OBJECTIVES: To assess cell proliferation and analyze oncogenetic abnormalities in cases of juvenile polyposis of the stomach (JPs), with or without coexisting tumors. METHODS: The Ki-67 labeling indices (KLI) were compared for juvenile polyps and coexisting tumors in three cases of JPs along with values for gastritis, foveolar epithelial hyperplastic polyps, adenomas, and carcinomas. Expression of p53, Bcl-2, and c-ErbB-2 in tumors was examined immunohistochemically, and a search for c-Ki-ras mutations was made by DNA direct sequencing. RESULTS: The KLI for JPs did not significantly differ between cases, being consistently lower than the values for both hyperplastic polyps and gastritis. The KLI for the papillary tumors and a signet ring cell carcinoma found in association with JPs tended to be lower than those for their conventional counterparts. P53, but not Bcl-2 and c-ErbB-2, was focally expressed in the papillary tumors, whereas all three were absent in the signet ring cell carcinoma, in the JPs. No c-Ki-ras mutations were detected in the papillary tumors. CONCLUSIONS: The cell proliferation of JPs is relatively low and the polyps can be considered hamartomatous. However, neoplastic change clearly can occur in association with a relative increase in proliferative activity being observed in coexisting tumors. Low cellular proliferative activity and absence of oncogenetic abnormalities in tumors of JPs, compared with their conventional counterpart tumors, suggest that pathways of tumorigenesis and genetic alteration in JPs may be different from those in their conventional counterparts.
OBJECTIVES: To assess cell proliferation and analyze oncogenetic abnormalities in cases of juvenile polyposis of the stomach (JPs), with or without coexisting tumors. METHODS: The Ki-67 labeling indices (KLI) were compared for juvenile polyps and coexisting tumors in three cases of JPs along with values for gastritis, foveolar epithelial hyperplastic polyps, adenomas, and carcinomas. Expression of p53, Bcl-2, and c-ErbB-2 in tumors was examined immunohistochemically, and a search for c-Ki-ras mutations was made by DNA direct sequencing. RESULTS: The KLI for JPs did not significantly differ between cases, being consistently lower than the values for both hyperplastic polyps and gastritis. The KLI for the papillary tumors and a signet ring cell carcinoma found in association with JPs tended to be lower than those for their conventional counterparts. P53, but not Bcl-2 and c-ErbB-2, was focally expressed in the papillary tumors, whereas all three were absent in the signet ring cell carcinoma, in the JPs. No c-Ki-ras mutations were detected in the papillary tumors. CONCLUSIONS: The cell proliferation of JPs is relatively low and the polyps can be considered hamartomatous. However, neoplastic change clearly can occur in association with a relative increase in proliferative activity being observed in coexisting tumors. Low cellular proliferative activity and absence of oncogenetic abnormalities in tumors of JPs, compared with their conventional counterpart tumors, suggest that pathways of tumorigenesis and genetic alteration in JPs may be different from those in their conventional counterparts.