Revisiting DNA damage repair, p53-mediated apoptosis and cisplatin sensitivity in germ cell tumors Review uri icon


MeSH Major

  • Apoptosis
  • Cisplatin
  • DNA Repair
  • Drug Resistance, Neoplasm
  • Neoplasms, Germ Cell and Embryonal
  • Testicular Neoplasms
  • Tumor Suppressor Protein p53


  • Testicular germ cell tumors (TGCTs), ie, seminomas and nonseminomas, account for 1% to 3% of all neoplasms in men. They are the most common cancer in young white males and are unique in their responsiveness to cisplatin-based chemotherapy. For this reason, TGCTs are considered a model for curative disease. However, up to now, the molecular mechanisms behind this exceptional responsiveness to DNA-damaging agents have remained unclear. A hypersensitive apoptotic response, as well as a reduction in the proficiency to repair cisplatin-induced DNA damage might account for this behavior. In this review, building on recent findings of p53-induced apoptosis and DNA-repair mechanisms in TGCTs, we will discuss the molecular bases that drive tumor sensitivity to cisplatin, emphasizing the new therapeutic approaches proposed to eventually constrain tumor recurrence, and target TGCTs which are unresponsive to standard therapies.

publication date

  • July 17, 2013



  • Review



  • eng

Digital Object Identifier (DOI)

  • 10.1387/ijdb.130135mb

PubMed ID

  • 23784838

Additional Document Info

start page

  • 273

end page

  • 80


  • 57


  • 2-4