Evidence map›Paper›PMID 27622834›Full record

ArticleInternational journal of radiation biology2016

DNA repair pathway choice at various conditions immediately post irradiation.

Min Liu, Hongyan Wang, Solah Lee, Bailong Liu, Lihua Dong, Ya Wang

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of radiation biology, 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
0.5field-weighted citation impact, top 28% 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, 5 citations in OpenAlex.

  1. Expert reviews in molecular medicine · 2022
    Review
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

6 authors at 2 institutions in 2 countries.

Min Liua Department of Radiation Oncology , the First Hospital, Jilin University , Changchun , China.
Hongyan Wangb Department of Radiation Oncology , School of Medicine and the Winship Cancer Institute, Emory University , Atlanta , Georgia , USA.
Solah Leeb Department of Radiation Oncology , School of Medicine and the Winship Cancer Institute, Emory University , Atlanta , Georgia , USA.
Bailong Liua Department of Radiation Oncology , the First Hospital, Jilin University , Changchun , China.
Lihua Donga Department of Radiation Oncology , the First Hospital, Jilin University , Changchun , China.
Ya Wangb Department of Radiation Oncology , School of Medicine and the Winship Cancer Institute, Emory University , Atlanta , Georgia , USA.
Emory University · USFirst Hospital of Jilin University · CN

Funding

Winship Cancer Institute Cancer Center Support GrantP30CA138292 · NCI · EMORY UNIVERSITY · PI Suresh S Ramalingam · 2009 to 2026
$47.5M
miR-21 signaling in tumor response to radiation treatmentR01CA186129 · NCI · EMORY UNIVERSITY · PI WANG, YA · 2014 to 2018
$1.6M
Mechanism for miR-21-modulated radioresistanceR21CA185882 · NCI · EMORY UNIVERSITY · PI WANG, YA · 2015 to 2016
$373k
NCI NIH HHS P30 CA138292NCI NIH HHS R01 CA186129NCI NIH HHS R21 CA185882
6 · The paper itself

Abstract

purposeTo clarify which DNA double-strand break repair pathway, non-homologous end-joining (NHEJ), homologous recombination repair (HRR) or both, plays a key role in potentially lethal damage repair (PLDR). METHODS AND MATERIALS: Combining published data and our new potentially lethal damage repair (PLDR) data, we explain whether similar to sublethal damage repair (SLDR), PLDR also mainly depends on NHEJ versus HRR. The PLDR data used the same cell lines: wild type, HRR or NHEJ-deficient fibroblast cells, as those SLDR data published by our laboratory previously. The PLDR condition that we used was as commonly described by many other groups: the cells were collected immediately or overnight post ionizing radiation for colony formation after cultured to a plateau phase with a low concentration of serum medium.

resultsEnough data from other groups and our lab showed that wild type or HRR-deficient cells had efficient PLDR, but NHEJ deficient cells did not.

conclusionNHEJ contributes more to PLDR than HRR in mammalian cells, which is similar to SLDR. Since both SLDR and PLDR are relevant to clinical tumor status while undergoing radiotherapy, such clarification may benefit radiotherapy in the near future.

Indexed as

Adaptation, PhysiologicalAnimalsCell CycleDNADNA DamageDNA RepairDose-Response Relationship, DrugEvidence-Based MedicineHumansMetabolic Networks and PathwaysRadiation DosageDNADNA double strand break (DSB)DNA repair; homologous recombination repair (HRR); ionizing radiationnon-homologous end-joining (NHEJ); sublethal damage repair (SLDR); potentially lethal damage repair (PLDR); heavy ion

Identifiers

PMID27622834
PMCPMC5183539
OpenAlexW2519040550

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.