Evidence map›Paper›PMID 32151273›Full record

ReviewActa neuropathologica communications2020

Low-grade developmental and epilepsy associated brain tumors: a critical update 2020.

Rutger Juriaan Slegers, Ingmar Blumcke

Open access · goldAbstract readReview
In one paragraph

Review in Acta neuropathologica communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
14.8field-weighted citation impact, top 1% 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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 182 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Long-term outcomes of epilepsy surgery: A 25-year experience from a tertiary referral center.Epileptic disorders : international epilepsy journal with videotape · 2025
    Article
  10. Review
  11. Review
  12. Review
  13. Autoimmune encephalitis-associated epilepsy.Nature reviews. Neurology · 2025
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

15 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 2 countries.

Rutger Juriaan SlegersFaculty of Health, Medicine and Life Sciences, Maastricht University, Universiteitssingel 40, NL - 6229ER, Maastricht, The Netherlands.
Ingmar BlumckeDepartment of Neuropathology, University Hospitals Erlangen, Schwabachanalge 6, 91054, Erlangen, Germany. bluemcke@uk-erlangen.de.
Maastricht University · NLUniversitätsklinikum Erlangen · DE

Funding

Deutsche Forschungsgemeinschaft BL 421/4-1
6 · The paper itself

Abstract

Brain tumors represent the second most frequent etiology in patients with focal seizure onset before 18 years of age and submitted to epilepsy surgery. Hence, this category of brain tumors, herein defined as low-grade, developmental, epilepsy-associated brain tumors (LEAT) is different from those frequently encountered in adults as (A): 77% of LEAT occur in the temporal lobe; (B): the vast majority of LEAT are of low malignancy and classified as WHO I°; (C): LEAT are often composed of mixed glial and neuronal cell components and present with variable growth patterns including small cysts or nodules; (D): LEAT do not share common gene driving mutations, such as IDH1 or 1p/19q co-deletions. Characteristic entities comprise the ganglioglioma (GG), the dysembryoplastic neuroepithelial tumor (DNT), the angiocentric glioma (AG), the isomorphic diffuse glioma (IDG) and the papillary glio-neuronal tumor (PGNT), representing 73.2% of 1680 tumors collected in a large German series of 6747 patients submitted to epilepsy surgery. In the realm of exciting discoveries of genetic drivers of brain tumors new genes have been also reported for LEAT. BRAF V600E mutations were linked to GG with CD34 expression, FGFR1 mutations to DNT, MYB alterations to AG and also IDG and PRKCA fusions to PGNT, suggesting the possibility to also develop a genetically driven tumor classification scheme for LEAT. Rare availability of LEAT in a single center is a challenging obstacle, however, to systematically unravel the neurobiological nature and clinical behavior of LEAT. Other challenges in need of clarification include malignant tumor progression of LEAT entities, seizure relapse in patients following bulk tumor resection and the controversial issue of associated focal cortical dysplasia as additional pathomechanism. In order to advance our understanding and promote reliable diagnostic work-up of LEAT, we recommend, therefore, international collaboration to achieve our goals.

Indexed as

Arachnoid CystsAstrocytomaBrain NeoplasmsCentral Nervous System CystsDermoid CystEpidermal CystEpilepsies, PartialGangliogliomaHumansMolecular Diagnostic TechniquesNeoplasm GradingNeoplasms, NeuroepithelialOligodendrogliomaProtein Kinase C-alphaProto-Oncogene ProteinsProto-Oncogene Proteins B-rafBRAF protein, humanFGFR1 protein, humanMYBL1 protein, humanMYB protein, humanPRKCA protein, humanProtein Kinase C-alphaProto-Oncogene ProteinsProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-mybReceptor, Fibroblast Growth Factor, Type 1Trans-ActivatorsAstrocytomaGangliogliomaOligodendrogliomaPathologySeizure

Identifiers

PMID32151273
PMCPMC7063704
OpenAlexW3011566957

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.