Gastric adenocarcinoma (GA) presents a challenge in understanding the complex interactions of environmental factors with genotype in carcinogenesis. The National Cancer Centre has taken a multifaceted approach to this problem with comparative genomic hybridization of freshly resected GAs. Data from nine cases of intestinal and five cases of diffuse histological types showed the common aberrations to be loss of 4pq (four cases) and gains of 17pq (five cases) and 20pq (four cases). We also documented amplifications in 22q (six cases), 20q (five cases) and 1pq (two cases). High-level gains were present in 20q11.2q12 (three cases), 10q24.3q25.1 (one case) and 12q14 (one case). Two cases of diffuse GA showed no change. High-level amplifications in 10q24.3q25.1 and 12q14 have not been reported previously. High-level amplification of 12q14 could be associated with overexpression of MDM2, CDK4 and RAP1B. Three cytochrome P450 hydroxylases map to 10q24. Loss of 4pq is a common abnormality in cases of GA; its biological significance may be related to loss of function of caspase 3, caspase 6 and PTPN13, which is frequently deleted in liver and ovarian cancers. High-level gain of 20q or 20pq was another striking finding of this preliminary study. Amplified genes of probable importance from this genomic region are those for DNA methyltransferase 3B, E2F transcription factor 1, EHT and matrix metalloproteinase 5. Gain of 17pq or 17q has been frequently reported in cases of GA, and candidate genes of relevance to gastric carcinogenesis are HER-2/neu, and those encoding survivin and gastrin.