Proximal adenomas in hereditary non-polyposis colorectal cancer are prone to rapid malignant transformation

• Published in: Gut 2002-03, Vol.50 (3), p.382-386
• Main Authors: Rijcken, F E M, Hollema, H, Kleibeuker, J H
• Format: Article
• Language: English
• Subjects: Adenoma; Adenoma - pathology; adenoma-carcinoma sequence; adenomas; Adult; Age; Aged; Aged, 80 and over; bovine serum albumin; BSA; Cancer; Cell Transformation, Neoplastic - pathology; Colonic Neoplasms - pathology; Colorectal cancer; Colorectal Neoplasms, Hereditary Nonpolyposis - pathology; Development and progression; Disease Progression; dysplasia; Endoscopy; Female; Follow-Up Studies; Genetic aspects; hereditary non-polyposis colorectal cancer; HNPCC; Humans; Male; Medical research; Middle Aged; mismatch repair; MMR; Mutation; Patients; PBS; phosphate buffered saline; Proteins; proximal colon; Rectal Neoplasms - pathology; Rodents; Studies; Tumorigenesis; Tumors
• ISSN: 0017-5749; 1468-3288; 1458-3288
• DOI: 10.1136/gut.50.3.382

Background: Hereditary non-polyposis colorectal cancer (HNPCC) is thought to arise from adenomas. HNPCC mostly occurs in the proximal colon. We investigated whether this proximal preponderance is due to a proximal preponderance of adenomas or (also) differences in transformation rates from adenomas to cancer between the distal and proximal colon. Methods: A total of 100 HNPCC adenomas were evaluated and compared with 152 sporadic adenomas for location, size, and dysplasia. Twenty five adenomas from patients with a known mismatch repair (MMR) gene mutation were stained for expression of MLH1 and MSH2. Results: HNPCC adenomas were more often located proximally (50% v 26%; p=0.018) and were smaller in comparison with sporadic adenomas. They were similarly dysplastic. However, all proximal HNPCC adenomas ≥5 mm were highly dysplastic compared with 17% of the larger proximal sporadic polyps (p