[KIT receptor in testicular seminoma]

KIT receptor expression is observed in the majority of seminomas. Activation of KIT tyrosine kinase due to somatic mutations has been demonstrated. Mutations of the c-kit gene in testicular seminomas are located in exon 17. Inhibitors of KIT tyrosine kinase activity can have a therapeutic role, particularly in seminomas with a c-kit mutation sensitive to imatinib mesylate. A clinical trial plans to examine the efficacy of imatinib mesylate in the treatment of metastatic seminomas refractory to chemotherapy. Tyrosine kinase inhibitors can also be tested in patients with minimal retroperitoneal lymph node involvement before radiotherapy. If they are active, future therapeutic trials could include the use of these inhibitors as adjuvant therapy for patients with stage I seminoma in order to decrease the potential risk of second tumour.