摘要
AIM： To understand the local pathophysiological alterations and gene ontology-based functional classification of colonic biopsies into inflammatory and neoplastic diseases. 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, 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-l, bystin-like, calgranulin-A, TRAIL receptor 3）. IBD samples were characterized by overregulated chemokine （C-X-C motif） ligand 13, replication protein A1, E74-1ike factor 2 and downregu- fated TNF receptor-associated factor 6, BCL2-interacting killer genes. In adenomas upregulation of TNF receptorassociated factor 6, replication protein A1, E74-1ike factor 2 and underexpression of BCL2-associated X protein, calgranulin-A genes were found. CRC cases had significantly increased epidermal growth factor receptor, topoisomerase-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-PCR confirmed 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 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.
基金
Supported by Epigenomics Inc
