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Germ Cell Cancer, Testicular Dysgenesis Syndrome and Epigenetics

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Book cover Epigenetics and Human Reproduction

Part of the book series: Epigenetics and Human Health ((EHH))

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Abstract

Testicular dysgenesis syndrome (TDS) comprises a series of disorders, which are linked by an aberrant development of the testis, including abnormal differentiation of somatic cells and delayed maturation of germ cells. Environmental factors (including endocrine disrupters) are thought to impair development of the testis. It is likewise though that epigenetic patterns can be regulated by environmental stimuli and we here review the current knowledge on epigenetic patterns in testicular dysgenesis, which to a large extend is limited to testicular cancer. Testicular Germ Cell Tumors (TGCTs) of young adults originate from a precursor cell, carcinoma in situ testis, which has features of arrested and transformed gonocytes, including high expression of embryonic pluripotency genes and low genome methylation. Overt TGCTs are capable of a marked re-programming with loss of germinal phenotype and increased somatic differentiation. These features suggest a role for epigenetic changes in the pathogenesis and progression of TGCT. In addition to chromatin modifications and gene imprinting, other regulatory mechanisms have been emerging, i.e., miRNAs, which are instrumental in the regulation of gene transcription. It is possible that epigenetic reprogramming during early development may also be a cause of genital malformations and reduced spermatogenesis, but more research is needed to identify the causative environmental factors, their precise targets and affected pathways.

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Almstrup, K., Mlynarska, O., Meyts, E.RD. (2011). Germ Cell Cancer, Testicular Dysgenesis Syndrome and Epigenetics. In: Rousseaux, S., Khochbin, S. (eds) Epigenetics and Human Reproduction. Epigenetics and Human Health. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-14773-9_2

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