分子生物学的立場からみた表面型起源の大腸癌

Colon Cancer Developed from Superficial Type Adenoms : From a Molecular Biological Point of View

要旨　非遺伝性大腸腫瘍256病巣（隆起型腺腫95病巣，表面型腺腫62病巣，浸潤癌99病巣）について，K-ras codon 12における点突然変異について解析した．隆起型腺腫は67％に変異がみられたのに対して，表面型腺腫では21％と有意に低率であり，中でも平坦・陥凹型病変の変異頻度は8％と特に低率であった．浸潤癌のK-ras変異頻度を発育形態別にみると，隆起型sm，pm癌はそれぞれ56％，78％であったのに対して，non-polypoid growth type（NPG群）sm，pm癌では6％，23％であった．これらの結果から，隆起型腺腫→隆起型浸潤癌，平坦・陥凹型腺腫→NPG群浸潤癌の発癌経路が推定された．

　To clarify genetic changes in colorectal tumorigenesis, K-ras codon 12 point mutations were examined in 95 polypoid adenomas , 62 flat adenomas, and 99 invasive carcinomas. The mutation frequency in flat adenomas was 21% (13/62), significantly lower than that in polypoid adenomas (67%: 64/95). Among flat adenomas, completely flat or depressed ones (type Ⅱb or type Ⅱc) exhibited especially low mutation frequency (8%). As for invasive carcinomas, the mutation frequency was higher in polypoid carcinomas than in nonpolypoid ones (submucosal carcinoma : 56% vs. 6%, carcinomas invading as far as the muscularis propria 78% vs. 23%). From these results, it is assumed that polypoid adenomas develop to polypoid carcinomas and flat adenomas to non-polypoid carcinomas.