Abstract
In the human embryo, the genetic program that orchestrates germ cell specification involves the activation of epigenetic and transcriptional mechanisms that make the germline a unique cell population continuously poised between germness and pluripotency. Germ cell tumors, neoplasias originating from fetal or neonatal germ cells, maintain such dichotomy and can adopt either pluripotent features (embryonal carcinomas) or germness features (seminomas) with a wide range of phenotypes in between these histotypes. Here, we review the basic concepts of cell specification, migration and gonadal colonization of human primordial germ cells (hPGCs) highlighting the analogies of transcriptional/epigenetic programs between these two cell types.
Highlights
In mammals, the unique core regulatory circuitry of transcriptional factors, epigenetics and signaling inputs regulating germline specification is becoming revealed.In the present work, we critically review old and new evidence that the unique pluripotency status is imposed on human primordial germ cells (hPGCs) by epigenetics traits regulated by pluripotency, and germline transcription factors that make these cells prone to undergo tumorigenesis
We critically review old and new evidence that the unique pluripotency status is imposed on hPGCs by epigenetics traits regulated by pluripotency, and germline transcription factors that make these cells prone to undergo tumorigenesis
Gunnar Teilum first proposed a theory concerning the malignant potential of extragonadal germ cells known as the “germ cell theory”, suggesting that EGCTs originate from stray PGCs, which have undergone a malignant transformation during embryonic development [5]
Summary
The unique core regulatory circuitry of transcriptional factors, epigenetics and signaling inputs regulating germline specification is becoming revealed. We critically review old and new evidence that the unique pluripotency status is imposed on hPGCs by epigenetics traits regulated by pluripotency, and germline transcription factors that make these cells prone to undergo tumorigenesis. Such notion is discussed under the view that PGCs might be part of a pluripotent stem/progenitor cell pool exhibiting common markers that contribute to various somatic cell lineages (see [1,2,3])
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