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We have examined genetic alterations in 11 surgically removed oral squamous cell carcinomas (OSCCs) using comparative genomic hybridization (CGH) and laser scanning cytometry (LSC), which allow quantitative analysis of chromosomal abnormalities. CGH analysis revealed gains and/or losses of DNA sequence copy number in all tumors. Gains in DNA sequence copy number were detected frequently for chromosome arms 3q25-28 (6/11), 5p (6/11) and 8q (5/11), and losses in chromosome arms 18q (4/11), 19q (4/11), 17p (3/11), and 19p (3/11). Amplification of 5p was observed in two tumors. LSC detected DNA aneuploidy with DNA indices ranging from 1.30 to 1.82 in 6 of 11 tumors. The number of chromosomal aberrations was higher in DNA aneuploid tumors than in diploid tumors (8.17 vs 3.60/tumor, P<0.05). Furthermore, the average number of chromosomal aberrations was significantly higher in stage T2 tumors and larger tumors than in stage T1 tumors (7.71 vs 3.25/tumor, P<0.05). Our results suggest that DNA aneuploidy and large tumor size reflect an underlying chromosomal instability.

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We detected genetic alterations in 14 cell lines established from 14 human oral squamous cell carcinomas (OSCCs) using comparative genomic hybridization (CGH), which allows a comprehensive analysis of chromosomal imbalances and identification of nonrandom genetic aberrations specific to OSCCs. All cell lines showed gains and losses of DNA copy number. DNA losses were detected for chromosomes 18q (10/14) and 4q (9/14) with minimal overlapping regions of 18q 12–32 and 4q31‐qter, respectively. In contrast, the common sites for increased copy number were chromosomes 5p (12/14), 8q23‐ter (11/14), 20p (8/14), 20q (8/14), and 3q25‐ter (7/14). These results suggest that losses of 18q12–22 and 4q31‐ter and gains of 5p and 8q23‐ter play important roles in the development and/or progression of OSCC.