Evidence map›Paper›PMID 26975496›Full record

ArticleThe British journal of radiology2016

Characterization of in vitro radiosensitization in mammalian cells using biomathematical modelling: implications for hypofractionated radiotherapy with a combined modality approach.

Yuji Seo, Keisuke Tamari, Yasuo Yoshioka, Fumiaki Isohashi, Osamu Suzuki, Kazuhiko Hayashi, Yutaka Takahashi, SungJae Baek, Keisuke Otani, Kazuhiko Ogawa

Open access · greenAbstract read
In one paragraph

Article in The British journal of radiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 99% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Article
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

10 authors at 1 institution in 1 country.

Yuji SeoDepartment of Radiation Oncology, Osaka University Graduate School of Medicine, Osaka, Japan.
Keisuke TamariDepartment of Radiation Oncology, Osaka University Graduate School of Medicine, Osaka, Japan.
Yasuo YoshiokaDepartment of Radiation Oncology, Osaka University Graduate School of Medicine, Osaka, Japan.
Fumiaki IsohashiDepartment of Radiation Oncology, Osaka University Graduate School of Medicine, Osaka, Japan.
Osamu SuzukiDepartment of Radiation Oncology, Osaka University Graduate School of Medicine, Osaka, Japan.
Kazuhiko HayashiDepartment of Radiation Oncology, Osaka University Graduate School of Medicine, Osaka, Japan.
Yutaka TakahashiDepartment of Radiation Oncology, Osaka University Graduate School of Medicine, Osaka, Japan.
SungJae BaekDepartment of Radiation Oncology, Osaka University Graduate School of Medicine, Osaka, Japan.
Keisuke OtaniDepartment of Radiation Oncology, Osaka University Graduate School of Medicine, Osaka, Japan.
Kazuhiko OgawaDepartment of Radiation Oncology, Osaka University Graduate School of Medicine, Osaka, Japan.
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveIt is unclear whether radiosensitization is beneficial when radiotherapy is administered at a high dose per fraction. The aim of this study was to assess the impact of radiation dose on the effectiveness of a broad range of radiosensitizers.

methodsWe analyzed 653 pairs of clonogenic survival curves in 285 published articles, in which modifications of radiosensitivity were studied using the colony-forming assay. The modifications of radiosensitivity were arbitrarily classified into 20 classes. The survival curves were fitted to two biomathematical models: the linear-quadratic model and the repair-misrepair (RMR) model.

resultsWe found that radiosensitization was predominantly characterized by an increase of the α value (α-sensitization) without an increase of the β value (β-sensitization). A subset analysis revealed that all 20 classes showed significant α-sensitization. In contrast, only oxygen/hypoxic sensitizers (oxygen) and poly(adenosine diphosphate-ribose) polymerase inhibition (PARPi) exhibited β-sensitization. An analysis using the RMR model revealed two major sources of radiosensitization: an increased residual DNA lesion through repair inhibition and a shift from linear repairs to quadratic misrepairs, leading to enhanced lethal chromosomal aberrations.

conclusionOxygen and PARPi were found to show β-sensitization, which was favourable for eliciting a comparable degree of sensitization in the higher dose range. Reduced fidelity of the repair was suggested to be a possible mechanism of β-sensitization. Further study targeting β-sensitization is needed to develop a novel combined modality therapy with high-dose-per-fraction radiotherapy. ADVANCES IN KNOWLEDGE: Radiosensitization can be classified into two groups, α- and β-sensitizations. These two phenomena may stem from distinct underlying mechanisms.

Indexed as

Models, BiologicalAnimalsCell Physiological PhenomenaCell SurvivalCombined Modality TherapyComputer SimulationDNA DamageDose-Response Relationship, RadiationHumansRadiation Dose HypofractionationRadiation-Sensitizing AgentsRadiation ToleranceRadiation-Sensitizing Agents

Identifiers

PMID26975496
PMCPMC5258145
OpenAlexW2298717128

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.