Evidence map›Paper›PMID 32401689›Full record

ArticleRadiation research2020

Cellular Response to Proton Irradiation: A Simulation Study with TOPAS-nBio.

Hongyu Zhu, Aimee L McNamara, Stephen J McMahon, Jose Ramos-Mendez, Nicholas T Henthorn, Bruce Faddegon, Kathryn D Held, Joseph Perl, Junli Li, Harald Paganetti and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Radiation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 56 citations in OpenAlex.

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  11. Cellular lethal damage ofFrontiers in medicine · 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

11 authors at 7 institutions in 3 countries.

Hongyu ZhuDepartment of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts 02114.
Aimee L McNamaraDepartment of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts 02114.
Stephen J McMahonCentre for Cancer Research and Cell Biology, Queens University Belfast, Belfast, United Kingdom.
Jose Ramos-MendezDepartment of Radiation Oncology, University of California San Francisco, California 94143.
Nicholas T HenthornDivision of Molecular and Clinical Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.
Bruce FaddegonDepartment of Radiation Oncology, University of California San Francisco, California 94143.
Kathryn D HeldDepartment of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts 02114.
Joseph PerlSLAC National Accelerator Laboratory, Menlo Park, California.
Junli LiDepartment of Engineering Physics, Tsinghua University, Beijing 100084, P.R. China.
Harald PaganettiDepartment of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts 02114.
Jan SchuemannDepartment of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts 02114.
Massachusetts General Hospital · USHarvard University · USUniversity of California, San Francisco · USQueen's University Belfast · GBSLAC National Accelerator Laboratory · USTsinghua University · CNUniversity of Manchester · GB

Funding

TOPAS - nBio, a Monte Carlo tool for radiation biology researchR01CA187003 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI SCHUEMANN, JAN PATRICK OSCAR · 2015 to 2024
$4.8M
NCI NIH HHS R01 CA187003
6 · The paper itself

Abstract

The cellular response to ionizing radiation continues to be of significant research interest in cancer radiotherapy, and DNA is recognized as the critical target for most of the biologic effects of radiation. Incident particles can cause initial DNA damages through physical and chemical interactions within a short time scale. Initial DNA damages can undergo repair via different pathways available at different stages of the cell cycle. The misrepair of DNA damage results in genomic rearrangement and causes mutations and chromosome aberrations, which are drivers of cell death. This work presents an integrated study of simulating cell response after proton irradiation with energies of 0.5-500 MeV (LET of 60-0.2 keV/µm). A model of a whole nucleus with fractal DNA geometry was implemented in TOPAS-nBio for initial DNA damage simulations. The default physics and chemistry models in TOPAS-nBio were used to describe interactions of primary particles, secondary particles, and radiolysis products within the nucleus. The initial DNA double-strand break (DSB) yield was found to increase from 6.5 DSB/Gy/Gbp at low-linear energy transfer (LET) of 0.2 keV/µm to 21.2 DSB/Gy/Gbp at high LET of 60 keV/µm. A mechanistic repair model was applied to predict the characteristics of DNA damage repair and dose response of chromosome aberrations. It was found that more than 95% of the DSBs are repaired within the first 24 h and the misrepaired DSB fraction increases rapidly with LET and reaches 15.8% at 60 keV/µm with an estimated chromosome aberration detection threshold of 3 Mbp. The dicentric and acentric fragment yields and the dose response of micronuclei formation after proton irradiation were calculated and compared with experimental results.

Indexed as

Models, BiologicalMonte Carlo MethodProtonsChromosome AberrationsDNA Breaks, Double-StrandedFibroblastsHumansLinear Energy TransferProtons

Identifiers

PMID32401689
PMCPMC7484135
OpenAlexW3025451886

What OpenQuestion holds

Textmetadata
LicenceTDM
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.