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Ras Oncogene p21 Levels Parallel Malignant Potential of Different Human Colonic Benign Conditions
Fabrizio Michelassi, MD;
Steve Leuthner;
Mark Lubienski, MD;
David Bostwick, MD;
Jennifer Rodgers, HT;
Mark Handcock;
George E. Block, MD
Arch Surg. 1987;122(12):1414-1416.
Abstract
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Ras oncogenes are a specific family of genes believed to play a role in malignant transformation and tumor growth in humans. To gain a better understanding of the role these oncogenes may play in malignant transformation, we evaluated the levels of a ras gene protein product (p21) in formaldehyde-fixed, paraffin-embedded specimens of normal human colonic mucosa, hyperplastic polyps, tubular adenomas, villous adenomas, and epithelium from a patient with ulcerative colitis. The p21 protein content was measured using the RAP-5 monoclonal antibody in a semiquantitative immunohistochemical assay. The titer value was expressed as the highest dilution of antibody giving definite staining using the avidinbiotin peroxidase method. Differences in p21 titer values among all classes of polyps were significant (hyperplastic polyps values were less than tubular adenomas values, which were less than villous adenoma values). The p21 titers obtained from ulcerative colitis specimens were similar to those obtained from villous adenomas. We conclude that the levels of ras oncogene protein product increase with the malignant potential of benign human colonic conditions. These findings suggest that the ras oncogene protein product may play an important role in the malignant transformation of benign lesions of the human colon. If these findings are confirmed, as technology progresses to allow molecular probes to measure gene products in biopsy specimens, high-risk patients could be monitored and treated before actual malignant transformation occurs.
(Arch Surg 1987;122:1414-1416)
Author Affiliations
From the Departments of Surgery (Drs Michelassi, Lubienski, and Block, and Mr Leuthner and Ms Rodgers), Pathology (Dr Bostwick), and Statistics (Mr Handcock), University of Chicago.
Footnotes
Accepted for publication Sept 16, 1987.
Read before the Annual Meeting of the Society of Surgical Oncology, London, April 29, 1987.
Reprint requests to Department of Surgery, University of Chicago Medical Center, 5841 S Maryland Ave, Chicago, IL 60637 (Dr Michelassi).
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