本文選題：MTDH + E-cadherin��； 參考：《重慶醫(yī)科大學(xué)》2016年博士論文

【摘要】：膀胱癌是泌尿系最常見(jiàn)的惡性腫瘤,臨床上,膀胱癌多采用腫瘤切除,術(shù)后輔助化療。然而,由于膀胱癌的高轉(zhuǎn)移性,膀胱癌的復(fù)發(fā)率及死亡率仍然很高。故研究膀胱癌的轉(zhuǎn)移機(jī)制是很有必要的。MTDH是近年來(lái)發(fā)現(xiàn)的癌基因,已有報(bào)道其在惡性腫瘤中表達(dá)較高。上皮間質(zhì)轉(zhuǎn)化(EMT)是上皮細(xì)胞獲得間質(zhì)表型,易于侵襲轉(zhuǎn)移的特性,其經(jīng)典上皮標(biāo)志物為E-cadherin。有報(bào)道顯示,在惡性腫瘤中,MTDH可促進(jìn)EMT發(fā)生,而EMT是膀胱癌發(fā)生侵襲、轉(zhuǎn)移的重要原因。目前,在膀胱癌中尚無(wú)MTDH與EMT的相關(guān)研究。本研究擬通過(guò)分析在膀胱癌組織及細(xì)胞中MTDH與E-cadherin的表達(dá)關(guān)系,探討MTDH與EMT是否存在某種聯(lián)系,進(jìn)而采用基因沉默及過(guò)表達(dá)技術(shù),深入研究MTDH對(duì)EMT的影響,及MTDH促進(jìn)膀胱癌細(xì)胞侵襲、轉(zhuǎn)移的機(jī)制。第一部分MTDH和E-cadherin在膀胱癌組織及細(xì)胞中的表達(dá)及臨床意義目的檢測(cè)MTDH、E-cadherin在膀胱癌組織及細(xì)胞中的表達(dá),探討MTDH、E-cadherin與臨床病理特征的關(guān)系,以及MTDH與E-cadherin表達(dá)的相關(guān)性。方法1.應(yīng)用免疫組化(immunohistochemistry,IHC)SP法檢測(cè)膀胱癌組織中MTDH和EMT上皮標(biāo)志物E-cadherin的表達(dá)水平。分析MTDH、E-cadherin蛋白表達(dá)與臨床病理特征之間的關(guān)系,Spearman’s法分析MTDH與E-cadherin表達(dá)可能存在的相關(guān)性。2.Real-time PCR方法檢測(cè)MTDH與E-cadherin在膀胱癌細(xì)胞株、尿路上皮細(xì)胞株中m RNA的表達(dá)水平。3.Western blot方法檢測(cè)在膀胱癌細(xì)胞株、尿路上皮細(xì)胞株MTDH與E-cadherin蛋白的表達(dá)水平。結(jié)果1.與癌旁組織比較,癌組織MTDH的蛋白表達(dá)水平明顯增高,E-cadherin的表達(dá)水平明顯降低。MTDH、E-cadherin表達(dá)與患者年齡、性別、腫瘤大小、數(shù)量無(wú)關(guān),與腫瘤遠(yuǎn)處轉(zhuǎn)移、臨床分期、病理分級(jí)有關(guān)。MTDH與E-cadherin的蛋白表達(dá)之間呈負(fù)相關(guān)(r=-0.722,P0.05)。2.膀胱癌細(xì)胞株5637、T24中MTDH m RNA表達(dá)水平相對(duì)于人尿路上皮細(xì)胞株SV-HUC-1中顯著升高;E-cadherin m RNA表達(dá)水平在膀胱癌細(xì)胞株5637、T24中相對(duì)于人尿路上皮細(xì)胞株SV-HUC-1中顯著降低。3.膀胱癌細(xì)胞株5637、T24中MTDH蛋白表達(dá)水平相對(duì)于人尿路上皮細(xì)胞株SV-HUC-1中顯著升高;E-cadherin的蛋白表達(dá)水平在膀胱癌細(xì)胞株5637、T24中相對(duì)于其在人尿路上皮細(xì)胞株SV-HUC-1中顯著降低。結(jié)論MTDH在膀胱癌組織及細(xì)胞中高表達(dá),E-cadherin在癌旁組織及正常細(xì)胞中高表達(dá)。MTDH與腫瘤臨床病理學(xué)特征密切相關(guān),可作為判斷腫瘤臨床病理的分子指標(biāo)。MTDH與E-cadherin呈負(fù)相關(guān),相互之間存在負(fù)向調(diào)控。第二部分MTDH基因沉默對(duì)膀胱癌細(xì)胞功能學(xué)影響及其機(jī)制研究目的探討抑制MTDH表達(dá)對(duì)膀胱癌細(xì)胞增殖、凋亡、遷移、侵襲的影響及MTDH沉默對(duì)上皮間質(zhì)轉(zhuǎn)化相關(guān)標(biāo)志物的影響方法1.Real-time PCR檢測(cè)si RNA-MTDH轉(zhuǎn)染5637和T24細(xì)胞后MTDH m RNA變化情況,Western blot方法檢測(cè)si RNA-MTDH轉(zhuǎn)染5637和T24細(xì)胞后,MTDH蛋白表達(dá)情況,分析si RNA的抑制效率,最終篩選出沉默效率最高的si RNA。2.