Evidence map›Paper›PMID 31102330›Full record

ReviewAndrology2019

Meiotic gene activation in somatic and germ cell tumours.

J Feichtinger, R J McFarlane

Open access · hybridAbstract readReview
In one paragraph

Review in Andrology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Special Issue "Advances in Genome Regulation in Cancer".International journal of molecular sciences · 2023
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Transcriptomics of Meiosis in the Male Mouse.Frontiers in cell and developmental biology · 2021
    Review
  15. Article
  16. 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

2 authors at 2 institutions in 2 countries.

J FeichtingerDivision of Cell Biology, Histology and Embryology, Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Medical University of Graz, Graz, Austria.ORCID 0000-0002-3667-5857
R J McFarlaneNorth West Cancer Research Institute, School of Medical Sciences, Bangor University, Bangor, Gwynedd, UK.ORCID 0000-0002-3139-3092
Bangor University · GBMedical University of Graz · AT

Funding

Austrian Science Fund FWF T 923
6 · The paper itself

Abstract

backgroundGerm cell tumours are uniquely associated with the gametogenic tissues of males and females. A feature of these cancers is that they can express genes that are normally tightly restricted to meiotic cells. This aberrant gene expression has been used as an indicator that these cancer cells are attempting a programmed germ line event, meiotic entry. However, work in non-germ cell cancers has also indicated that meiotic genes can become aberrantly activated in a wide range of cancer types and indeed provide functions that serve as oncogenic drivers. Here, we review the activation of meiotic factors in cancers and explore commonalities between meiotic gene activation in germ cell and non-germ cell cancers.

objectivesThe objectives of this review are to highlight key questions relating to meiotic gene activation in germ cell tumours and to offer possible interpretations as to the biological relevance in this unique cancer type. MATERIALS AND

methodsPubMed and the GEPIA database were searched for papers in English and for cancer gene expression data, respectively.

resultsWe provide a brief overview of meiotic progression, with a focus on the unique mechanisms of reductional chromosome segregation in meiosis I. We then offer detailed insight into the role of meiotic chromosome regulators in non-germ cell cancers and extend this to provide an overview of how this might relate to germ cell tumours.

conclusionsWe propose that meiotic gene activation in germ cell tumours might not indicate an unscheduled attempt to enter a full meiotic programme. Rather, it might simply reflect either aberrant activation of a subset of meiotic genes, with little or no biological relevance, or aberrant activation of a subset of meiotic genes as positive tumour evolutionary/oncogenic drivers. These postulates provide the provocation for further studies in this emerging field.

Indexed as

AnimalsFemaleHumansMaleMeiosisNeoplasms, Germ Cell and EmbryonalTranscriptional Activationgenome stabilitygerm cell tumourmeiosisoncogenesis

Identifiers

PMID31102330
PMCPMC6766858
OpenAlexW2946552508

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.