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1.
Chinese Journal of Experimental and Clinical Virology ; (6): 452-454, 2008.
Article in Chinese | WPRIM | ID: wpr-332469

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the expression of vasoactive intestinal peptide (VIP) in gastric adenocarcinoma, and to evaluate the correlation of VIP level with clinical pathologic parameters.</p><p><b>METHODS</b>The level of VIP in sera from gastric adenocarcinoma patients and healthy people was investigated by ELISA. Moreover, the differential gene expression between gastric adenocarcinoma, gastric dysplasia, and the corresponding normal gastric mucosa were determined by RT-PCR. Western Blot was also used to measure the expression of VIP in the gastric adenocarcinoma and the normal gastric mucosa.</p><p><b>RESULTS</b>The serum level of VIP was (5.794 +/- 0.014) ng/ ml in normal control and was (14.437 +/- 0.825) ng/ml in gastric adenocarcinoma patients, showing significant difference (P < 0.05). Meanwhile,the V/B of gastric adenocarcinoma tissues was greater than that of gastric dysplasia and the corresponding normal gastric mucosa (P <0.01), the values of V/B were 1.5261 +/- 0.3028, 0.9334 +/- 0.2872,and 0.9051 +/- 0.2794, respectively. The values of V/B between normal gastric mucosa and gastric dysplasia were not different significantly (P > 0.05). There were significantly negative correlation between the VIP mRNA expression of the differentiation degree of tumor (P < 0.05). The VIP mRNA expression was higher in gastric adenocarcinoma with lymph node metastasis than that without lymph node matastsis (P < 0.05). The VIP protein expression of the gastric adenocarcinoma tissues was greater than that of normal control.</p><p><b>CONCLUSION</b>This findings provide a direct evidence to support the possibility that VIP play a cofactor role in the pathogenesis of gastric adenocarcinoma.</p>


Subject(s)
Humans , Adenocarcinoma , Blood , Genetics , Gastric Mucosa , Metabolism , Gene Expression , RNA, Messenger , Metabolism , Reverse Transcriptase Polymerase Chain Reaction , Stomach Neoplasms , Blood , Genetics , Vasoactive Intestinal Peptide , Blood , Genetics
2.
Chinese Journal of Oncology ; (12): 662-665, 2007.
Article in Chinese | WPRIM | ID: wpr-298523

ABSTRACT

<p><b>OBJECTIVE</b>To determine the dynamic expression of survivin gene in hepatocarcinogenesis of rats induced by aflatoxin B1 (AFB1).</p><p><b>METHODS</b>78 Sprague-Dawley rats were used in this study. Hepatocellular carcinoma was induced in the rats by aflatoxin B1. Liver and HCC tissues were examined by immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>The earliest hepatocellular carcinoma occurred at 46th week after AFB1 treatment. The HCC incidence was 54.9% (28/51) at 46th week and 64.9% (24/37) at 58th week. The positive rates of survivin protein expression in 24 HCC, para-cancerous liver tissues of experimental group were 41.7% and 54.2%, respectively, with no significant difference between them (P > 0.05). No survivin expression was detected in the experimental group before 46th week, neither in the rats without HCC occurrence nor the normal controls. The level of survivin mRNA expression in HCC at 58th week was significantly higher than that in pre-HCC, no-HCC and normal liver tissues in the control group (P < 0.01). The level of survivin mRNA expression in para-carcinoma tissues was also significantly higher than that in no-HCC and normal liver tissues of the control (P < 0.01). The level of survivin mRNA in pre-HCC at 12th, 20th, 36th, 46th weeks were significantly higher than those in normal liver tissues taken from control group during the same periods (P < 0.01).</p><p><b>CONCLUSION</b>The over-expression of survivin gene is related to the occurrence of HCC and may play an important role in the carcinogenesis of HCC.</p>


Subject(s)
Animals , Male , Rats , Aflatoxin B1 , Apoptosis Regulatory Proteins , Genetics , Metabolism , Gene Expression Regulation, Neoplastic , Liver , Metabolism , Liver Neoplasms, Experimental , Metabolism , Microtubule-Associated Proteins , Genetics , Metabolism , RNA, Messenger , Metabolism , Random Allocation , Rats, Sprague-Dawley
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