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Deletion analysis of the p16/CDKN2 gene in head and neck squamous cell carcinoma using quantitative polymerase chain

J D Rawnsley1, E S Srivatsan, R Chakrabarti

  • 1Department of Surgery, University of California-Los Angeles School of Medicine, USA.

Abstract

Insights

This study investigated deletions of the p16/CDKN2 tumor suppressor gene in head and neck squamous cell carcinoma (HNSCC). Findings suggest a higher frequency of homozygous and hemizygous deletions than previously reported in HNSCC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The p16/CDKN2/MTS1 gene, located on chromosome 9p21-22, is a potential tumor suppressor.
  • Alterations in this gene are implicated in various cancers, including head and neck squamous cell carcinoma (HNSCC).

Purpose of the Study:

  • To determine the frequency of hemizygous and homozygous deletions of the p16/CDKN2 gene in HNSCC.
  • To assess the role of p16/CDKN2 gene alterations in the development of HNSCC.

Main Methods:

  • Quantitative polymerase chain reaction (PCR) was employed to analyze DNA samples from 21 HNSCC tumors and 12 normal tissues.
  • Fluorescent quantification of PCR products for p16/CDKN2 and a control marker on chromosome 8p (D8S265) allowed for ratio comparisons.

Main Results:

  • Analysis revealed varying deletion patterns: 38% of tumors showed high p16/CDKN2-D8S265 ratios (>0.75), 38% had intermediate ratios (0.25-0.75), and 24% exhibited low ratios (<0.25).
  • The average ratio in the low-ratio group was 0.06, indicating substantial gene loss.

Conclusions:

  • The observed deletion rates suggest a higher incidence of homozygous and probable hemizygous deletion of p16/CDKN2 in HNSCC than previously documented.
  • These findings underscore the potential significance of p16/CDKN2 gene alterations in HNSCC pathogenesis.

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