Steffensen I L, Paulsen J E, Alexander J
Avdeling for miljømedisin Statens institutt for folkehelse, Oslo.
Tidsskr Nor Laegeforen. 1997 May 30;117(14):2046-51.
The incidence of colon cancer has increased during the last 30 years in Norway and is now the second most common newly diagnosed type of cancer in women and the third in men. Familial adenomatous polyposis, hereditary colorectal cancer, is caused primarily by inactivation of the tumour suppressor gene adenomatous polyposis coli (APC). The protein coded for by this gene has a possible role in cell-cell signalling or adhesion by binding to catenins which bind to the cell adhesion molecule E-cadherin, or in anchoring the cytoskeleton. Both germ-line and somatic APC gene mutations result in a truncated protein, due to introduction of a stop codon. The positions of the germ-line mutations seem to correlate with the seriousness of polyposis. The food mutagen PhIP causes specific mutations in the Apc gene in rats, and is a possible environmental mutagen also in humans. The Min mouse with mutated Apc-gene is a good model for studies of both induction and prevention of inherited and sporadic intestinal cancer.
在过去30年里，挪威结肠癌的发病率有所上升，目前是女性新诊断出的第二大常见癌症类型，男性中的第三大常见癌症类型。家族性腺瘤性息肉病，即遗传性结直肠癌，主要由肿瘤抑制基因腺瘤性息肉病基因（APC）失活引起。该基因编码的蛋白质可能通过与结合细胞粘附分子E-钙粘蛋白的连环蛋白结合，在细胞间信号传导或粘附中发挥作用，或者在锚定细胞骨架方面发挥作用。由于引入了终止密码子，种系和体细胞APC基因突变都会导致截短蛋白的产生。种系突变的位置似乎与息肉病的严重程度相关。食物诱变剂PhIP会在大鼠的Apc基因中引起特定突变，在人类中也可能是一种环境诱变剂。具有突变Apc基因的Min小鼠是研究遗传性和散发性肠道癌症的诱导和预防的良好模型。
