Evidence map›Paper›PMID 28779875›Full record

ReviewMutation research2017

Paths from DNA damage and signaling to genome rearrangements via homologous recombination.

Jac A Nickoloff

Abstract readReview
In one paragraph

Review in Mutation research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Article
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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

1 author.

Jac A NickoloffDepartment of Environmental and Radiological Health Sciences, Colorado State University, 1618 Campus Delivery, Fort Collins, CO 80523, United States. Electronic address: J.Nickoloff@colostate.edu.

Funding

METNASE ROLES IN NHEJ, DNA INTEGRATION AND TRANSLOCATIONR01GM084020 · NIGMS · COLORADO STATE UNIVERSITY · PI NICKOLOFF, JAC A · 2009 to 2016
$2.4M
NIGMS NIH HHS R01 GM084020
6 · The paper itself

Abstract

DNA damage is a constant threat to genome integrity. DNA repair and damage signaling networks play a central role maintaining genome stability, suppressing tumorigenesis, and determining tumor response to common cancer chemotherapeutic agents and radiotherapy. DNA double-strand breaks (DSBs) are critical lesions induced by ionizing radiation and when replication forks encounter damage. DSBs can result in mutations and large-scale genome rearrangements reflecting mis-repair by non-homologous end joining or homologous recombination. Ionizing radiation induces genetic change immediately, and it also triggers delayed events weeks or even years after exposure, long after the initial damage has been repaired or diluted through cell division. This review covers DNA damage signaling and repair pathways and cell fate following genotoxic insult, including immediate and delayed genome instability and cell survival/cell death pathways.

Indexed as

DNA DamageGene RearrangementGenome, HumanGenomic InstabilityHomologous RecombinationSignal TransductionHumansDNA damageDNA repairGenome instabilityRadiation

Identifiers

PMID28779875
PMCPMC9157578

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.