Evidence map›Paper›PMID 9358774›Full record

ArticleThe American journal of pathology1997

Subependymal astrocytic hamartomas in the Eker rat model of tuberous sclerosis.

R S Yeung, C D Katsetos, A Klein-Szanto

Abstract read
In one paragraph

Article in The American journal of pathology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 93 citations in OpenAlex.

  1. Genetics of familial acromegaly and pituitary gigantism.The Journal of clinical endocrinology and metabolism · 2026
    Review
  2. Endoscopic endonasal resection of olfactory tract hamartoma for pediatric epilepsy.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2024
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Mechanistic Target of Rapamycin Pathway in Epileptic Disorders.Journal of Korean Neurosurgical Society · 2019
    Article
  8. Review
  9. Article
  10. Review
  11. Novel animal models of pediatric epilepsy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2012
    Review
  12. Review
  13. Review
  14. The tuberous sclerosis complex.Annals of the New York Academy of Sciences · 2010
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  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

3 authors at 1 institution in 1 country.

R S YeungDivision of Medical Sciences, Fox Chase Cancer Center, Philadelphia, Pennsylvania, USA. ryeung@u.washington.edu
C D Katsetos
A Klein-Szanto
Fox Chase Cancer Center · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Margaret von Mehren · 1985 to 2026
$138.8M
CANCER SUSCEPTIBILITY IN AN ANIMAL MODELR01CA061889 · NCI · UNIVERSITY OF WASHINGTON · PI YEUNG, RAYMOND · 2000 to 2004
$1.7M
CANCER SUSCEPTIBILITY IN AN ANIMAL MODELR29CA061889 · NCI · UNIVERSITY OF WASHINGTON · PI YEUNG, RAYMOND · 1994 to 1998
–
NCI NIH HHS CA06927NCI NIH HHS CA61889
6 · The paper itself

Abstract

Tuberous sclerosis (TSC) is an autosomal dominant syndrome that is linked to two genetic loci: TSC1 (9q34) and TSC2 (16p13). Brain manifestations such as cortical tubers and subependymal hamartoma/giant cell astrocytomas are major causes of TSC-related morbidity. In this study, we describe the central nervous system involvement in a unique rodent model of tuberous sclerosis. The Eker rat carries a spontaneous germline mutation of the TSC2 gene and is predisposed to multiple neoplasia. In a series of 45 adult Eker carriers (TSC2 +/-), three types of focal intracranial lesions were found, of which the subependymal and subcortical hamartomas were most prevalent (65%). There exist remarkable phenotypic similarities between the Eker rat and human subependymal lesions. Our study indicates that the predominant cellular phenotype of the subependymal hamartomas is astroglial and suggests that the neuronal contribution within these lesions is, in part, the result of pre-existing myelinated axons. The hamartomas did not show evidence of loss of the wild-type TSC2 allele; it remains to be determined whether TSC2 inactivation is necessary for their pathogenesis. This genetically-defined rodent model may be useful in elucidating the molecular and developmental basis of the subependymal giant cell astrocytoma in humans.

Indexed as

Disease Models, AnimalAnimalsAstrocytesBrain DiseasesCalbindinsEpendymaGlial Fibrillary Acidic ProteinHamartomaImmunohistochemistryLoss of HeterozygosityMyelin Basic ProteinNeurofilament ProteinsRatsRats, Inbred F344Rodent DiseasesS100 Calcium Binding Protein GCalbindinsGlial Fibrillary Acidic ProteinMyelin Basic ProteinNeurofilament ProteinsS100 Calcium Binding Protein GTubulin

Identifiers

PMID9358774
PMCPMC1858083
OpenAlexW1752565791

What OpenQuestion holds

Textmetadata
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.