通過(guò)CCK8法檢測(cè)MTDH基因沉默后5637和T24的增殖能力的變化,流式細(xì)胞術(shù)檢測(cè)MTDH基因沉默對(duì)5637和T24細(xì)胞凋亡的影響,細(xì)胞劃痕實(shí)驗(yàn)檢測(cè)MTDH基因沉默對(duì)5637、T24細(xì)胞遷移能力的影響,Transwell實(shí)驗(yàn)檢測(cè)MTDH基因沉默對(duì)5637、T24細(xì)胞的侵襲能力的影響。3.Real-time PCR方法檢測(cè)si RNA2-MTDH轉(zhuǎn)染5637、T24細(xì)胞后上皮間質(zhì)轉(zhuǎn)化相關(guān)標(biāo)志物E-cadherin、N-cadherin、Vimentin m RNA的表達(dá)變化。Western blot檢測(cè)si RNA2-MTDH轉(zhuǎn)染5637、T24細(xì)胞后上皮間質(zhì)轉(zhuǎn)化相關(guān)標(biāo)志物E-cadherin、N-cadherin、Vimentin蛋白的表達(dá)變化。細(xì)胞免疫熒光技術(shù)檢測(cè)si RNA2-MTDH轉(zhuǎn)染5637、T24細(xì)胞后上皮間質(zhì)轉(zhuǎn)化相關(guān)標(biāo)志物E-cadherin、N-cadherin、Vimentin熒光表達(dá)變化。結(jié)果1.從基因及蛋白水平驗(yàn)證si RNA2-MTDH沉默效率大于70%,篩選確定si RNA2用于后續(xù)實(shí)驗(yàn)。2.CCK8法實(shí)驗(yàn)結(jié)果顯示:與對(duì)照組相比,MTDH基因沉默后膀胱癌細(xì)胞5637、T24的增殖能力明顯降低,流式細(xì)胞儀檢測(cè)結(jié)果提示MTDH基因沉默后5637、T24凋亡率較對(duì)照組明顯增加,細(xì)胞劃痕實(shí)驗(yàn)、Transwell實(shí)驗(yàn)結(jié)果提示MTDH基因沉默后5637、T24細(xì)胞遷移及侵襲能力顯著降低。3.Real-time PCR、Western blot實(shí)驗(yàn)提示si RNA2-MTDH轉(zhuǎn)染5637、T24細(xì)胞后上皮相關(guān)標(biāo)志物E-cadherin m RNA及蛋白表達(dá)顯著增高,而間質(zhì)標(biāo)志物N-cadherin、Vimentin m RNA及蛋白表達(dá)顯著降低。細(xì)胞免疫熒光技術(shù)檢測(cè)提示si RNA2-MTDH轉(zhuǎn)染5637、T24細(xì)胞后相關(guān)標(biāo)志物E-cadherin熒光表達(dá)增強(qiáng),陽(yáng)性細(xì)胞數(shù)增多;而N-cadherin、Vimentin熒光表達(dá)減弱,陽(yáng)性細(xì)胞數(shù)減少。結(jié)論MTDH基因沉默抑制膀胱癌細(xì)胞增殖,促進(jìn)其凋亡,抑制膀胱癌細(xì)胞遷移及侵襲,促進(jìn)上皮標(biāo)志物表達(dá),抑制間質(zhì)標(biāo)志物表達(dá),抑制上皮間質(zhì)轉(zhuǎn)化。第三部分MTDH過(guò)表達(dá)對(duì)膀胱癌細(xì)胞功能學(xué)影響及其機(jī)制研究目的探討MTDH過(guò)表達(dá)對(duì)膀胱癌細(xì)胞增殖、凋亡、遷移、侵襲的影響及MTDH過(guò)表達(dá)對(duì)上皮間質(zhì)轉(zhuǎn)化相關(guān)標(biāo)志物的影響方法1.構(gòu)建MTDH過(guò)表達(dá)慢病毒載體GV341-MTDH及GV341-NC,制備慢病毒濃縮液LV-MTDH,LV-NC,感染5637、T24細(xì)胞,建立過(guò)表達(dá)MTDH的LV-MTDH單克隆細(xì)胞株及陰性對(duì)照組LV-NC細(xì)胞株。Real-time PCR檢測(cè)5637和T24細(xì)胞過(guò)表達(dá)MTDH后MTDH m RNA變化情況,Western blot方法檢測(cè)5637和T24細(xì)胞過(guò)表達(dá)MTDH后,MTDH蛋白表達(dá)情況。2.通過(guò)CCK8法檢測(cè)5637和T24細(xì)胞MTDH過(guò)表達(dá)后增殖能力的變化,流式細(xì)胞術(shù)檢測(cè)MTDH基因過(guò)表達(dá)對(duì)5637和T24細(xì)胞凋亡的影響,細(xì)胞劃痕實(shí)驗(yàn)檢測(cè)MTDH基因過(guò)表達(dá)對(duì)5637、T24細(xì)胞遷移能力的影響,Transwell實(shí)驗(yàn)檢測(cè)MTDH基因過(guò)表達(dá)對(duì)5637、T24細(xì)胞的侵襲能力的影響。