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Article

High frequency of p16 (CDKN2/MTS-1/INK4A) inactivation in head and neck squamous cell carcinoma.

Cancer research - 15 Aug 1996

Reed A L, Califano J, Cairns P, Westra W H, Jones R M, Koch W, Ahrendt S, Eby Y, Sewell D, Nawroz H, Bartek J, Sidransky D

Abstract excerpt

The tumor suppressor gene p16 (CDKN2/MTS-1/INK4A) can be inactivated by multiple genetic mechanisms. We analyzed 29 invasive primary head and neck squamous cell carcinomas (HNSCC) for p16 inactivation with immunohistochemistry utilizing a new monoclonal antibody (mAb), DCS-50. p16 staining of the...

Topics

Blotting, Southern
Carcinoma, Squamous Cell
Carrier Proteins
Cyclin-Dependent Kinase Inhibitor p16
DNA, Neoplasm
Exons
Genes, Tumor Suppressor
Head and Neck Neoplasms
Humans
Immunohistochemistry
Methylation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Mutation

Source

Identifiers

PMID: 8705996

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 30 Aug 2026. Prepared record publication-8705996-2026-08-30.1. Manifest publication-graph-cohort-2026-08-30.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 30 Aug 2026.

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High frequency of p16 (CDKN2/MTS-1/INK4A) inactivation in head and neck squamous cell carcinoma.PMID 8705996Read ↗

Inactivation of p16INK4a in primary tumors and cell lines of head and neck squamous cell carcinoma.Semantic proximity Read ↗

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Somatic INK4a-ARF locus mutations: a significant mechanism of gene inactivation in squamous cell carcinomas of the head and neck.Semantic proximity Read ↗

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