Evidence map›Paper›PMID 31130628›Full record

ArticleCancers2019

TCam-2 Cells Deficient for SOX2 and FOXA2 Are Blocked in Differentiation and Maintain a Seminoma-Like Cell Fate In Vivo.

Daniel Nettersheim, Saskia Vadder, Sina Jostes, Alena Heimsoeth, Hubert Schorle

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. EditingInternational journal of molecular sciences · 2021
    Review
  12. Review
  13. Article
  14. Cancers · 2020
    Article
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

5 authors at 2 institutions in 1 country.

Daniel NettersheimDepartment of Urology, Urological Research Lab, Translational Urooncology, University Hospital Düsseldorf, 40225 Düsseldorf, Germany. Daniel.Nettersheim@med.uni-duesseldorf.de.ORCID 0000-0002-4483-845X
Saskia VadderDepartment of Developmental Pathology, Institute of Pathology, Bonn University Medical School, 53127 Bonn, Germany. Saskia.Vadder@gmx.de.
Sina JostesDepartment of Developmental Pathology, Institute of Pathology, Bonn University Medical School, 53127 Bonn, Germany. Sina.Jostes@ukbonn.de.
Alena HeimsoethDepartment of Developmental Pathology, Institute of Pathology, Bonn University Medical School, 53127 Bonn, Germany. Alena.Heimsoeth@uk-koeln.de.
Hubert SchorleDepartment of Developmental Pathology, Institute of Pathology, Bonn University Medical School, 53127 Bonn, Germany. Hubert.Schorle@ukbonn.de.ORCID 0000-0001-8272-0076
University of Bonn · DEDüsseldorf University Hospital · DE

Funding

Deutsche Forschungsgemeinschaft SCHO 503/16-1
6 · The paper itself

Abstract

Testicular germ cell tumors (GCTs) are very common in young men and can be stratified into seminomas and non-seminomas. While seminomas share a similar gene expression and epigenetic profile with primordial germ cells, the stem cell population of the non-seminomas, the embryonal carcinoma (EC), resembles malignant embryonic stem cells. Thus, ECs are able to differentiate into cells of all three germ layers (teratomas) and even extra-embryonic-tissue-like cells (yolk-sac tumor, choriocarcinoma). In the last years, we demonstrated that the cellular microenvironment considerably influences the plasticity of seminomas (TCam-2 cells). Upon a microenvironment-triggered inhibition of the BMP signaling pathway in vivo (murine flank or brain), seminomatous TCam-2 cells reprogram to an EC-like cell fate. We identified SOX2 as a key factor activated upon BMP inhibition mediating the reprogramming process by regulating pluripotency, reprogramming and epigenetic factors. Indeed, CRISPR/Cas9 SOX2-deleted TCam-2 cells were able to maintain a seminoma-cell fate in vivo for about six weeks, but after six weeks in vivo still small sub-populations initiated differentiation. Closer analyses of these differentiated clusters suggested that the pioneer factor FOXA2 might be the driving force behind this induction of differentiation, since many FOXA2 interacting genes and differentiation factors like

Indexed as

embryonal carcinomaFOXA2germ cell tumorsmicroenvironmentreprogrammingseminomaSOX2

Identifiers

PMID31130628
PMCPMC6562827
OpenAlexW2946152502

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.