AIM: To understand the local pathophysiological altera- tions and gene ontology-based functional classification of colonic biopsies into inflammatory and neoplastic dis- eases. METHODS: Total RNA was extracted from frozen biop- sies and amplified by T7-method. Expression profile was evaluated by Atlas Glass 1K microarrays. After microar- ray quality control, applicable data were available from 10 adenomas, 6 colorectal adenocarcinomas (CRCs), and 6 inflammatory bowel diseases (IBDs). Multivariate statistical and cell functional analyses were performed. Real-time RT-PCR and immunohistochemistry were used for validation. RESULTS: Discriminant analysis of selected genes, could correctly reclassify all 22 samples using 4 parameters (heat shock transcription factor-1, bystin-like, calgranu- lin-A, TRAIL receptor 3). IBD samples were characterized by overregulated chemokine (C-X-C motif) ligand 13, replication protein A1, E74-like factor 2 and downregu- lated TNF receptor-associated factor 6, BCL2-interacting killer genes. In adenomas upregulation of TNF receptor- associated factor 6, replication protein A1, E74-like factor 2 and underexpression of BCL2-associated X protein, cal- granulin-A genes were found. CRC cases had significantly increased epidermal growth factor receptor, topoisomer- ase-1, v-jun, TNF receptor-associated factor 6 and TRAIL receptor 3, and decreased RAD51 and RAD52 DNA repair gene, protein phosphatase-2A and BCL2-interacting killer mRNA levels. Epidermal growth factor receptor RT-PCR and immunohistochemistry, topoisomerase-1 RT-PCRconfirmed the chip results. CONCLUSION: Different histological alterations can be reclassified by functional, multivariate analysis using cDNA microarrays. Further studies with expanded sample number are needed for subclassification of pathological alterations. AIM: To understand the local pathophysiological alteraisms and gene ontology-based functional classification of colonic biopsies into inflammatory and neoplastic dis- eases. METHODS: Total RNA was extracted from frozen biopsies and amplified by T7-method. Expression profile was evaluated by Atlas Glass 1K microarrays. After microarray quality control, suitable data were available from 10 adenomas, 6 colorectal adenocarcinomas (CRCs), and 6 inflammatory bowel diseases (IBDs). Multivariate statistical and cell functional analyzes were performed. -PCR and immunohistochemistry were used for validation. RESULTS: Discriminant analysis of selected genes, could correctly reclassify all 22 samples using 4 parameters (heat shock transcription factor-1, bystin-like, calgranu-lin-A, TRAIL receptor 3) samples were characterized by overregulated chemokine (CXC motif) ligand 13, replication protein A1, E74-like factor 2 and downreguated TNF receptor-associated factor 6 , BCL2-interacting killer genes. In adenomas upregulation of TNF receptor-associated factor 6, replication protein A1, E74-like factor 2 and underexpression of BCL2-associated X protein, cal- granulin-A genes were found. epidermal growth factor receptor, topoisomer-ase-1, v-jun, TNF receptor-associated factor 6 and TRAIL receptor 3, and decreased RAD51 and RAD52 DNA repair genes, protein phosphatase-2A and BCL2- Receptor RT-PCR and immunohistochemistry, topoisomerase-1 RT-PCRconfirmed the chip results. CONCLUSION: Different histological alterations can be reclassified by functional, multivariate analysis using cDNA microarrays. Further studies with expanded sample number are needed for subclassification of pathological alterations.