Molecular Genetic Correlates of p16, cdk4, and pRb Immunohistochemistry in Glioblastomas

摘要: The vast majority of glioblastomas have CDKN2A , CDK4 or RB gene alterations that perturb the p16-cdk4-pRb cell cycle regulatory cascade. To explore whether immunohistochemical methods provide an alternative means assessing this pathway, we studied 25 using a combination molecular genetic and assays. Homozygous deletion was detected in 12 (48%) cases, amplification 4 (16%) tumors, loss heterozygosity at 8 22 (36%) informative cases. Five (20%) had diffuse p16 positivity. Significantly, all these either LOH, suggesting immunopositivity only occurs those tumors with another component pathway. Nineteen (76%) cases were uniformly immunonegative for pl6, homozygous deletions, but remaining 7 lacked mutations promoter methylation. All stained diffusely cdk4, irrespective status. Extensive pRb staining present most maintained both alleles, absent loss, there notable discrepancies. Thus, immunohistochemistry cannot replace analysis critical cascade; instead, combined results hint complex regulation checkpoint. From practical point view, although pl6 immunonegativity does not necessarily indicate deletion, positive p 16 immunostaining strongly suggests excludes deletion.