Evidence map›Paper›PMID 34764346›Full record

ArticleScientific reports2021

Chronic pathophysiological changes in the normal brain parenchyma caused by radiotherapy accelerate glioma progression.

Yuichiro Tsuji, Naosuke Nonoguchi, Daisuke Okuzaki, Yusuke Wada, Daisuke Motooka, Yuki Hirota, Taichiro Toho, Nobuhiko Yoshikawa, Motomasa Furuse, Shinji Kawabata and 6 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 7 citations in OpenAlex.

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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

16 authors at 4 institutions in 1 country.

Yuichiro TsujiDepartment of Neurosurgery, Osaka Medical and Pharmaceutical University, 2-7 Daigaku-Machi, Takatsuki, Osaka, 569-8686, Japan. yuuichirou.tsuji@ompu.ac.jp.
Naosuke NonoguchiDepartment of Neurosurgery, Osaka Medical and Pharmaceutical University, 2-7 Daigaku-Machi, Takatsuki, Osaka, 569-8686, Japan. naosuke.nonoguchi@ompu.ac.jp.
Daisuke OkuzakiGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Yusuke WadaDepartment of Advanced Pathobiology, Graduate School of Life and Environmental Sciences, Osaka Prefecture University, 1-58 Rinku Ourai-Kita, Izumisano, Osaka, 598-8531, Japan.
Daisuke MotookaGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Yuki HirotaDepartment of Neurosurgery, Osaka Medical and Pharmaceutical University, 2-7 Daigaku-Machi, Takatsuki, Osaka, 569-8686, Japan.
Taichiro TohoDepartment of Neurosurgery, Osaka Medical and Pharmaceutical University, 2-7 Daigaku-Machi, Takatsuki, Osaka, 569-8686, Japan.
Nobuhiko YoshikawaDepartment of Radiology, Osaka Medical and Pharmaceutical University, Osaka, Japan.
Motomasa FuruseDepartment of Neurosurgery, Osaka Medical and Pharmaceutical University, 2-7 Daigaku-Machi, Takatsuki, Osaka, 569-8686, Japan.
Shinji KawabataDepartment of Neurosurgery, Osaka Medical and Pharmaceutical University, 2-7 Daigaku-Machi, Takatsuki, Osaka, 569-8686, Japan.
Shin-Ichi MiyatakeDepartment of Neurosurgery, Osaka Medical and Pharmaceutical University, 2-7 Daigaku-Machi, Takatsuki, Osaka, 569-8686, Japan.
Hiroyuki NakamuraLaboratory for Chemistry and Life Science, Institute of Innovative Research, Tokyo Institute of Technology, 4259 Nagatsuta-cho, Midori-ku, Yokohama, Kanagawa, 226-8503, Japan.
Ryohei YamamotoDepartment of Advanced Pathobiology, Graduate School of Life and Environmental Sciences, Osaka Prefecture University, 1-58 Rinku Ourai-Kita, Izumisano, Osaka, 598-8531, Japan.
Shota NakamuraGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Toshihiko KuroiwaDepartment of Neurosurgery, Tesseikai Neurosurgical Hospital, 28-1, Nakanohommachi, Shijyonawate, Osaka, 575-8511, Japan.
Masahiko WanibuchiDepartment of Neurosurgery, Osaka Medical and Pharmaceutical University, 2-7 Daigaku-Machi, Takatsuki, Osaka, 569-8686, Japan.
Osaka University of Pharmaceutical Sciences · JPOsaka University · JPOsaka Prefecture University · JPTokyo Institute of Technology · JP

Funding

JSPS KAKENHI JP15K21510JSPS KAKENHI JP17K10911JSPS KAKENHI JP26293327
6 · The paper itself

Abstract

Radiation therapy is one of standard treatment for malignant glioma after surgery. The microenvironment after irradiation is considered not to be suitable for the survival of tumor cells (tumor bed effect). This study investigated whether the effect of changes in the microenvironment of parenchymal brain tissue caused by radiotherapy affect the recurrence and progression of glioma. 65-Gy irradiation had been applied to the right hemisphere of Fisher rats. After 3 months from irradiation, we extracted RNA and protein from the irradiated rat brain. To study effects of proteins extracted from the brains, we performed WST-8 assay and tube formation assay in vitro. Cytokine production were investigated for qPCR. Additionally, we transplanted glioma cell into the irradiated and sham animals and the median survival time of F98 transplanted rats was also examined in vivo. Immunohistochemical analyses and invasiveness of implanted tumor were evaluated. X-ray irradiation promoted the secretion of cytokines such as CXCL12, VEGF-A, TGF-β1 and TNFα from the irradiated brain. Proteins extracted from the irradiated brain promoted the proliferation and angiogenic activity of F98 glioma cells. Glioma cells implanted in the irradiated brains showed significantly high proliferation, angiogenesis and invasive ability, and the post-irradiation F98 tumor-implanted rats showed a shorter median survival time compared to the Sham-irradiation group. The current study suggests that the microenvironment around the brain tissue in the chronic phase after exposure to X-ray radiation becomes suitable for glioma cell growth and invasion.

Indexed as

AnimalsBrainBrain NeoplasmsCell Line, TumorCell ProliferationGliomaMaleRadiation DosageRadiation OncologyRadiotherapy DosageRatsRats, Inbred F344Tumor Microenvironment

Identifiers

PMID34764346
PMCPMC8585920
OpenAlexW3213468498

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.