Serrated neoplasias and de novo carcinomas in ulcerative colitis: A histological study in colectomy specimens

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Journal of Gastroenterology and Hepatology

Volume 22 Issue 7 Page 1024-1031, July 2007

To cite this article: A Rubio (2007) Serrated neoplasias and de novo carcinomas in ulcerative colitis: A histological study in colectomy specimens Journal of Gastroenterology and Hepatology 22 (7), 1024–1031. doi:10.1111/j.1440-1746.2007.04944.x

Abstract

GASTROENTEROLOGY

A Rubio

Gastrointestinal and Liver Pathology Research Laboratory, Department of Pathology, Karolinska Institute and University Hospital, Stockholm, Sweden

Dr CA Rubio, Gastrointestinal and Liver Pathology Research Laboratory, Department of Pathology, Karolinska Institute and University Hospital, Stockholm 17176, Sweden. Email: carlos.rubio@...

Abstract

Background and Aim: Cancer in ulcerative colitis (UC) originates in dysplastic crypts, adenomatous growths (UCAG), and UC-associated adenomas (UCAD). The aim of the present study was to compare the histological phenotypes between UCAG, UCAD, and sporadic colorectal adenomas in non-colitics (non-UCAD), as well as between UC-associated carcinomas (UCC) and carcinomas in non-colitic patients (non-UCC).

Methods: Three thousand and forty nine sections from 96 colectomy specimens in patients with UC-pancolitis and carcinoma were reviewed.

Results: Villous phenotypes were more frequent in UCAG (48%) than in UCAD (26%) and non-UCAD (11%), and serrated phenotypes more frequent in UCAD (29%) than in UCAG (12%) and non-UCAD (8%). Tubular phenotypes were far less frequent in UCAG (14%) than in UCAD (45%) and non-UCAD (80%). Villous and signet ring cell cancer phenotypes were more frequent in UCC (22% and 8%, respectively) than in non-UCC (9% and 0.8%, respectively). Six UCC (5.6%) were de novo carcinomas.

Conclusions: Invasive carcinomas were found in one-half of the UCAG and in one-third of the UCAD, indicating that both lesions are important in cancer development in UC. The different proportions of histological phenotypes found in UCAG, UCAD, and non-UCAD on the one hand, and UCC and non-UCC on the other, suggest that chronic protracted inflammation might have modified the stem cell receptors that receive the molecular signals that program structural configurations in neoplastic glands. This is the first study reporting the occurrence of serrated and microtubular UCAG and of de novo carcinomas in UC.