Ｔｈｅ ｅｘｐｒｅｓｓｉｏｎ ｏｆ ｐ５３ ｗａｓ ｓｔｕｄｉｅｄ ｉｎ ｔｉｓｓｕｅ ｏｆ ｔｈｉｒｔｙ ｃａｓｅｓ ｏｆ ｂｉｌｉａｒｙ ｔｒａｃｔ ａｄｅｎｏｃａｒｃｉｎｏｍａ ａｎｄ ｔｈｒｅｅ ｃａｓｅｓ ｏｆ ｂｉｌｉａｒｙ ａｄｅｎｏｍａ ｂｙ ＳＡＢＣ ｉｍｍｕｎｏｈｉｓｔｏｃｈｅｍｉｓｔｒｙ ｍｅｔｈｏｄ．Ｉｔ ｒｅｖｅａｌｅｄ ｔｈａｔ ３０％ ｏｆ ｔｈｅ ｆｏｒｍｅｒ ｃａｓｅｓ ｗａｓ ｐｏｓｉｔｉｖｅ ｓｔａｉｎ ａｎｄ ａｌｌ ｎｅｇａｔｉｖｅ ｉｎ ｔｈｅ ｌａｔｔｅｒ．Ｎｏ ｒｅｌａｔｉｏｎｓｈｉｐ ｗａｓ ｆｏｕｎｄ ｂｅｔｗｅｅｎ ｔｈｅ ｐ５３ ｅｘｐｒｅｓｓｉｏｎ ａｎｄ ｔｈｅ ｌｏｃａｔｉｏｎ，ｔｉｓｓｕｅ ｔｙｐｅ ａｎｄ ｌｙｍｐｈ ｎｏｄｅ ｍｅｔａｓｔａｓｉｓ ｏｆ ｔｈｅ ｂｉｌｉａｒｙ ｔｒａｃｔ ａｄｅｎｏｃａｒｃｉｎｏｍａ．
【摘要】 目的 探讨丙型肝炎病毒非结构蛋白NS4B对肝细胞内p53表达的影响，以及在肝癌发生中的作用与机制。 方法 设置空白对照组、空白载体组、转染NS4B组、转染p53组、共转染NS4B及p53组。使用脂质体介导转染法，转染丙型肝炎病毒非结构蛋白重组质粒PCXN2-NS4B及突变型p53基因重组质粒pC53-CX22AN3进入Chang肝细胞内，并用G418筛选获得稳定表达细胞。采用免疫细胞化学法检测p53表达率。 结果 空白对照组无p53表达，空白载体组及转染NS4B组呈弱阳性表达，转染p53组及共转染组呈阳性表达；转染p53组、共转染组分别与空白对照组、空白载体组及转染NS4B组比较，差异均有统计学意义 （Plt;0.05）。 结论 NS4B可能抑制p53表达，也可能阻止其进入细胞核，但NS4B与突变型p53关系不明确。NS4B导致肝细胞异常增生，诱导肝癌发生可能不依赖p53的异常表达及突变。【Abstract】 Objective To investigate the effect of hepatitis C Virus on-structural protein 4B(HCV NS4B) on expression of p53 in hepatic cell, and to study the role and mechanism in development of hepatocellular carcinoma. Methods The experiment was divided into negative control, pure vector PCXN2, PCXN2-NS4B, PC53-cx22AN3, and co-transfection group. Recombinant plasmid PCXN2-NS4B and mutant p53 gene--PC53-cx22AN3, PC53-cx22AN3 with PCXN2-NS4B, blank vectors were transfected into Chang liver cell by liposome-mediated transfection respectively. Positive cells were screened by G418. The expression rate of p53 was measured by immunocytochemistry. Result No expression rate of p53 gene in control group was found, lower positive expression in group PCXN2 and PCXN2-NS4B. The expression of p53 gene in group PC53-CX22AN3 and co-transfection was ber than the others (Plt;0.005). Conclusion HCV-NS4B may inhibit the expression of p53 gene, and it may play a crucial role in inhibiting p53 transfered to hepatic cells nuclear. But it isn’t clear that the. HCV-NS4B can enhance the role of mutant p53 gene. It suggested that HCV-NS4B induce proliferation of hepatic cell not through regulating the expression of p53.
Objective To explore the expressions of caudal-related homeodomain transcription factor-2 （CDX-2）and tumor suppressor gene KAI-1 in colon carcinoma tissues and to analyze their clinical significances. Methods Immu-nohistochemical SP method was used to detect the expressions of CDX-2 and KAI-1 in 50 cases of colon carcinoma tissues and corresponding adjacent tissues （from cancer tissue ≤2cm） and 25 cases of normal colon mucosa tissues. The relation-ships of the expressions of CDX-2 and KAI-1 to the clinicopathologic features were analyzed. Results ①The positive rates of CDX-2 expression and KAI-1 expression in the colon carcinoma tissues were significantly lower than those in the normal colon mucosa tissues 〔CDX-2：34% （17/50） versus 88% （22/25）， P＜0.05；KAI-1：30% （15/50） versus 92% （23/25）， P＜0.05〕 and adjacent tissues of colon carcinoma 〔CDX-2：34% （17/50） versus 54% （27/50）， P＜0.05；KAI-1：30% （15/50） versus 58% （29/50）， P＜0.05〕， which in the adjacent tissues of colon carcinoma were significantly lower than those in the normal colon mucosa tissues （P＜0.05）. ②The positive expressions of CDX-2 and KAI-1 were related to lymph node metastasis， depth of invasion， and degree of tumor differentiation （P＜0.05）. ③Spearman rank correl-ation analysis showed that the CDX-2 expression was positively correlated with KAI-1 expression （rs=0.544， P＜0.01）. Conclusions CDX-2 and KAI-1 may be closely related to the development， invasion， metastasis， and prognosis of colon carcinoma， the combination of CDX-2 and KAI-1 in evaluation of their function has a certain guiding significance in the treatment for colon carcinoma.
