Evidence map›Paper›PMID 34112938›Full record

ArticleScientific reports2021

Differential methylation of G-protein coupled receptor signaling genes in gastrointestinal neuroendocrine tumors.

Seyoun Byun, Kajsa E Affolter, Angela K Snow, Karen Curtin, Austin R Cannon, Lisa A Cannon-Albright, Ramya Thota, Deborah W Neklason

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

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  7. The Journal of international medical research · 2022
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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

8 authors at 3 institutions in 1 country.

Seyoun ByunHuntsman Cancer Institute, University of Utah, 2000 Circle of Hope, Salt Lake City, UT, 84112-5550, USA.
Kajsa E AffolterHuntsman Cancer Institute, University of Utah, 2000 Circle of Hope, Salt Lake City, UT, 84112-5550, USA.
Angela K SnowHuntsman Cancer Institute, University of Utah, 2000 Circle of Hope, Salt Lake City, UT, 84112-5550, USA.
Karen CurtinHuntsman Cancer Institute, University of Utah, 2000 Circle of Hope, Salt Lake City, UT, 84112-5550, USA.
Austin R CannonDivision of General Surgery, Department of Surgery, University of Utah School of Medicine, Salt Lake City, USA.
Lisa A Cannon-AlbrightHuntsman Cancer Institute, University of Utah, 2000 Circle of Hope, Salt Lake City, UT, 84112-5550, USA.
Ramya ThotaMedical Oncology, Intermountain Healthcare, Salt Lake City, USA.
Deborah W NeklasonHuntsman Cancer Institute, University of Utah, 2000 Circle of Hope, Salt Lake City, UT, 84112-5550, USA. deb.neklason@hci.utah.edu.
University of Utah · USHuntsman Cancer Institute · USIntermountain Healthcare · US

Funding

From genomics to natural language processing: A protected environment for research computing in the health scienceS10OD021644 · OD · UNIVERSITY OF UTAH · PI CHEATHAM, THOMAS E. · 2017 to 2017
$494k
Genetic and Environmental Etiology of Familial Small Intestinal Carcinoid CancerR21CA205796 · NCI · UNIVERSITY OF UTAH · PI NEKLASON, DEBORAH WOOD · 2016 to 2017
$461k
NCI NIH HHS R21 CA205796NIH HHS S10 OD021644
6 · The paper itself

Abstract

Neuroendocrine tumors (NETs) of the small intestine undergo large chromosomal and methylation changes. The objective of this study was to identify methylation differences in NETs and consider how the differentially methylated genes may impact patient survival. Genome-wide methylation and chromosomal copy number variation (CNV) of NETs from the small intestine and appendix were measured. Tumors were divided into three molecular subtypes according to CNV results: chromosome 18 loss (18LOH), Multiple CNV, and No CNV. Comparison of 18LOH tumors with MultiCNV and NoCNV tumors identified 901 differentially methylated genes. Genes from the G-protein coupled receptor (GPCR) pathways are statistically overrepresented in the differentially methylated genes. One of the highlighted genes from the GPCR pathway is somatostatin (SST), a clinical target for NETs. Patient survival based on low versus high methylation in all samples identified four significant genes (p < 0.05) OR2S2, SMILR, RNU6-653P, and AC010543.1. Within the 18LOH molecular subtype tumors, survival differences were identified in high versus low methylation of 24 genes. The most significant is TRHR (p < 0.01), a GPCR with multiple FDA-approved drugs. By separating NETs into different molecular subtypes based on chromosomal changes, we find that multiple GPCRs and their ligands appear to be regulated through methylation and correlated with survival. These results suggest opportunities for better treatment strategies for NETs based on molecular features.

Indexed as

AdultAgedAged, 80 and overDisease-Free SurvivalDNA Copy Number VariationsDNA MethylationFemaleGastrointestinal NeoplasmsGene Expression Regulation, NeoplasticGenome, HumanHumansIntestine, SmallMaleMiddle AgedNeoplasm ProteinsNeuroendocrine TumorsNeoplasm ProteinsReceptors, G-Protein-Coupled

Identifiers

PMID34112938
PMCPMC8192774
OpenAlexW3133667273

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Registered trials

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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.