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Article

Loss of P16INK4 expression is frequent in high grade gliomas.

Cancer research - 1 May 1995

Nishikawa R, Furnari F B, Lin H, Arap W, Berger M S, Cavenee W K, Su Huang H J

Abstract excerpt

P16INK4 is a cell cycle regulator that specifically binds to and inactivates cyclin-dependent kinase 4 (CDK4). Its encoding gene (p16/CDKN2) maps to chromosome 9p21, a region that undergoes frequent loss of heterozygosity in a variety of human tumors. We have analyzed the p16/CDKN2 gene and its expression in a series of primary glioma samples. Although homozygous deletion or mutation of the p16/CDKN2 gene was...

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Source

Identifiers

PMID: 7728764

Genes

CDK4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

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Loss of P16INK4 expression is frequent in high grade gliomas.PMID 7728764Read ↗

p16 Immunohistochemical Expression as a Surrogate Assessment of CDKN2A Alteration in Gliomas Leading to Prognostic SignificancesSemantic proximity Read ↗

Expression of p19 INK4d, CDK4, CDK6 in glioblastoma multiformeSemantic proximity Read ↗

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p14ARF deletion and methylation in genetic pathways to glioblastomas.Semantic proximity Read ↗

Identification of p18 INK4c as a tumor suppressor gene in glioblastoma multiforme.Semantic proximity Read ↗

Expression of the p16INK4A/Cdkn2a gene is prevalently downregulated in human pheochromocytoma tumor specimens.Semantic proximity Read ↗

Point mutations can inactivate in vitro and in vivo activities of p16(INK4a)/CDKN2A in human glioma.Semantic proximity Read ↗

CDKN2 (p16/MTS1) gene deletion or CDK4 amplification occurs in the majority of glioblastomas.Semantic proximity Read ↗

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