ObjectiveTo detect the expression of somatostatin receptor Ⅱ(SSTR2) mRNA in the specimens of colorectal cancer patients and discuss the relationship between the expression and characteristics of the tumor.MethodsAll tissue samples of 36 cases, including normal colonic mucosa (10 cm beyond the tumor), mucosa adjacent to the tumor (within 2 cm of the tumor), tumor, and mesenteric lymph node, were collected immediately after surgical resection. The SSTR2 mRNA were detected by RT-PCR in 135 samples of the 36 cases. The SSTR2 mRNA expression rate in different samples was compared.ResultsThe SSTR2 mRNA expression rate of normal colonic mucosa, mucosa adjacent to tumor, tumor, mesenteric node without metastasis, and mesenteric node with metastasis was 67.6%(23/34), 75.0%(24/32),91.4%(32/35),93.8%(15/16) and 81.8%(9/11) respectively. Expression rate of tumor significantly increased compared with normal colonic mucosa (χ2=6.37, P＜0.05). The expression rate of the tumor in different groups, such as patients of different sex, serum CEA level, tumor size, location, histological grade and pathological stage, showed no difference (P＞0.05）.ConclusionThe expression rate of SSTR2 mRNA of colorectal adenocarcinoma increases. The expression rate does not correlate with the histological grade and pathological stage of the tumor.
Objective To review the research progress in relationship between hereditary diffuse gastric cancer (HDGC) and CDH1 gene. Methods Literatures on HDGC which were published in recent years were collected and analyzed. Results Aberrant CDH1 gene is significantly correlated with HDGC: mutations of CDH1 exons play the most important role in pathogenesis of HDGC. Screening CDH1 gene mutation is useful for diagnosis of HDGC as well as the treatments. Alterations of CDH1 other than exon mutation, such as intron mutation, gene promoter methylation and single nucleotide polymorphism may result in downregulation of the gene expression. Further study should be done to confirm the roles of these alterations. Conclusions Alterations of CDH1 gene are significantly associated with the pathogenesis of HDGC. Detecting alterations of CDH1 gene are important for diagnosis and management of HDGC as well as to get insights of the pathogenesis of the disease.
【Abstract】ObjectiveTo investigate the inhibitory effects of somatostatin analogue (SSTA) on the colonic carcinoma cell growth in vitro and in vivo and its possible mechanism. MethodsThe somatostatin receptor type Ⅱ (SSTR2) mRNA of colonic carcinoma cell line HCT116 was detected by using RTPCR and hybridization in situ. The effects of octreotide (Oct) or NC-8-12 (specific agonist of SSTR2 ) on the proliferation of HCT116 was measured with MTT after HCT116 stimulated by insulin or epidermal growth factor (EGF) and incubated with Oct or NC-8-12 simultaneously for 24 hours. The expression of cyclin D1 was detected with flow cytometry. The HCT116 were implanted in nude mice subcutaneously and treated with Oct or NC-8-12. The tumor volume and tumor weight were measured according to schedule. Results①SSTR2 mRNA was detected in HCT116 and the tumor implanted in nude mice; ②Insulin and EGF increased the proliferation of HCT116 significantly, and this proliferation could be inhibited by Oct and NC-8-12 partially; ③Insulin increased the Cyclin D1 expression of HCT116, its level decreased slightly when treated with Oct or NC-8-12 but not significantly (Pgt;0.05); ④The weight and volume of implanted tumor in nude mice treated with Oct or NC-8-12 showed no significant difference compared with the control group (Pgt;0.05). ConclusionBoth Oct and NC-8-12 could inhibit the proliferation of colonic carcinoma cell line HCT116 in vitro, which indicated that SSTR2 may mediated the inhibition. Oct and NC-8-12 have no effect on the growth of implanted HCT116 in nude mice in this experiment.
Objective Heparan sulfate proteoglycans (HSPGs) is an important component of the extracellular matrix. syndecan-1, a member of syndecan family, belongs to HSPGs and plays an important role in cell morphology and intracellular arrangement. The present study was designed to investigate the expression of syndecan-1 in patients with colorectal cancer, to analyse its relationship to cancer progression and clinical prognosis. Methods Paraffin-embeded specimens were collected from 31 patients with colorectal cancers from 2003 to 2004 in Peking Union Medical College Hospital. Syndecan-1 protein expression was measured by immunohistochemistry. Its expression was evaluated with relationship to clinicopathological factors, including tumor infiltration, tumor differentiation, lymph node metastasis, accompanying with colorectal adenoma and 2-year survivals. Results Immunohistochemistry in 31 specimens showed syndecan-1 were detected positive in 1 colorectal cancer tissue (3.2%), while positive in 29 normal tissues (93.5%), with significant difference (P＜0.01). No prognostic differences could be found in the clinic outcome because of the high expression rate of syndecan-1 in normal tissues and low expression rate in cancer tissues. Conclusion Syncecan-1 is expressed in normal colorectal tissues and rarely expressed in cancer tissues.
Objective Heparanase can specifically cleave carbohydrate chains of heparan sulphate proteoglycans, which is an important component of the extracellular matrix. This study was designed to investigate the expression of heparanase in patients with colorectal cancer, and to analyze its relationships with progression of the cancer and clinical prognosis. Methods Samples were collected from 36 patients with colorectal cancers from 2003 to 2004 in Peking Union Medical College Hospital, and were embeded by Paraffin and fresh-frozened. The expression of heparanase mRNA and its protein were measured by RT-PCR and immunohistochemistry. The relationships between these expressions and the clinicopathologic information (tumor invasion, tumor differentiation, lymph node involvement, accompanying with colorectal adenoma and 2-year survival) were also evaluated. Results The expressions of heparanase mRNA in colorectal cancer (19/31， 61.3%) were significantly higher than those in normal colorectal tissues (6.5%). The overexpressions in normal tissues were positively correlated to the incidence of adenoma in patients with colorectal cancer （r=0.352， P=0.024）. The result of immunohistochemistry also showed that heparanase mainly expressed in the vascular endothelium within cancer tissues and the peripheral invased region outside cancer tissues. The 2-year disease-free-survival in patients with negative heparanase expression (88.9%) was higher than that with positive heparanase expression (50.0%), but there was no significant difference （P=0.078）. Conclusion Heparanase overexpressed in colorectal cancer tissues, and thus it may take a role as an indicator for the formation and prognosis of colorectal cancer.