Comparative analysis of cell adhesion molecules, cell cycle regulatory proteins, mismatch repair genes, cyclooxygenase-2, and DPC4 in carcinomas arising in inflammatory bowel disease and sporadic colon cancer

• Published in: Oncology reports Vol. 11; no. 5; p. 951
• Main Authors: Hill, Kalisha A, Wang, Kim L, Stryker, Steven J, Gupta, Rohit, Weinrach, David M, Rao, M S
• Format: Journal Article
• Language: English
• Published: Greece 01-05-2004
• Subjects: Adaptor Proteins, Signal Transducing; Base Pair Mismatch - physiology; beta Catenin; Cadherins - metabolism; Carrier Proteins; Cell Adhesion Molecules - metabolism; Cell Cycle Proteins - metabolism; Colonic Neoplasms - complications; Colonic Neoplasms - enzymology; Colonic Neoplasms - metabolism; Cyclin D1 - metabolism; Cyclin-Dependent Kinase Inhibitor p21; Cyclin-Dependent Kinase Inhibitor p27; Cyclins - metabolism; Cyclooxygenase 2; Cytoskeletal Proteins - metabolism; DNA-Binding Proteins - metabolism; Gene Expression Profiling; Humans; Hyaluronan Receptors - metabolism; Inflammatory Bowel Diseases - complications; Inflammatory Bowel Diseases - enzymology; Inflammatory Bowel Diseases - metabolism; Isoenzymes - metabolism; Membrane Proteins; MutL Protein Homolog 1; MutS Homolog 2 Protein; Neoplasm Proteins - metabolism; Nuclear Proteins; Prostaglandin-Endoperoxide Synthases - metabolism; Proto-Oncogene Proteins - metabolism; Smad4 Protein; Trans-Activators - metabolism; Tumor Suppressor Proteins - metabolism
• DOI: 10.3892/or.11.5.951
• ISSN: 1021-335X

Colon carcinoma arising in inflammatory bowel disease often exhibits aggressive behavior compared to sporadic carcinomas. The rationale for the different biological behaviors of these two groups of tumors is not fully understood. In this study, we have examined carcinomas arising in inflammatory bowel disease (IBD) and sporadic carcinomas (SCA) for molecular differences that may provide clues for the behavioral disparity of these tumors. Thirty-eight colon carcinomas (12 from ulcerative colitis, 5 from Crohn's disease, and 21 SCA) were analyzed by immunohistochemistry for cell adhesion molecules (E-cadherin, beta-catenin, CD44), cell cycle regulatory proteins (cyclin D1, p27, p21), mismatch repair proteins (hMLH1, hMSH2), cyclooxygenase-2 and DPC4. Carcinomas arising in IBD showed significant decrease in expression of cell adhesion molecules, the cell cycle inhibitor protein, p21, and increased expression of cyclooxygenase-2 compared to sporadic carcinomas. No differences were observed in the expression of cell cycle regulatory proteins p27, cyclin D1, DPC4 and mismatch repair proteins between these two groups of tumors. Decreased expression of p21 as well as adhesion molecules may provide increased impetus for the aggressive behavior of tumors arising in inflammatory bowel disease.