Evidence map›Paper›PMID 28045896›Full record

ArticlePLoS genetics2017

A Signature of Genomic Instability Resulting from Deficient Replication Licensing.

Steven C Pruitt, Maochun Qin, Jianmin Wang, Dimiter Kunnev, Amy Freeland

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  10. Ribosomal DNA and the nucleolus in the context of genome organization.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2019
    Review
  11. Article
  12. 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

5 authors at 1 institution in 1 country.

Steven C PruittDepartment of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, New York, United States of America.ORCID http://orcid.org/0000-0002-3966-8214
Maochun QinDepartment of Biostatistics and Bioinformatics, Roswell Park Cancer Institute, Buffalo, New York, United States of America.
Jianmin WangDepartment of Biostatistics and Bioinformatics, Roswell Park Cancer Institute, Buffalo, New York, United States of America.
Dimiter KunnevDepartment of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, New York, United States of America.
Amy FreelandDepartment of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, New York, United States of America.
Roswell Park Comprehensive Cancer Center · US

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MARK G FRATTINI · 1985 to 2026
$116.6M
Replication Licensing in Genome Stability, Cancer and AgingR01CA130995 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI KNUDSEN, ERIK · 2008 to 2022
$5.3M
Cell Proliferation in Genome and Tissue IntegrityR01AG041854 · NIA · ROSWELL PARK CANCER INSTITUTE CORP · PI PRUITT, STEVEN C · 2012 to 2016
$1.7M
NCI NIH HHS P30 CA016056NCI NIH HHS R01 CA130995NIA NIH HHS R01 AG041854
6 · The paper itself

Abstract

Insufficient licensing of DNA replication origins has been shown to result in genome instability, stem cell deficiency, and cancers. However, it is unclear whether the DNA damage resulting from deficient replication licensing occurs generally or if specific sites are preferentially affected. To map locations of ongoing DNA damage in vivo, the DNAs present in red blood cell micronuclei were sequenced. Many micronuclei are the product of DNA breaks that leave acentromeric remnants that failed to segregate during mitosis and should reflect the locations of breaks. To validate the approach we show that micronuclear sequences identify known common fragile sites under conditions that induce breaks at these locations (hydroxyurea). In MCM2 deficient mice a different set of preferred breakage sites is identified that includes the tumor suppressor gene Tcf3, which is known to contribute to T-lymphocytic leukemias that arise in these mice, and the 45S rRNA gene repeats.

Indexed as

DNA ReplicationGenomic InstabilityAnimalsBasic Helix-Loop-Helix ProteinsDNA DamageErythrocytesMiceMicronuclei, Chromosome-DefectiveMicronucleus TestsMinichromosome Maintenance Complex Component 2Basic Helix-Loop-Helix ProteinsMcm2 protein, mouseMinichromosome Maintenance Complex Component 2Tcf3 protein, mouse

Identifiers

PMID28045896
PMCPMC5242545
OpenAlexW2571290222

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.