CDKN2/p16 inactivation and p16 immunohistochemistry in astrocytic gliomas.

Piva,R; Cavalla,P; Bortolotto,S; Cordera,S; Grosso,R; Richiardi,P; Dutto,A; Schiffer,D

doi:10.3892/ijo.12.1.55

CDKN2/p16 inactivation and p16 immunohistochemistry in astrocytic gliomas.

Authors:
- R Piva
- P Cavalla
- S Bortolotto
- S Cordera
- R Grosso
- P Richiardi
- A Dutto
- D Schiffer
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Affiliations: Department of Neuroscience, University of Turin, via Cherasco, 15 I-10126 Turin, Italy.
Published online on: January 1, 1998 https://doi.org/10.3892/ijo.12.1.55
Pages: 55-63

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Abstract

CDKN2/p16 inactivation is the most frequent alteration in the molecular regulation of G1-S transition. CDKN2/p16 homozygous deletions was studied in paraffin-embedded sections of 45 astrocytic tumours by multiplex PCR. Immunohistochemistry for p16 and proliferation marker Ki-67 MIB-1 was performed in adjacent sections; their labelling index (LI) have been calculated. CDKN2/p16 gene was not deleted in astrocytomas, while homozygous deletion was found in 26.7% anaplastic astrocytomas, and in 55.0% of glioblastomas. Analysis of CDKN2/p16 homozygous deletion in discrete areas of the same tumour, showed that the deletion occurred independently of the phenotypic aspect of the areas. Nevertheless a genotypic and phenotypic heterogeneity is present in few cases. p16 immunohistochemistry mostly corresponds to the genotypic pattern. No correlation was found between CDKN2/p16 homozygous deletion and MIB-1 LI.