| Theme | Update in management of colitic cancer | |
|---|---|---|
| Title | Role of genomic alterations in ulcerative colitis-associated colorectal neoplasia | |
| Publish Date | 2009/05 | |
| Author | Natsuko Saito | Department of Surgical and Molecular Pathology, Dokyo University School of Medicine / Saito Clinic |
| Author | Shigehiko Fujii | Department of Surgical and Molecular Pathology, Dokyo University School of Medicine |
| Author | Akira Sekikawa | Department of Surgical and Molecular Pathology, Dokyo University School of Medicine |
| Author | Kazuhito Ichikawa | Department of Surgical and Molecular Pathology, Dokyo University School of Medicine |
| Author | Shigeki Tomita | Department of Surgical and Molecular Pathology, Dokyo University School of Medicine |
| Author | Hirokazu Fukui | Department of Surgical and Molecular Pathology, Dokyo University School of Medicine |
| Author | Joji Imura | Department of Surgical and Molecular Pathology, Dokyo University School of Medicine |
| Author | Yoshikuni Saito | Saito Clinic |
| Author | Takahiro Fujimori | Department of Surgical and Molecular Pathology, Dokyo University School of Medicine |
| [ Summary ] | We analysed the differences between carcinogenesis in ulcerative colitis associated tumors and sporadic colorectal cancer. It is now believed, and widely accepted, that sporadic colorectal cancers develop through three pathways, the adenoma-carcinoma sequence (ACS), the hereditary nonpolyposis colorectal cancer (HNPCC) pathway and the de novo pathway. On the other hand, ulcerative colitis-associated tumors develop through the pathway, known as the chronic colitis-dysplasia-carcinoma sequence, which is caused by chronic infl ammation. Ulcerative colitis-related carcinogenesis also appears to differ from sporadic colorectal carcinogenesis in relation to different frequencies of specific aberrations. In our examination of current literature , the mutation rates for BRAF, rates of DNA hypermethylation and microsatellite instability were not statistically significant in either. However, the mutation rates for APC and K ras in ulcerative colitis associated tumors were lower than for sporadic colorectal cancer. Thus, genetic investigation plays an important role in adjunctive diagnosis. The establishment and application of genetic diagnosis is desirable for clinical approaches for early detection and treatment, especially screen of high-risk patients who's genetic makeup may lead to ulcerative colitis-associated tumors. |
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