Ki‐67 distribution, α‐methylacyl‐CoA racemase (AMACR) expression and mucin phenotypes are associated with non‐polypoid growth in ulcerative colitis‐associated neoplasia

Abstract

AimsUlcerative colitis‐associated neoplasia (UCAN) is characterised by multifocal tumourigenesis. A wide range of metachronous lesions have been reported to occur after endoscopic treatment of UCAN, which suggests the development of sporadic tumours in lesions treated as UCAN. Therefore, we aimed to evaluate differences of immunohistochemistry (IHC) in features and clinicopathological characteristics of intramucosal lesions in patients with ulcerative colitis (UC).Methods and resultsWe examined 35 intramucosal lesions resected for carcinoma or dysplasia by total colectomy from patients with UC and 71 sporadic adenomas (SAs) endoscopically resected from patients without UC. UC lesions were divided into the conventional UCAN group, defined as p53 mutant pattern and normal expression of β‐catenin, and the non‐conventional UCAN group, defined as the rest. Ki‐67 distribution, α‐methylacyl‐CoA racemase (AMACR) expression and mucin phenotypes were compared using IHC, and clinicopathological characteristics were investigated. Conventional and non‐conventional UCAN lesions were located in the left colon and rectum. Relative to the SA lesions, UCAN lesions occurred in much younger patients and exhibited more frequent basal distribution of Ki‐67 in tumour crypts. Conventional UCAN lesions tended to be non‐polyploid and exhibited a higher frequency of normal AMACR expression than SA lesions. UC lesions were heterogeneous—only two of the eight patients with multiple lesions had lesions (both non‐conventional UCAN lesions) exhibiting concordant IHC staining features.ConclusionsThe basal pattern of Ki‐67 distribution, normal expression of AMACR and a non‐intestinal mucin phenotype were determined as characteristic features suggestive of UCAN. Non‐polypoid growth was another a key feature of UCAN.