ABSTRACT
Lymph-node metastasis is an important indicator in the diagnosis of colon cancer. In order to determine the genes involved in metastasis, genomic copy-number aberrations in the primary tumours and lymph-node metastases were analysed in 12 patients using comparative genomic hybridization. This method detects genomic copy-number changes at the chromosomal level and the identification of the regions of aberration on any chromosome. Copy-number gains at 6p12 and losses at 8p12 were observed in a greater number of the primary tumours than in the metastases. These aberrations appear to be involved in lymph-node metastasis of colon cancer, and may allow measurement of the risk of lymph-node metastasis from a given colon cancer.
Subject(s)
Adenocarcinoma/genetics , Chromosome Aberrations , Colonic Neoplasms/genetics , Lymph Nodes/pathology , Lymphatic Metastasis/genetics , Adenocarcinoma/secondary , Adenocarcinoma/surgery , Chromosomes, Human, Pair 6 , Chromosomes, Human, Pair 8 , Colonic Neoplasms/pathology , Colonic Neoplasms/surgery , DNA, Neoplasm/analysis , Female , Gene Amplification , Gene Dosage , Genome , Humans , Lymphatic Metastasis/pathology , Male , Nucleic Acid HybridizationABSTRACT
Colorectal cancer is thought to be more common in men than in women. The chromosomal locations of DNA gains and losses in surgical specimens of colorectal tumours were detected by comparative genomic hybridization and were compared by gender. Five chromosomal regions, 7p, 8p, 8q, Xp and Xq, contained multiple gains that were significantly more common in males than in females, and within these regions, the differences were significant for Xp21, Xp11.3, Xp11.4 and Xq26. Regions 1p, 3q, 11q, 12p, 12q and 15q contained multiple sites of gain that were significantly more common in females than in males. Tumours from male and female patients showed significantly more losses at 11p and 15q, and at 4q and Xq, respectively. The fact that gains in X-chromosomal regions were detected with a significantly higher frequency in tumours from male patients suggests that the difference between the genders might be explained by X-chromosomal inactivation.