Testicular germ cell tumors (TGCTs) represent the most common malignancy in men
aged 15-35. Due to these tumors’ biological and clinical characteristics, they can serve as an appropriate
system for studying molecular mechanisms associated with cisplatin-based treatment resistance.
This review describes treatment resistance from clinical and molecular viewpoints. Cisplatin
resistance is determined by various biological mechanisms, including the modulation of the DNA
repair capacity of cancer cells, alterations to apoptotic cell death pathways, deregulation of gene expression
pathways, epigenetic alterations and insufficient DNA binding. Moreover, this review describes
TGCTs as a model system that enables the study of the cellular features of cancer stem cells
in metastatic process and describes experimental models that can be used to study treatment resistance
in TGCTs. All of the abovementioned aspects may help to elucidate the molecular mechanisms
underlying cisplatin resistance and may help to identify promising new therapeutic targets.
HNF1β is a sensitive and specific novel marker for yolk sac tumor: a tissue microarray analysis of 601 testicular germ cell tumors