OBJECTIVE: To study the significance of beta -catenin, p53 and PCNA in PJS harmatoma. METHOD: Paraffin sections of 29 hamartomas of 18 patient with Peutz-Jeghers syndrome, 19 patients with colorectal mucosa and 10 persons with normal mucosa were examined using LSAB. Positive cells were detected under light microscope. RESULTS: All 10 persons with normal mucosa showed p53 negative and beta - catenin positive. The beta - catenin protein was predominantly localized to the plasma membrane. PCNA index (PI) in normal mucosa was 10.56 +/- 7.51. The PI of hamartoma and cancer was 44.57 +/- 21.15 and 32.96 +/- 18.88. The PI of the two groups was significantly higher than that of the normal group. In hamartoma, the positive cells were mainly located in the low 1/3 part of the mucous glands. The positive rate of p53 was 24.1% (7/29) in hamartomatouspolyps and 57.9% (11/19) in colorectal carcinoma (chi(2) = 5.581, P < 0.05). Abnormal expression rate of beta- catenin in colorectal carcinoma was 73.7% (14/19) and 41.3% (12/29) in hamartomatous polyps. Some epithelial cells showed nuclear localization of beta- catenin and concentration of cytoplasm. (chi(2) = 4.825, P < 0.05). CONCLUSIONS: The proliferation activity of hamartomatous polyps increased significantly by multifactory interaction. p53 and beta- catenin play a role in the early stage of hamartoma- adenoma-carcinoma sequence but have a different mechanism in inducing colorectal cancer.
OBJECTIVE: To study the significance of beta -catenin, p53 and PCNA in PJS harmatoma. METHOD:Paraffin sections of 29 hamartomas of 18 patient with Peutz-Jeghers syndrome, 19 patients with colorectal mucosa and 10 persons with normal mucosa were examined using LSAB. Positive cells were detected under light microscope. RESULTS: All 10 persons with normal mucosa showed p53 negative and beta - catenin positive. The beta - catenin protein was predominantly localized to the plasma membrane. PCNA index (PI) in normal mucosa was 10.56 +/- 7.51. The PI of hamartoma and cancer was 44.57 +/- 21.15 and 32.96 +/- 18.88. The PI of the two groups was significantly higher than that of the normal group. In hamartoma, the positive cells were mainly located in the low 1/3 part of the mucous glands. The positive rate of p53 was 24.1% (7/29) in hamartomatouspolyps and 57.9% (11/19) in colorectal carcinoma (chi(2) = 5.581, P < 0.05). Abnormal expression rate of beta- catenin in colorectal carcinoma was 73.7% (14/19) and 41.3% (12/29) in hamartomatous polyps. Some epithelial cells showed nuclear localization of beta- catenin and concentration of cytoplasm. (chi(2) = 4.825, P < 0.05). CONCLUSIONS: The proliferation activity of hamartomatous polyps increased significantly by multifactory interaction. p53 and beta- catenin play a role in the early stage of hamartoma- adenoma-carcinoma sequence but have a different mechanism in inducing colorectal cancer.