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Objective:To study the risk factors affecting the prognosis of patients with type Ⅰ endometrial cancer.Methods:A total of 279 patients with type Ⅰ endometrial cancer admitted to the First Affiliated Hospital of Southwest Medical University were enrolled from January 2010 to January 2015. The clinical data of all patients were retrospectively analyzed. The Kaplan-Meier method was used to estimate patients′ survival rate. Cox regression risk model was used to analyze the risk factors that might affect the prognosis of patients with endometrial cancer.Results:Of 279 patients with endometrial cancer, postoperative recurrence was observed in 36 patients. The 5-year disease free survival rate was 87.10%(243/279). The 2, 3 and 5-year survival rates were 95.9% (95% CI: 93.6%-98.3%), 94.3% (95% CI: 91.6%-97.2%), and 90.4% (95% CI: 86.6%-94.3%). Univariate analysis showed that obesity ( HR=2.194, 95% CI: 1.031-4.671, P=0.041), myometrial invasion ( HR=2.957, 95% CI: 1.382-6.329, P=0.005), tissue grading (G2: HR=3.271, 95% CI: 1.336-8.010, P=0.010; G3: HR=9.933, 95% CI: 3.565-27.672, P<0.001), tumor size ( HR=8.067, 95% CI: 2.426-26.821, P=0.001), abdominal cytology ( HR=3.293, 95% CI: 1.523-7.121, P=0.002), surgery-pathological staging (Ⅲ stage: HR=28.357, 95% CI: 11.516-69.828, P<0.001), nature of lymph node ( HR=14.629, 95% CI: 5.023-42.606, P<0.001), cervical interstitial infiltration ( HR=3.806, 95% CI: 1.653-8.764, P=0.002), accessory metastasis ( HR=9.101, 95% CI: 3.831-21.622, P<0.001) and lymphovascular space invasion ( HR=5.011, 95% CI: 2.233-11.249, P<0.001) were all correlated with the prognosis of the patients. Multivariate analysis showed that the independent risk factors for the prognosis of endometrial cancer patients were depth of myometrial invasion ( HR=2.503, 95% CI: 1.115-5.616, P=0.026), histological grading (G2: HR=3.143, 95% CI: 1.205-8.198, P=0.019; G3: HR=3.655, 95% CI: 1.151-11.610, P=0.028), surgery-pathological staging (Ⅲ stage: HR=27.701, 95% CI: 9.608-79.869, P<0.001) and lymphovascular space invasion ( HR=3.297, 95% CI: 1.370-7.936, P=0.008). Conclusion:Obesity, myometrial invasion, tissue grading, tumor size, abdominal cytology, surgery-pathological staging, nature of lymph node, cervical interstitial infiltration, adnexal metastasis and lymphovascular space invasion all affect the prognosis of patients. Depth of myometrial invasion, histological grading, surgical-pathological staging and lymphovascular space invasion are independent risk factors for the prognosis of patients with Ⅰ endometrial cancer.
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Polyamine biosynthesis is controlled primarily by omithine Decarboxylase (ODC) and S-adenosylmethionine decarboxylase (AdoMetDC). Antisense ODC and AdoMetDC sequences were cloned into an adenoviral vector (Ad-ODC-AdoMetDCas). To study the inhibitory effects of Ad-ODC-AdoMetDCas on polyamine biosynthesis and esophageal cancer cell apoptosis, adenovirus-mediated gene tmnsduction efficiency was assessed with counting GFP-positive cells using MTT. The malignant phenotype of Eca109 cells was assessed by growth curve. Western blot and HPLC were used to detect ODC and AdoMetDC expression and polyamine content in Ecal09 cells. TUNEL was used to analyze cell apoptosis. The change of morphology of apoptotic cells was observed by electron microscope. It was demonstrated approximate 70% of Eca 109 cells were infected with Ad-ODC-AdoMetDCas when MOI reached 50. The expression of ODC was inhibited in the infected tumor cells. Ad-ODC-AdoMetDCas could inhibit Ecal09 cell growth and invasive ability. TUNEL proved that Ad-ODC-AdoMetDCas can lead to cell apoptosis. Characterized morphology was observed by electronmicroscope (ehromatincondensation,nuclear disintegration,formation of apoptoticbodies).It was suggested Ad-ODC-AdoMetDCas has significant inhibitory effects on esophageal cancer cell proliferation, leads to cell apoptosis and bears therapeutic potential for the treatment of esophageal cancer.
