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KMID : 0361019950380060916
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Korean Journal of Otolaryngology - Head and Neck Surgery
1995 Volume.38 No. 6 p.916 ~ p.927
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Increased Polysomies of Chromosome 7 and 17 and p53 Overexpression in Squamous Cell Carcinoma of the Larynx
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Abstract
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This study was carried out to understand the relationship between specific chromosome changes and their phenotypic consequences at the tissue level of human laryngeal cancers. Fourteen paraffin-embedded human laryngeal squamous cell carcinoma
samples
were investigated for the evidence of genetic alterations. Using chromosome 7 and 17-specific repetitive α-satellite DNA probes. The mean chromosome index was 1.26 for chromosome 7 and 1.07 for chromosome 17. Normal lymphocytes and stromal cells
showed
one or two chromosome signals per cell in most cases. There was three or more chromosome signals per cell with 35.1% of cancer cells for chromosome 7 and 12.3% for chromosome 17. An increase in copy number, particularly of chromosome 7 was
associated
with a less favorable phenotype, including high nuclear grade. The tumor-suppressor protein p53 is overexpressed in 64.3% of squamous cell carcinomas of the larynx. There was a significant difference in the frequency of p53 negativity between
tumors
from patients, died of cancer (80%) and those who had been disease-free for more than 5 years (11%). PCNA immunostaining revealed growth dysregulation of tumor cells and intratumoral heterogeneity. PCNA labelling inden ranged from 11% to 80% in
tumor
cells. There was no significant correlation between p53 protein overexpression and PCNA LI.
There results suggest that chromosome polysomy for chromosomes 7 and 17 are present in laryngeal squamous cell carcinomas. There is a strong correlation between genotypic abnormalities and tumor phenotype in human laryngeal cancer, p53
overexpression
and growth dysregulation revealed by PCNA LI could be an excellent biomarkers and give an additional biological information in laryngeal cancer patients. This capabability will prove to be an important tool for determining the underlying genetic
basis
for tumor development, tissue phenotype heterogeneity and progression by allowing genetic determination to be made on paraffin-embedded tissue sections where tumor histologic architecture is preserved. (Korean J Otolaryngol 38:6, 1995)
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