Article: article from journal or magazin.
Frequent p16INK4 (MTS1) gene inactivation in testicular germ cell tumors
American Journal of Pathology
Journal Article Research Support, Non-U.S. Gov't --- Old month value: Sep
The molecular mechanisms responsible for the development of testicular germ cell tumors (GCTs) have not as yet been elucidated. The aim of the present study was to determine whether genetic alterations of p16INK4 (MTS1) and/or cyclin-dependent kinase 4 (CDK4) occur in the genesis of these tumors. We have analyzed these two genes in 29 testicular GCTs, seminomas, and nonseminomas. None of the tumors showed either p16INK4 or CDK4 mutations. Only 1 of the 29 GCTs displayed loss of heterozygosity of the p16INK4 gene. No homozygous deletions of p16INK4 were detected. Evidence of hypermethylation of p16INK4 exon 1, however, was demonstrated in 13 of the 26 (50%) GCTs analyzed. Tumor samples having exon 1 of p16INK4 methylated expressed significantly lower levels of p16INK4 mRNA, as analyzed by reverse transcriptase polymerase chain reaction. These results suggest that p16INK4 inactivation plays a role in the genesis of GCTs.
Adolescent Adult Base Sequence Carrier Proteins/*genetics Child Child, Preschool Chromosome Deletion Cyclin-Dependent Kinase Inhibitor p16 DNA Methylation *Gene Expression Regulation, Neoplastic Genes, Tumor Suppressor/*genetics Heterozygote Humans Male Middle Aged Neoplasms, Germ Cell and Embryonal/*genetics Polymerase Chain Reaction Polymorphism, Genetic Polymorphism, Single-Stranded Conformational Proteins/genetics RNA, Messenger/metabolism Testicular Neoplasms/*genetics Tumor Suppressor Protein p14ARF
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