follows: cell survival by clonogenic assay, cell death modes by morphologic observation of DAPI-stained nuclei, DNA double-strand breaks (DSBs) by immunostaining of phosphorylated H2AX (γH2AX), and cell cycle by flow cytometry and immunostaining of Ser10-phosphorylated histone H3.

resultsThe p53-/- cells were more resistant than the p53+/+ cells to X-ray irradiation, while the sensitivities of the p53+/+ and p53-/- cells to carbon-ion beam irradiation were comparable. X-ray and carbon-ion beam irradiations predominantly induced apoptosis of the p53+/+ cells but not the p53-/- cells. In the p53-/- cells, carbon-ion beam irradiation, but not X-ray irradiation, markedly induced mitotic catastrophe that was associated with premature mitotic entry with harboring long-retained DSBs at 24 h post-irradiation.

conclusionsEfficient induction of mitotic catastrophe in apoptosis-resistant p53-deficient cells implies a strong cancer cell-killing effect of carbon-ion beam irradiation that is independent of the p53 status, suggesting its biological advantage over X-ray treatment.

Indexed as

Radiation, IonizingApoptosisCell Line, TumorDNA Breaks, Double-StrandedG2 Phase Cell Cycle CheckpointsHCT116 CellsHeavy Ion RadiotherapyHistonesHumansM Phase Cell Cycle CheckpointsPhosphorylationTumor Suppressor Protein p53HistonesTumor Suppressor Protein p53

Identifiers

PMID25531293
PMCPMC4274003
OpenAlexW2044228695

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.