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[Objective 1 by detecting colon adenocarcinoma cells during the development of proliferation and apoptosis, apoptosis, proliferation ratio and P53, COX-2 and bcl-2 positive expression rate of to explore cell proliferation and apoptosis in colon cancer becomes the role of law and related adjustment factors. [Method] collect the complete archive paraffin blocks of Pathology, the First Affiliated Hospital of Kunming Medical College, 2000-2010 surgical colon resected specimens clinical data, a total of 81 cases. Including normal colorectal mucosa in 15 cases, 18 cases of colorectal adenomas, colon adenocarcinoma Duke 's A 15 cases, the Duke's B 18 cases, Duke's C period 15 cases. SP method of immunohistochemical detection of Ki-67, bcl-2, P53, COX-2 in each group expression, calculation of Ki-67, bcl-2, P53, COX-2 positive expression rate of Ki-67 positive The expression rate of cell proliferation index (proliferation index, PI). By TUNEL [terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling technique labeled apoptotic cells, calculate the apoptotic index (apoptotic index, AI), and apoptosis / proliferation ratio of (AI / PI), results of the use of SPSS11.5 software for statistical analysis. [Results] Ki-67 protein localized in the nucleus in normal colonic mucosa of Ki-67 expression in the crypt bottom, and a pale yellow yellow particles; colon adenoma and adenocarcinoma of Ki-67 expression dispersed, yellow brown particles. bcl-2 protein expression in cytoplasm, bcl-2 expression in the normal colonic mucosa mostly negative and light yellow fine particles, and are mainly located in the mucosal surface;, bcl-2 expression in colon adenoma and adenocarcinoma dispersed, mostly a pale yellow yellow particles. P53 protein located in the nucleus, P53 almost no expression in normal colonic mucosa; P53 expression in colon adenomas less, and mostly negative or a light yellow yellow granules, P53 expression in colon adenocarcinoma was diffuse distribution of yellow - brown particles. COX-2 protein expression in cytoplasm, diffuse positive expression in the normal colonic mucosa, colonic adenoma and adenocarcinoma, COX-2, and yellow - brown particles. TUNEL detection of apoptotic cells were stained brown, and the cells were round and adjacent pericyte detachment concentrated cytoplasm, nuclear chromatin condensation was chunky cohesion surrounding the nuclear membrane, nucleolus cracking. In the normal colonic mucosa of apoptotic cells in the mucosal surface, and very few, occasional individual apoptotic cells in the glands, the crypts are nowhere to be seen at the bottom of apoptotic cells; significantly increased the number of apoptotic cells in colonic adenomas, The mucosal surface less the crypt bottom apoptosis cells increased; showed focal distribution of apoptotic cells in the colon adenocarcinoma. In the normal colonic mucosa, the colonic adenomas colon adenocarcinoma Dukes'A period, Dukes'B period, Dukes of apoptosis index were 1.6%, 6.7%, 4.5%, 3.7%, 3.2%, among the groups differences in the overall comparison was statistically significant (p lt; 0.001), ki-67 positive expression rates were 31.0%, 74.1%, 59.5%, 72.3%, 68.1%, and the difference between groups overall comparison was statistically significant ( p lt; 0.000), apoptosis proliferation than were 0.04,0.08,0.05,0.04,0.04 between each group, the difference was statistically significant (p lt; 0.001). The positive expression rate of bcl-2 in normal colonic mucosa, colorectal adenomas, colon adenocarcinoma Dukes'A period, Dukes'B period, Dukes'C period were 13.3%, 70.6%, 63.6%, 83.5%, 80.5%, each group the difference between the overall comparison was statistically significant (p lt; 0.001); positive expression rate of P53 in normal colonic mucosa, colorectal adenomas, colon adenocarcinoma Dukes'A period, Dukes'B period, Dukes'C respectively 7.1%, 61.1%, 48.5%, 79.6%, 67.1%, and the overall difference between groups was statistically significant (p lt; 0.001); positive expression of COX-2 in normal colonic mucosa, colorectal adenomas, respectively the colon adenocarcinoma Dukes'A period, Dukes'B period the, Dukes'C period was 85.8%, 76.4%, 84.0%, 82.1%, 67.1%, and the overall difference between groups had no statistical significance (p gt; 0.05 ). The negative correlation between bcl-2 and P53 expression and AI / PI, rs were -0.570, -0.490 (P lt; 0.001), while no correlation between the expression of COX-2 and AI / PI, rs = 0.217 (P gt; 0.05). [Conclusion] 1. Colon from normal mucosa to adenoma cell proliferation, apoptosis and apoptosis / proliferation ratio gradually increased, the tumor tissue is a strong growth, the remodeling phase of the internal structure of the organization; 2. Colon adenoma to adeno cancer cell proliferation, apoptosis and apoptosis / proliferation ratio decreased gradually reveal cancerous colon tissue, the biological characteristics of the tumor cells may result in a qualitative change in the process, has a fast-growing malignant characteristics of tumor cells clones will enable tumor development into apoptosis, proliferation balanced development stage; 3. colon from no lymph node metastasis in advanced cancer to lymph node metastasis in advanced cancer, although apoptosis / proliferation than the state of relative equilibrium, but still at a high level, highly malignant characteristics of tumor cell clones has been formed to create the conditions for tumor invasion and metastasis; 4. colon adenocarcinoma glandular epithelial cells in the development process bcl-2 and P53 AI / PI is closely related, and both tumor cell proliferation and apoptosis with two-way regulation, high expression promotes tumor proliferation, inhibition of apoptosis, while no significant correlation between colon gland epithelial cell expression of COX-2 and AI / PI.
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