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Polyamine biosynthesis is controlled primarily by ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase(AdoMetDC). Antisense ODC and AdoMetDC sequences were cloned into an adenoviral vector (Ad-ODC-AdoMetDCas). To evaluated the effect of recombinant adenovirus Ad-ODC-AdoMetDCas which can simultaneously express both antisense ornithine decarboxylase (ODC) and sadenosylmethionine decarboxylase (AdoMetDC), the human lung cancer cell line A-549, was infected with Ad-ODC-AdoMetDCas as well as with control vector. Viable cell counting, determination of polyamine concentrations, cell apoptosis,and Matrigel invasion assays were performed in order to assess properties of tumor growth and invasiveness. Furthermore,Ad-ODC-AdoMetDCas's anti-tumor effect was also evaluated in vivo in a nude mice xenograft model. It was demonstrated that adenovirus-mediated ODC and AdoMetDC antisense expression could inhibit tumor cell growth, lead to cell apoptosis and reduce tumor cell invasiveness. Polyamine levels were significantly decreased in Ad-ODC-AdoMetDCas-treated cells compared with controls.This adenovirus also induced tumor regression in established tumors in nude mice. It was suggested that as a new anticancer reagent,the recombinant adenovirus Ad-ODC-AdoMetDCas holds promising hope for the therapy of lung cancers.
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Objective To investigate the effect of raloxifene on the mRNA expression of endothelin-1 in vascular endothelial cells and assess the role of estrogen receptor. Methods Bovine carotid endothelial cells were pretreated with 10nM raloxifene for 24 hours, then total RNA was harvested and Northern blotting was performed to investigate the effect of raloxifene on the mRNA expression of endothelin-1. Furthermore, estrogen receptor inhibitor, 100nM ICI 182 780 was used to pretreat the cells together with raloxifene and the expression of endothelin-1 was observed too. Results The mRNA expression of endothelin-1 in bovine carotid endothelial cells was inhibited significantly by pretreatment with raloxifene and this effect could be blocked by ICI182 780 (0.16?0.05 vs 0.39?0.07, P
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AIM: To assess the effect of estrogen on the gene expression of caveolin-1 in rat vascular smooth muscle cells (VSMCs). METHODS: Wistar rats were ovariectomized and subjected to subcutaneous implantation of placebo pellets (OVX+V group) or estradiol pellets (OVX+E group). 2 weeks after implantation, the expression of caveolin-1 gene in endothelium-denuded aortic tissue was examined by RT-PCR. Furthermore, Northern blotting was used to analyze the mRNA expression of caveolin-1 in cultured rat VSMCs. RESULTS: RT-PCR showed that expression of caveolin-1 gene was significantly higher in OVX+E group than that in OVX+V group. Northern blot analysis showed that the mRNA expression of caveolin-1 was higher in VSMCs pretreated with 17?-estradiol (17?-E 2) than that in VSMCs without 17?-E 2 pretreatment. CONCLUSION: Estrogen up-regulates the gene expression of caveolin-1 in the vascular wall, partially indicating the cardiovascular effect of estrogen. [
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?-GT activity and its substrate GSH content in tissue homogenate, epithe-lium and stroma of normal and benign hyperplastic human prostates were measured tostudy their relationship with pathogenesis of benign prostatic hyperplasia (BPH). Theresults were: a) ?-GT activity in BPH tissues were very much increased; but GSHcontent was much decreased; b) The ?-GT activity in epithelium of both normal andBPH were much higher than that in relative stroma. However epithelium GSH contentwere lower than that of stroma. Thase results suggested that increand ?-GT activity anddecreased GSH content play an important role in pathogenesis of BPH.