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Andrology. 2019 Jul;7(4):415-427. doi: 10.1111/andr.12628. Epub 2019 May 17.

Meiotic gene activation in somatic and germ cell tumours.

Author information

1
Division of Cell Biology, Histology and Embryology, Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Medical University of Graz, Graz, Austria.
2
OMICS Center Graz, BioTechMed Graz, Graz, Austria.
3
North West Cancer Research Institute, School of Medical Sciences, Bangor University, Bangor, Gwynedd, UK.

Abstract

BACKGROUND:

Germ 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.

OBJECTIVES:

The 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 METHODS:

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

RESULTS:

We 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.

CONCLUSIONS:

We 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.

KEYWORDS:

genome stability; germ cell tumour; meiosis; oncogenesis

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