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Jeffrey D. Rawnsley, MD, MS; Eri S. Srivatsan, PhD; Rita Chakrabarti, PhD; Kathleen R. Billings, MD; Marilene B. Wang, MD

Arch Otolaryngol Head Neck Surg. 1997;123(8):863-867.

Abstract
Background
Recently, the p16/CDKN2/MTS1 gene in the 9p21-22 region has been offered as a candidate tumor suppressor gene. We examined the frequency of hemizygous and homozygous deletions of p16/CDKN2 in head and neck squamous cell carcinoma (HNSCC) using a quantitative polymerase chain reaction (PCR) method.

Design
Twenty-one HNSCC and 12 corresponding normal DNA samples were examined for deletion of p16/CDKN2 using PCR amplification and fluorescent quantification of DNA. All tumor and normal DNA samples were also amplified with fluorescein-labeled primers for a control DNA marker on chromosome 8p (D8S265). The ratios of the observed fluorescence of the p16/CDKN2 and 8p PCR products were compared.

Setting and participants
Patients with HNSCC scheduled to undergo surgical resection of their tumors were recruited. After the specimen was removed, a portion of the tissue was snap frozen for further DNA extraction.

Results
Eight tumors (38%) had p16/CDKN2-D8S265 ratios of greater than 0.75; 8 tumors (38%), from 0.25 to 0.75; and 5 tumors (24%), of less than 0.25, the average ratio in this last group being 0.06.

Conclusions
These ratios suggest a higher rate of homozygous deletion than previously reported and significant probable hemizygous deletion of the p16/CDKN2 gene in HNSCC.

Arch Otolaryngol Head Neck Surg. 1997;123:863-867

Author Affiliations
From the Division of Head and Neck Surgery, Department of Surgery, University of California—Los Angeles School of Medicine (Drs Rawnsley, Billings, and Wang), and the Division of General Surgery, Wadsworth Veterans Administration Hospital (Drs Srivatsan and Chakrabarti), Los Angeles, Calif.

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