Intestinal adaptation and experimental carcinogenesis after partial colectomy. Increased tumour yields are confined to the anastomosis.

Abstract

Small-bowel resection enhances experimental colorectal carcinogenesis, probably by stimulating epithelial cell proliferation. The possibility that similar mechanisms might explain metachronous large-bowel cancers in man was tested in Sprague-Dawley rats submitted to partial colectomy before or after a five-week course of azoxymethane (total dose 50 mg/kg). The timing of operation did not affect tumour yields at 40 weeks. Caecal resection augmented mucosal mass in the ileum and right colon but did not affect carcinogenesis. Right hemicolectomy only increased ileal segmental weight (by 22%); left hemicolectomy increased the protein and DNA contents of the residual right colon by 18-42%. Large-bowel tumours in 84 rats were distributed as follows: proximal colon 36, colonic anastomosis 51, distal colon 87, rectum 43. Consistent with this left-sided predominance, left hemicolectomy reduced the number of large-bowel tumours. A twofold increase in distal tumours after both transection and right hemicolectomy simply reflected the high incidence of anastomotic tumours. Furthermore, one rat given vehicle as opposed to carcinogen developed an invasive mucinous adenocarcinoma at the colorectal anastomosis, after left hemicolectomy. The large bowel shows limited adaptation to partial resection and is not at increased risk of carcinogenesis, except in the region of the suture line.