| Background and objectives: Gastric cancer, the major cause of carcinoma death, is one of the most common malignant tumors in the world, which has a very poor prognosis. The tumorigenesis of gastric cancer is a compositive process concerned of the activation of many oncogenes, inactivation of anti-oncogenes and the subsequent changes of cytobiological behaviors. Lots of oncogenes and anti-oncogenes play different roles in different biochemical pathways. They communicate and form a network to interact each other to regulate the development of tumor.TGF- β (transforming growth factor β ) signal transduction is involved hi fundamental biological processes, such as cell growth regulation, differentiation, adhesion, the formation of ECM (Extracellular matrix), immune regulation, tissue repair and apoptosis, et al. Nowadays, people focus on the relationship between TGF- β signal transduction and carcinogenesis. Recent progress has led to the elucidation of a general TGF-fi signaling pathway: Firstly, TGF- β ligand adhere to transforming growth factor β receptor I, II (T β R I ,T βRII) and T β R I is phosphorylated by T β RII. Then, Smad2 and SmadS are activated by T β R I and form heteromeric complexes with Smad4. These complexes translocate to the nucleus where they control expression of target genes. Nowadays, people focus on the relationship between TGF- β signal transduction and carcinogenesis.Smad4, a new anti-oncogene, play a key role in TGF- β signal transduction. Smad4 express a low level in many tumor tissues, but there exist lots of differences in gastric cancer. T β R I and T β RII, two lands of transmembrane receptor, are essential toTGF- 0 signal transduction. They can be adhered by TGF- P ligand and initiate TGF- β signal transduction. T β RII is an anti-oncogene, which also express a low level in many tumor tissues. The effect of Tβ R I in the development of gastric cancer also exist a lot of controversy. The aim of this study to evaluate the relationship between the expression of T ?R I, TPRII and Smad4 and clinicopathologocal factors in gastric cancer, to provide theoretical basis for evaluation of gastric cancer' s, therapy and prognosis of gastric cancer.Materials and Methods: (1) 67 surgically resected gastric cancer samples and 24 normal mucosa samples of stomach (the terminal of rescted samples) , which were adjacent to carcinoma mucosa, were all confirmed pathologically. All the tissues were fixed in 10% neutral formalin and embedden in paraffin. (2) SABC immunohistochemistry technique was used to detect the expression of T β RI and T β RII and SMAD4 in para-cancerous normal mucosa and gastric cancer tissues. (3) The data was analysized by statistical software SPSS 10.0. -test was used to analysize the difference between different groups. a=0.05 was considered as statistically significant value.Results: 1. The positive expression rate of T β R I (73.13%) in gastric cancer tissue is lower than that in normal mucosa (95.83%), (P<0. 05 ) ,which lies in the terminal of rescted samples. There is a significantly higher positive expression rate of T β RII in para-cancerous normal mucosa (95.83%) than that in gastric cancer tissues (49.25%),(P<0.01) . For SMAD4, the positive expression rate in gastric cancer tissues (44.78%) is much lower than that in para-cancerous normal mucosa (95.83%), (P<0. 01) .2.In gastric cancer tissues, there is no difference of the positive expression rate of Tβ R I between the better differentiation group (78.79%) and the worse differentiation group (67.65%),(P>0.05). there is no difference of the positive expression rate of T β RI between the serosal or extraserosal infiltration group (67.57%) and the subserosa group (80.00%), (P>0.05). there is no difference of the positive expression rate of T β RI between the lymphnode metastasis negtive group(82.14%) and the lymphnode metastasis positive group(66.67%),(JP>0.05). there is no difference of the positiveexpression rate of T P R I between the I / II...
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