Evidence map›Paper›PMID 31413324›Full record

ReviewNature reviews. Cancer2019

Human germ cell tumours from a developmental perspective.

J Wolter Oosterhuis, Leendert H J Looijenga

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 172 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
172citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

172 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Guideline
  4. Meta-Analysis of Gene Expressions in Testicular Germ Cell Tumor Histologies.International journal of molecular sciences · 2020
    Pooled it
  5. Trial
  6. Overlapping genetic etiology of pediatric and adult germ cell tumors.Journal of the National Cancer Institute · 2026
    Article
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112 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.

J Wolter OosterhuisLaboratory for Experimental Patho-Oncology, Department of Pathology, Erasmus MC Cancer Institute, Rotterdam, Netherlands. j.w.oosterhuis@erasmusmc.nl.ORCID http://orcid.org/0000-0002-6685-686X
Leendert H J LooijengaLaboratory for Experimental Patho-Oncology, Department of Pathology, Erasmus MC Cancer Institute, Rotterdam, Netherlands.ORCID http://orcid.org/0000-0002-8146-1911

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human germ cell tumours (GCTs) are derived from stem cells of the early embryo and the germ line. They occur in the gonads (ovaries and testes) and also in extragonadal sites, where migrating primordial germ cells are located during embryogenesis. This group of heterogeneous neoplasms is unique in that their developmental potential is in effect determined by the latent potency state of their cells of origin, which are reprogrammed to omnipotent, totipotent or pluripotent stem cells. Seven GCT types, defined according to their developmental potential, have been identified, each with distinct epidemiological and (epi)genomic features. Heritable predisposition factors affecting the cells of origin and their niches likely explain bilateral, multiple and familial occurrences of the different types of GCTs. Unlike most other tumour types, GCTs are rarely caused by somatic driver mutations, but arise through failure to control the latent developmental potential of their cells of origin, resulting in their reprogramming. Consistent with their non-mutational origin, even the malignant tumours of the group are characterized by wild-type TP53 and high sensitivity for DNA damage. However, tumour progression and the rare occurrence of treatment resistance are driven by embryonic epigenetic state, specific (sub)chromosomal imbalances and somatic mutations. Thus, recent progress in understanding GCT biology supports a comprehensive developmental pathogenetic model for the origin of all GCTs, and provides new biomarkers, as well as potential targets for treatment of resistant disease.

Indexed as

Epigenesis, GeneticAllelesAnimalsBiomarkers, TumorCell MovementDisease ProgressionEmbryonic DevelopmentFemaleGene Expression Regulation, DevelopmentalGene Expression Regulation, NeoplasticGenomic ImprintingGenomicsHumansKaryotypingMaleMutationBiomarkers, Tumor

Identifiers

What Socratic 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 Socratic graph.