Evidence map›Paper›PMID 24781529›Full record

ArticlePloS one2014

A pilot genome-scale profiling of DNA methylation in sporadic pituitary macroadenomas: association with tumor invasion and histopathological subtype.

Chao Ling, Matthew Pease, Lingling Shi, Vasu Punj, Mark S Shiroishi, Deborah Commins, Daniel J Weisenberger, Kai Wang, Gabriel Zada

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 3 pooled it
0.6field-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

35 citing papers in PubMed, 3 syntheses or guidelines pooled it, 46 citations in OpenAlex.

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  9. DNA Methylation in Pituitary Adenomas: A Scoping Review.International journal of molecular sciences · 2025
    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

9 authors at 1 institution in 2 countries.

Chao LingResearch Center of Basic Medical Sciences, Tianjin Medical University, Tianjin, China; Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
Matthew PeaseDepartment of Neurosurgery, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
Lingling ShiZilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
Vasu PunjNCCC Bioinformatics Core and Division of Hematology, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
Mark S ShiroishiDepartment of Radiology, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
Deborah ComminsDepartment of Pathology, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
Daniel J WeisenbergerUSC Epigenome Center, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
Kai WangZilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America; Department of Psychiatry, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America; Division of Bioinformatics, Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
Gabriel ZadaZilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America; Department of Neurosurgery, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
University of Southern California · US

Funding

Los Angeles Basin Clinical and Translational Science InstituteKL2RR031991 · NCRR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BUCHANAN, THOMAS A · 2010 to 2011
$1.6M
NCRR NIH HHS KL2 RR031991NCRR NIH HHS KL2RR031991
6 · The paper itself

Abstract

Pituitary adenomas (PAs) are neoplasms that may cause a variety of neurological and endocrine effects. Although known causal contributors include heredity, hormonal influence and somatic mutations, the pathophysiologic mechanisms driving tumorigenesis and invasion of sporadic PAs remain unknown. We hypothesized that alterations in DNA methylation are associated with PA invasion and histopathology subtype, and that genome-scale methylation analysis may complement current classification methods for sporadic PAs. Twenty-four surgically-resected sporadic PAs with varying histopathological subtypes were assigned dichotomized Knosp invasion scores and examined using genome-wide DNA methylation profiling and RNA sequencing. PA samples clustered into subgroups according to functional status. Compared with hormonally-active PAs, nonfunctional PAs exhibited global DNA hypermethylation (mean beta-value 0.47 versus 0.42, P = 0.005); the most significant site of differential DNA methylation was within the promoter region of the potassium voltage-gated channel KCNAB2 (FDR = 5.11×10-10). Pathway analysis of promoter-associated CpGs showed that nonfunctional PAs are potentially associated with the ion-channel activity signal pathway. DNA hypermethylation tended to be negatively correlated with gene expression. DNA methylation analysis may be used to identify candidate genes involved in PA function and may potentially complement current standard immunostaining classification in sporadic PAs. DNA hypermethylation of KCNAB2 and downstream ion-channel activity signal pathways may contribute to the endocrine-inactive status of nonfunctional PAs.

Indexed as

DNA MethylationAdenomaAdolescentAdultAgedAged, 80 and overCpG IslandsFemaleGene Expression Regulation, NeoplasticGenome, HumanHumansMaleMiddle AgedNeoplasm InvasivenessPituitary GlandPituitary NeoplasmsKCNAB2 protein, humanPotassium Channels, Voltage-GatedShaker Superfamily of Potassium Channels

Identifiers

PMID24781529
PMCPMC4004564
OpenAlexW2092378745

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.