Evidence map›Paper›PMID 22725639›Full record

Trial reportJournal of cutaneous pathology2012

Misregulation of Rad50 expression in melanoma cells.

Nathan L Avaritt, Richard Owens, Signe K Larson, Matthew Reynolds, Stephanie Byrum, Kim M Hiatt, Bruce R Smoller, Alan J Tackett, Wang L Cheung

Open access · greenAbstract readClinical Trial
In one paragraph

Trial report in Journal of cutaneous pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 48% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Rad50 promotes ovarian cancer progression through NF-κB activation.Journal of cellular and molecular medicine · 2021
    Article
  2. 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

9 authors at 1 institution in 1 country.

Nathan L Avaritt *Department of Biochemistry, University of Arkansas for Medical Sciences, Little Rock, AR 72205.
Richard Owens *Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, AR 72205.
Signe K LarsonDepartment of Biochemistry, University of Arkansas for Medical Sciences, Little Rock, AR 72205.
Matthew ReynoldsDepartment of Biochemistry, University of Arkansas for Medical Sciences, Little Rock, AR 72205.
Stephanie ByrumDepartment of Biochemistry, University of Arkansas for Medical Sciences, Little Rock, AR 72205.
Kim M HiattDepartment of Pathology, University of Arkansas for Medical Sciences, Little Rock, AR 72205.
Bruce R SmollerDepartment of Pathology, University of Arkansas for Medical Sciences, Little Rock, AR 72205.
Alan J TackettDepartment of Biochemistry, University of Arkansas for Medical Sciences, Little Rock, AR 72205.
Wang L CheungDepartment of Biochemistry, University of Arkansas for Medical Sciences, Little Rock, AR 72205.
University of Arkansas for Medical Sciences · US

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR029884 · NCRR · UNIV OF ARKANSAS FOR MED SCIS · PI LOWERY, CURTIS L · 2009 to 2011
$11.4M
Development of technology for high resolution epigenetic profiling of chromatinR01DA025755 · NIDA · UNIV OF ARKANSAS FOR MED SCIS · PI TACKETT, ALAN, TAVERNA, SEAN D. · 2008 to 2011
$1.6M
Arkansas Center for Clinical Translational ResearchKL2RR029883 · NCRR · UNIV OF ARKANSAS FOR MED SCIS · PI LOWERY, CURTIS L · 2009 to 2011
$588k
Identification of combinatorial histone post-translational modifications within tF32GM093614 · NIGMS · UNIV OF ARKANSAS FOR MED SCIS · PI BYRUM, STEPHANIE D · 2011 to 2012
$101k
NCRR NIH HHS KL2 RR029883NCRR NIH HHS KL2RR029883NCRR NIH HHS UL1 RR029884NCRR NIH HHS UL1RR029884NIDA NIH HHS R01 DA025755NIDA NIH HHS R01DA025755NIGMS NIH HHS F32 GM093614NIGMS NIH HHS F32GM093614
6 · The paper itself

Abstract

DNA double-strand breaks are increased in human melanoma tissue as detected by histone H2AX phosphorylation.(1-3) We investigated two of the downstream effectors of DNA double-strand breaks, Rad50 and 53BP1 (tumor suppressor p53 binding protein 1), to determine if they are altered in human primary melanoma cells. Melanoma cases showed high Rad50 staining (81.8%; 9/11) significantly more frequently than conventional or atypical melanocytic nevi (0%; 0/18). In contrast, the staining pattern for 53BP1 appears similar between melanoma and nevi. This is the first study that shows activation and misregulation of the DNA repair pathway in human melanoma cells. The staining features of Rad50, a component of an essential DNA double-strand break repair complex, are clearly increased in melanoma cells with regards to both staining intensity and the number of positive melanoma cells. Interestingly, among the melanoma cases with increased Rad50 staining, most demonstrated cytoplasmic rather than nuclear staining (88.9%, 8/9). Further studies are needed to determine the cause of this mislocalization and its affects, if any, on DNA double-strand break repair in melanoma.

Indexed as

Gene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticMelanomaAcid Anhydride HydrolasesDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA, NeoplasmDNA RepairDNA Repair EnzymesFemaleHistonesHumansIntracellular Signaling Peptides and ProteinsMaleMiddle AgedNeoplasm ProteinsAcid Anhydride HydrolasesDNA-Binding ProteinsDNA, NeoplasmDNA Repair EnzymesHistonesIntracellular Signaling Peptides and ProteinsNeoplasm ProteinsRAD50 protein, humanTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1

Identifiers

PMID22725639
PMCPMC4237308
OpenAlexW2053829862

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.