特集名 |
colitic cancer診断update |
題名 |
1. 発生 (1) 潰瘍性大腸炎合併腫瘍の発生 -- 炎症性発癌と一般大腸腫瘍との差異について |
発刊年月 |
2009年 05月 |
著者 |
味岡 洋一 |
新潟大学大学院医歯学総合研究科分子・診断病理学分野 |
著者 |
岩永 明人 |
新潟大学大学院医歯学総合研究科分子・診断病理学分野 |
著者 |
渡辺 順 |
新潟大学大学院医歯学総合研究科分子・診断病理学分野 |
著者 |
西倉 健 |
新潟大学大学院医歯学総合研究科分子・診断病理学分野 |
著者 |
渡辺 玄 |
新潟大学大学院医歯学総合研究科分子・診断病理学分野 |
著者 |
加藤 卓 |
新潟大学大学院医歯学総合研究科分子・診断病理学分野 |
【 要旨 】 |
長期経過潰瘍性大腸炎(UC)の大腸粘膜には,一般大腸に発生する腫瘍(腺腫,高分化腺癌)と組織学的には区別がつかないものと,それらとは異なる組織像を示すものとがある.癌の組織発生の点では,前者は一般大腸にみられる(1) adenoma carcinoma sequence,(2) de novo発癌,(3) serrated polyp neoplasia pathway,のいずれかと同系列の発癌過程の腫瘍,後者は炎症粘膜に特有な発癌過程(炎症性発癌)の腫瘍と考えられる.炎症性発癌病変は,(1) 表層分化を示す高分化腺癌,(2) 分化細胞を豊富にもつ高分化腺癌,(3) 細胞分化にきわめて乏しい高分化腺癌,(4) 粘膜内で脱分化をきたした低分化腺癌や印環細胞癌,(5) 一般大腸粘膜の腺腫とも癌とも判定が困難な腫瘍,に大別され,さらに一般大腸腫瘍とは異なる肉眼形態,p53蛋白過剰発現,細胞増殖動態を示す.腫瘍の組織像にこれら3要素を組み合わせることが,UCに偶発した一般大腸腫瘍と炎症性発癌病変とを病理学的に鑑別するためのポイントである. |
Theme |
Update in management of colitic cancer |
Title |
Histogenesis of colitis associated colorectal neoplasia |
Author |
Yoichi Ajioka |
Division of Molecular and Diagnostic Pathology, Graduate School of Medical and Dental Sciences, Niigata University |
Author |
Akito Iwanaga |
Division of Molecular and Diagnostic Pathology, Graduate School of Medical and Dental Sciences, Niigata University |
Author |
Jun Watanabe |
Division of Molecular and Diagnostic Pathology, Graduate School of Medical and Dental Sciences, Niigata University |
Author |
Ken Nishikura |
Division of Molecular and Diagnostic Pathology, Graduate School of Medical and Dental Sciences, Niigata University |
Author |
Gen Watanabe |
Division of Molecular and Diagnostic Pathology, Graduate School of Medical and Dental Sciences, Niigata University |
Author |
Takashi Kato |
Division of Molecular and Diagnostic Pathology, Graduate School of Medical and Dental Sciences, Niigata University |
[ Summary ] |
Intramucosal colorectal neoplasias complicated by long-standing ulcerative colitis (UC) can be divided histologically into two groups ; ones which are in distinguishible from tumors found in the colorectum, and ones which display unique feature be compared to tumors in the ordinary colorectum. From the view point of cancer histogenesis, the former tumors may be thought to be related to the lineage of the following 1) adenoma-carcinoma sequence, 2) de novo cancerization, 3) serrated polyp neoplasia pathway, in the ordinary colorectum. The latter tumors are thought to be of specific histogenetic pathway in the inflammatory mucosa (colitis-carcinoma sequence). Intramucosal neoplasias, which are thought to developed through colitis-arcinoma sequence are grouped as follows by their histological features ; 1) well differentiated tumors (WDT) with surperficial differentiation, 2) WDT with abundant differentiated cells, 3) WDT without differentiated cells, 4) dedifferentiated type tumor (poorly differentiated adenocarcinoma, signet ring cell carcinoma), and 5) tumors which cannot be classified as either benign or malignant. Furthermore, these tumors display unique macroscopic features such as p53 protein overexpression, and cell kinetics as compared to the ordinary intramucosal neoplasia of colorectum. Tumors in the line of the colitis-carcinoma sequence and in the lines for ordinary cancer histogenesis may be differentiated pathologically by the combination of these three features and the histological findings. |