Evidence map›Paper›PMID 22937135›Full record

ArticlePloS one2012

Prevalence of c-KIT mutations in gonadoblastoma and dysgerminomas of patients with disorders of sex development (DSD) and ovarian dysgerminomas.

Remko Hersmus, Hans Stoop, Gert Jan van de Geijn, Ronak Eini, Katharina Biermann, J Wolter Oosterhuis, Catharina Dhooge, Dominik T Schneider, Isabelle C Meijssen, Winand N M Dinjens and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 58 citations in OpenAlex.

  1. Germ cell tumors in children.Virchows Archiv : an international journal of pathology · 2025
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  8. New C3H KitScientific reports · 2022
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  11. Review
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  14. Review
  15. Zebrafish Germ Cell Tumors.Advances in experimental medicine and biology · 2016
    Review
  16. Article
  17. 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

13 authors at 5 institutions in 3 countries.

Remko HersmusDepartment of Pathology, Erasmus MC - University Medical Center Rotterdam, Josephine Nefkens Institute, Daniel den Hoed Cancer Center, Rotterdam, The Netherlands.
Hans Stoop
Gert Jan van de Geijn
Ronak Eini
Katharina Biermann
J Wolter Oosterhuis
Catharina Dhooge
Dominik T Schneider
Isabelle C Meijssen
Winand N M Dinjens
Hendrikus Jan Dubbink
Stenvert L S Drop
Leendert H J Looijenga
Erasmus MC Cancer Institute · NLErasmus MC · NLErasmus University Rotterdam · NLGhent University Hospital · BEKlinikum Dortmund · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activating c-KIT mutations (exons 11 and 17) are found in 10-40% of testicular seminomas, the majority being missense point mutations (codon 816). Malignant ovarian dysgerminomas represent ~3% of all ovarian cancers in Western countries, resembling testicular seminomas, regarding chromosomal aberrations and c-KIT mutations. DSD patients with specific Y-sequences have an increased risk for Type II Germ Cell Tumor/Cancer, with gonadoblastoma as precursor progressing to dysgerminoma. Here we present analysis of c-KIT exon 8, 9, 11, 13 and 17, and PDGFRA exon 12, 14 and 18 by conventional sequencing together with mutational analysis of c-KIT codon 816 by a sensitive and specific LightCycler melting curve analysis, confirmed by sequencing. The results are combined with data on TSPY and OCT3/4 expression in a series of 16 DSD patients presenting with gonadoblastoma and dysgerminoma and 15 patients presenting pure ovarian dysgerminomas without DSD. c-KIT codon 816 mutations were detected in five out of the total of 31 cases (all found in pure ovarian dysgerminomas). A synonymous SNP (rs 5578615) was detected in two patients, one DSD patient (with bilateral disease) and one patient with dysgerminoma. Next to these, three codon N822K mutations were detected in the group of 15 pure ovarian dysgerminomas. In total activating c-KIT mutations were found in 53% of ovarian dysgerminomas without DSD. In the group of 16 DSD cases a N505I and D820E mutation was found in a single tumor of a patient with gonadoblastoma and dysgerminoma. No PDGFRA mutations were found. Positive OCT3/4 staining was present in all gonadoblastomas and dysgerminomas investigated, TSPY expression was only seen in the gonadoblastoma/dysgerminoma lesions of the 16 DSD patients. This data supports the existence of two distinct but parallel pathways in the development of dysgerminoma, in which mutational status of c-KIT might parallel the presence of TSPY.

Indexed as

AdolescentAdultBiomarkers, TumorCell Cycle ProteinsChildChild, PreschoolDisorders of Sex DevelopmentDNA Mutational AnalysisDysgerminomaFemaleGonadoblastomaHumansInfantMaleMutationOctamer Transcription Factor-3Biomarkers, TumorCell Cycle ProteinsOctamer Transcription Factor-3Proto-Oncogene Proteins c-kitTSPY1 protein, human

Identifiers

PMID22937135
PMCPMC3429439
OpenAlexW2062379582

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Registered trials

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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.