Abstract

Testicular germ cell tumors (TGCTs) represent the most common solid tumors affecting young men. They constitute a distinct entity because of their embryonic origin and their unique biological behavior. Recent preclinical data regarding biological signaling machinery as well as genetic and epigenetic mechanisms associated with molecular patterns of tumors have contribute to explain the pathogenesis and the differentiation of TGCTs and to understand the mechanisms responsible for the development of resistance to treatment. In this review, we discuss the main genetic and epigenetic events associated with TGCTs development in order to better define their role in the pathogenesis of these tumors and in cisplatin-acquired resistance.

Highlights

  • Testicular germ cell tumors (TGCTs) represent the most common solid tumors affecting the young male population, with a peak incidence between the third and fourth decades of life [1]

  • Recent preclinical data regarding biological signaling machinery as well as genetic and epigenetic mechanisms associated with molecular patterns of tumors have contribute to explain the pathogenesis and the differentiation of TGCTs and to understand the mechanisms responsible for the development of resistance to treatment

  • Nonseminomatous TGCTs include embryonal carcinoma (EC), which has similarities to stem cells and is able to differentiate into several somatic lineages whereas the cells that constitute seminomas tumors resemble to primordial germ cells (PGCs) and/or the cells in the carcinoma in situ (CIS), making TGCTs an intriguing model for investigate gametogenesis and germ cell development in both normal and cancer systems

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Summary

Introduction

Testicular germ cell tumors (TGCTs) represent the most common solid tumors affecting the young male population, with a peak incidence between the third and fourth decades of life [1]. Recent preclinical data regarding biological signaling machinery as well as genetic and epigenetic mechanisms associated with molecular patterns of tumors have contribute to explain the pathogenesis and the differentiation of TGCTs and to understand the mechanisms responsible for the development of resistance to treatment.

Results
Conclusion

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