Evidence map›Paper›PMID 24367530›Full record

SynthesisPloS one2013

The role of epigenetic modification in tumorigenesis and progression of pituitary adenomas: a systematic review of the literature.

Matthew Pease, Chao Ling, William J Mack, Kai Wang, Gabriel Zada

Open access · goldAbstract readSystematic Review
In one paragraph

Synthesis in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. DNA Methylation in Pituitary Adenomas: A Scoping Review.International journal of molecular sciences · 2025
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. [Update on mechanisms of pituitary tumorigenesis.]Revista de la Facultad de Ciencias Medicas (Cordoba, Argentina) · 2021
    Review
  18. Aggressive pituitary tumours and pituitary carcinomas.Nature reviews. Endocrinology · 2021
    Review
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Matthew PeaseDepartment of Neurosurgery, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
Chao LingZilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
William J MackDepartment of Neurosurgery, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America ; Zilkha Neurogenetic Institute, 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 ZadaDepartment of Neurosurgery, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America ; Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
University of Southern California · US

Funding

Southern California Clinical and Translational Science InstituteKL2TR000131 · NCATS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BUCHANAN, THOMAS A · 2012 to 2015
$2.1M
NCATS NIH HHS KL2 TR000131
6 · The paper itself

Abstract

backgroundPituitary adenomas (PAs) are commonly occurring neoplasms with diverse endocrine and neurological effects. Although somatic gene mutations are uncommon in sporadic PAs, recent studies lend support to epigenetic modification as a potential cause of tumorigenesis and tumor progression.

methodsA systematic literature review of the PubMed and Google Scholar databases was conducted to identify abstracts (n=1,082) pertaining to key targets and mechanisms implicated in epigenetic dysregulation of PAs published between 1993-2013. Data regarding histopathological subtype, target genes, mode of epigenetic modification, and clinical correlation were recorded and analyzed.

resultsOf the 47 that studies met inclusion criteria and focused on epigenomic assessment of PAs, only 2 were genome-scale analyses. Current evidence supports epigenetic alteration in at least 24 PA genes, which were categorized into four groups based on function and epigenetic alteration: 1) Sixteen tumor suppressor genes silenced via DNA methylation; 2) Two oncogenes overexpressed via histone acetylation and hypomethylation; 3) Three imprinted genes with selective allelic silencing; and 4) One epigenome writer inducing abnormal genome-scale activity and 5) Two transcription regulators indirectly modifying the genome. Of these, 5 genes (CDKN2A, GADD45y, FGFR2, caspase-8, and PTAG) showed particular susceptibility to epigenetic modification, with abnormal DNA methylation in >50% of PA samples. Several genes displayed correlations between epigenetic modification and clinically relevant parameters, including invasiveness (CDKN2A; DAPK; Rb1), sex (MAGE-A3), tumor size (GNAS1), and histopathological subtype (CDKN2A; MEG3; p27; RASSF1A; Rb1).

conclusionsEpigenetic modification of selected PA genes may play a key role in tumorigenesis and progression, which may translate into important diagnostic and therapeutic applications.

Indexed as

Apoptosis Regulatory ProteinsCaspase 8Cyclin-Dependent Kinase Inhibitor p16DNA MethylationEpigenesis, GeneticHumansPituitary NeoplasmsReceptor, Fibroblast Growth Factor, Type 2Apoptosis Regulatory ProteinsCaspase 8Cyclin-Dependent Kinase Inhibitor p16FGFR2 protein, humanReceptor, Fibroblast Growth Factor, Type 2RHBDD3 protein, human

Identifiers

PMID24367530
PMCPMC3867353
OpenAlexW2017730226

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.