Evidence map›Paper›PMID 24035864›Full record

ReviewMolecular and cellular endocrinology2014

Genetic and epigenetic mutations of tumor suppressive genes in sporadic pituitary adenoma.

Yunli Zhou, Xun Zhang, Anne Klibanski

Abstract readReview
In one paragraph

Review in Molecular and cellular endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Pituitary Adenoma:Medicina (Kaunas, Lithuania) · 2024
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
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  15. Review
  16. HMGA2 cooperates with either p27Cell cycle (Georgetown, Tex.) · 2018
    Article
  17. Expression of E-cadherin, Slug and NCAM and its relationship to tumor invasiveness in patients with acromegaly.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017
    Article
  18. Article
  19. 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

3 authors at 2 institutions in 1 country.

Yunli ZhouNeuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, United States.
Xun ZhangNeuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, United States.
Anne KlibanskiNeuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, United States. Electronic address: aklibanski@partners.org.
Harvard University · USMassachusetts General Hospital · US

Funding

HORMONE REGULATION AND PATHOGENESIS OF PITUITARY TUMORSR01DK040947 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI KLIBANSKI, ANNE · 1989 to 2010
$2.7M
NIDDK NIH HHS R01 DK040947NIDDK NIH HHS R01DK40947
6 · The paper itself

Abstract

Human pituitary adenomas are the most common intracranial neoplasms. Approximately 5% of them are familial adenomas. Patients with familial tumors carry germline mutations in predisposition genes, including AIP, MEN1 and PRKAR1A. These mutations are extremely rare in sporadic pituitary adenomas, which therefore are caused by different mechanisms. Multiple tumor suppressive genes linked to sporadic tumors have been identified. Their inactivation is caused by epigenetic mechanisms, mainly promoter hypermethylation, and can be placed into two groups based on their functional interaction with tumor suppressors RB or p53. The RB group includes CDKN2A, CDKN2B, CDKN2C, RB1, BMP4, CDH1, CDH13, GADD45B and GADD45G; AIP and MEN1 genes also belong to this group. The p53 group includes MEG3, MGMT, PLAGL1, RASSF1, RASSF3 and SOCS1. We propose that the tumor suppression function of these genes is mainly mediated by the RB and p53 pathways. We also discuss possible tumor suppression mechanisms for individual genes.

Indexed as

Epigenesis, GeneticAdenomaAnimalsHumansMutationPituitary NeoplasmsRetinoblastoma ProteinTumor Suppressor Protein p53Retinoblastoma ProteinTumor Suppressor Protein p53EpigeneticGenetic mutationp53RBSporadic pituitary adenomaTumor suppression

Identifiers

PMID24035864
PMCPMC3943596
OpenAlexW1999582566

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.