| 特集名 | colitic cancer診断update | |
|---|---|---|
| 題名 | 1. 発生 (2) 潰瘍性大腸炎合併大腸腫瘍における遺伝子異常の役割 | |
| 発刊年月 | 2009年 05月 | |
| 著者 | 斎藤 奈津子 | 獨協医科大学病理学（人体分子）／斉藤内科医院 |
| 著者 | 藤井 茂彦 | 獨協医科大学病理学（人体分子） |
| 著者 | 関川 昭 | 獨協医科大学病理学（人体分子） |
| 著者 | 市川 一仁 | 獨協医科大学病理学（人体分子） |
| 著者 | 冨田 茂樹 | 獨協医科大学病理学（人体分子） |
| 著者 | 福井 広一 | 獨協医科大学病理学（人体分子） |
| 著者 | 井村 穣二 | 獨協医科大学病理学（人体分子） |
| 著者 | 斎藤 芳国 | 斉藤内科医院 |
| 著者 | 藤盛 孝博 | 獨協医科大学病理学（人体分子） |
| 【 要旨 】 | 潰瘍性大腸炎（ulcerative colitis；UC）合併大腸腫瘍は，散発性大腸腫瘍とは異なった経路で発生し，遺伝子学的特徴も両者で異なる点が多い．またUC合併大腸腫瘍では，その非腫瘍性粘膜においてもさまざまな遺伝子変化が起こっていることが明らかになっている．これらの遺伝子異常は，UC合併大腸腫瘍の病理診断において補助的診断として有用であるとともに，腫瘍発生の新たな危険因子となり，高危険症例の拾い上げが可能となることが期待されている． | |
| Theme | Update in management of colitic cancer | |
|---|---|---|
| Title | Role of genomic alterations in ulcerative colitis-associated colorectal neoplasia | |
| 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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