Frequent p16INK4 (MTS1) gene inactivation in testicular germ cell tumors.

摘要: The molecular mechanisms responsible for the development of testicular germ cell tumors (GCTs) have not as yet been elucidated. aim present study was to determine whether genetic alterations p16INK4 (MTS1) and/or cyclin-dependent kinase 4 (CDK4) occur in genesis these tumors. We analyzed two genes 29 GCTs, seminomas, and nonseminomas. None showed either or CDK4 mutations. Only 1 GCTs displayed loss heterozygosity gene. No homozygous deletions were detected. Evidence hypermethylation exon 1, however, demonstrated 13 26 (50%) analyzed. Tumor samples having methylated expressed significantly lower levels mRNA, by reverse transcriptase polymerase chain reaction. These results suggest that inactivation plays a role GCTs.