ObjectiveTo summarize the role of survivin gene in tumor. MethodsThe research status on biological characteristics the role of survivin gene in tumor for gene therapy and clinical application was retrospectively analyzed after related domestic and foreign literatures were reviewed. ResultsSurvivin gene was by far found to be the best powerful apoptosis inhibition gene, which played antiapoptosis role mainly through inhibiting directly the activity of caspase-3 and caspase-7 in the downstream of cascade reaction. Survivin gene promoted tumor cell proliferation and differentiation through speeding up tumor cells transition of G1→S phase and eluding the recognition of tumor cells to the apoptosis in G2/M phase. Survivin gene played important role in the intermediate links of vasiformation through angiogenic factor (VEGF, bFGF, Ang-1, and COX-2). ConclusionSurvivin gene may inhibit the apoptosis, promote the proliferation and differentiation of tumor cells and tumor angiogenesis, suggested that survivin gene has potential to act as a novel tumor marker and become an indicator of malignant tumor.
Objective To investigate the expression of suppressor gene Runt-related transcription factor 3 (Runx3) in gastric carcinoma and its relationship with clinicopathologic parameters. Methods RT-PCR and Western blot were used to determine the mRNA expression and protein expression of Runx3 gene in primary tumor and corresponding normal tissues respectively in 52 patients with gastric carcinoma. The relationship between Runx3 expression and clinicopathologic parameters was analyzed. Results RT-PCR and Western blot analysis in 52 patients with gastric carcinoma showed down-regulation of Runx3 mRNA and Runx3 protein in 59.6% (31/52) and 48.1% （25/52） of the primary tumors tested, and in none of the normal tissues (P＜0.05) respectively. There was a significant negative correlation between the expression level of Runx3 gene and the clinicopathologic parameters such as tumor size, differentiation, infiltrative depth, lymph node metastasis and TNM stage (P＜0.05， P＜0.01). Runx3 gene transcription was coincident with its protein expression (r=0.840, P＜0.01）. Conclusion The expression of Runx3 gene is down-regulated in gastric carcinoma, which suggests that Runx3 gene plays an important role in carcinogenesis and the progression of gastric carcinoma. It may be a new target of diagnosis and treatment of gastric carcinoma.
【Abstract】ObjectiveTo investigate the relationship between tumor suppressor gene DPC4 and the development and prognosis of pancreatic carcinoma. MethodsRelevant literatures of recent years were reviewed. ResultsDPC4 was located on chromosome 18. Its product was Smad 4 protein. Smad 4 protein was the central component of the transforming growth factor-beta signaling pathway, and all the biological effect was the results of interaction of Smad 4 and different Smads. The gene was deleted or inactive in about 50% of pancreatic carcinomas. The deletion of DPC4 had a great relation to the development and prognosis of pancreatic carcinoma. ConclusionThe alteration of tumor suppressor gene DPC4 is connected with the development and prognosis of pancreatic carcinoma. However, this research should be further studied.
Objective To study the expression and its clinical significance of p16 in human gastric carcinomas. MethodsThe expression of p16 protein and mRNA in human gastric carcinomas using SP immunohistochemical and in situ hybridization (ISH) methods were examined. Results Of the 85 cases tested, 65.88% (56 cases) showed positive staining of p16 protein in the primary lesions. The positive rate of p16 protein was significantly lower in the cases with deep invasion, poor differentiation or shorter survival periods (Ｐ＜0.05). The positive rate of p16 mRNA expression in human gastric carcinomas was 47.37% (in 38 cases). Conclusion p16 gene may correlate with the development and progress of gastric carcinomas. The expression of p16 gene may be a useful tool for showing biological behavior and prognosis of human gastric carcinomas.
Objective To investigate the effect of tumor suppressor gene on tumourigenesis in multiple primary malignant neoplasm (MPMN).Methods The retrospective analysis was used to summarize several common tumor suppressor genes correlation to MPMN. Results At current study of the tumor suppressor genes, the common genes studied in MPMN were p53, APC, p16, BRCA1, BRCA2 and PTEN/MMAC1, etc. The same mutation of tumor suppressor genes could be detected from PMNNs. Conclusion There are significant relations between MPMN and inactivation of tumor suppressor gene. By the study of tumor suppressor gene, it can reveal some common rules of tumourigenesis of MPMN.
ObjectiveTo summarize and analyze the relevant studies about the tumor suppressor phosphatase and tensin homolog deleted on chromosome ten (PTEN) and thyroid tumor then further elucidate?the possible mechanism of thyroid tumor formation and progression. Mothods Domestic and international literatures investigating the correlation between PTEN and thyroid tumor were retrieved and reviewed. ResultsThe abnormal expression of PTEN protein resulted by the mutation or methylation of PTEN gene may up-regulate the expression of its downstream effectors such as PI3K, mTOR, FAK, etc. This probably correlate with thyroid neoplasia and progression. Conciusions Abnormalites of PTEN and its downstream signal ways may correlate with the initiation and development of thyroid tumors. However, the specific mechanism still remains unclear and need more further researches