大腸腫瘍の組織構築と発育進展様式

Clinicopathological Features and Growth Pattern of Epithelial Tumors of the Colorectum

要旨　大腸早期癌165病変と陥凹型腺腫35病変の臨床病理学的特徴とp53蛋白発現を解析した．非隆起型癌（non-polypoid growth carcinoma; NPG癌）は隆起型癌（polypoid growth carcinoma; PG癌）に比べ男性に多く，右側結腸発生率が高く，長径が小さく，腺腫合併率が低く，両者の組織発生の違いが示唆された．更にNPG癌のうち粘膜内成分が表層全層型のものは，陥凹型腺腫と性差，発生部位，組織構築の点で共通性があり，それらの組織発生の関連性が示唆された．また，NPG癌，PG癌ともに腺腫内癌より純粋癌で脈管侵襲とリンパ節転移が高率であった．以上から，組織発生の違いにより発育進展様式や悪性度が異なると考えられた．p53蛋白発現は組織構築や悪性度とは相関はなかった．

　Clinicopathological features and p53 protein overexpression were evaluated on 165 lesions with early colorectal carcinoma 〔86 non-polypoid growth carcinomas (NPG-Ca), and 79 polypoid growth carcinomas (PG-Ca), and 35 depressed adenomas〕. Compared with PG-Cas, NPG-Cas were more frequently found in the proximal colon and men, and were smaller in diameter, and were less frequently accompanied by adenoma. This findings suggested that there was different carcinogenesis between NPG-Ca and PG-Ca. Among NPG-Cas, there were differences in sex ratio, location, incidence of submucosal invasion and lymphovascular permeation, between the lesions with intramucosal carcinomatous component in the superficial and whole thickness portion of the mucosa (SW-type) and those in the only deep portion of the mucosa (D-type). The SW-type accompanied submucosal invasion and lymphovascular permeation more frequently than the D-type. On the other hand, SW-type and the depressed adenoma had the same characteristics on the sex ratio, tumor location and histological architectures, which indicated that there might be common carcinogenesis between the SW-type carcinoma and the depressed adenoma. In both NPG-Ca and PG-Ca, pure carcinomas tended to have higher incidence of lymphovascular permeation and lymph node metastases than carcinomas mixed with adenomatous components. These results suggest that different pathways of carcinogenesis might result in different natural history of colorectal carcinoma. The immunohistochemical examination of p53 overexpression showed that there was no correlation between p53 overexpression and growth pattern or grades of malignancy.