3.Real-time PCR方法檢測(cè)5637、T24細(xì)胞MTDH過(guò)表達(dá)后上皮間質(zhì)轉(zhuǎn)化相關(guān)標(biāo)志物E-cadherin、N-cadherin、Vimentin m RNA的表達(dá)變化。Western blot檢測(cè)5637、T24細(xì)胞MTDH過(guò)表達(dá)后上皮間質(zhì)轉(zhuǎn)化相關(guān)標(biāo)志物E-cadherin、N-cadherin、Vimentin蛋白表達(dá)變化。細(xì)胞免疫熒光技術(shù)檢測(cè)5637、T24細(xì)胞MTDH過(guò)表達(dá)后E-cadherin、N-cadherin、Vimentin熒光表達(dá)變化。結(jié)果1.MTDH過(guò)表達(dá)慢病毒載體構(gòu)建成功,從基因及蛋白水平證實(shí)成功建立過(guò)表達(dá)MTDH的LV-MTDH單克隆細(xì)胞株及陰性對(duì)照組LV-NC細(xì)胞株。2.CCK8法實(shí)驗(yàn)結(jié)果顯示:與對(duì)照組相比,MTDH過(guò)表達(dá)后膀胱癌細(xì)胞5637、T24的增殖能力明顯增強(qiáng),流式細(xì)胞儀檢測(cè)結(jié)果提示MTDH過(guò)表達(dá)后5637、T24凋亡率較對(duì)照組明顯降低,細(xì)胞劃痕實(shí)驗(yàn)、Transwell實(shí)驗(yàn)結(jié)果提示MTDH基因過(guò)表達(dá)后5637、T24細(xì)胞遷移及侵襲能力顯著增強(qiáng)。3.Real-time PCR、Western blot實(shí)驗(yàn)提示5637、T24細(xì)胞MTDH基因過(guò)表達(dá)后上皮間質(zhì)轉(zhuǎn)化相關(guān)標(biāo)志物E-cadherin m RNA及蛋白表達(dá)明顯減弱,而N-cadherin、Vimentin m RNA及蛋白表達(dá)顯著增強(qiáng)。細(xì)胞免疫熒光技術(shù)檢測(cè)提示5637、T24細(xì)胞MTDH基因過(guò)表達(dá)后E-cadherin熒光表達(dá)減弱,陽(yáng)性細(xì)胞數(shù)減少;而N-cadherin、Vimentin熒光表達(dá)增強(qiáng),陽(yáng)性細(xì)胞數(shù)增多。結(jié)論MTDH基因過(guò)表達(dá)促進(jìn)膀胱癌細(xì)胞增殖,抑制其凋亡,增強(qiáng)膀胱癌細(xì)胞遷移及侵襲能力,抑制上皮標(biāo)志物表達(dá),提高間質(zhì)標(biāo)志物表達(dá),促進(jìn)上皮間質(zhì)轉(zhuǎn)化。第四部分MTDH過(guò)表達(dá)對(duì)T24、5637細(xì)胞Wnt/β-catenin信號(hào)通路及其下游靶基因的調(diào)控目的探討MTDH過(guò)表達(dá)對(duì)T24、5637細(xì)胞Wnt/β-catenin信號(hào)通路及其下游靶基因的調(diào)控方法1.Western blot檢測(cè)MTDH過(guò)表達(dá)對(duì)5637、T24細(xì)胞Wnt/β-catenin信號(hào)通路、下游靶基因及基質(zhì)金屬蛋白酶MMP9蛋白表達(dá)的影響2.免疫熒光檢測(cè)MTDH過(guò)表達(dá)5637和T24細(xì)胞對(duì)β-catenin熒光表達(dá)的影響結(jié)果1.Western blot實(shí)驗(yàn)提示5637、T24細(xì)胞MTDH基因過(guò)表達(dá)后Wnt通路被激活,細(xì)胞內(nèi)β-catenin總蛋白表達(dá)增多,胞核β-catenin蛋白表達(dá)顯著增多,而胞質(zhì)β-catenin蛋白表達(dá)明顯減低,c-Myc及MMP9蛋白表達(dá)顯著增加。2.免疫熒光實(shí)驗(yàn)提示:5637、T24細(xì)胞MTDH基因過(guò)表達(dá)后,β-catenin蛋白熒光表達(dá)增強(qiáng),陽(yáng)性細(xì)胞數(shù)增多,且胞核內(nèi)表達(dá)顯著增強(qiáng)。結(jié)論慢病毒載體介導(dǎo)的MTDH基因過(guò)表達(dá)經(jīng)Wnt/β-catenin信號(hào)通路,促進(jìn)上皮間質(zhì)轉(zhuǎn)化,增強(qiáng)膀胱癌細(xì)胞侵襲能力。
[Abstract]:Bladder cancer is the most common malignant tumor of the urinary system. In clinic, tumor resection and adjuvant chemotherapy are mostly used in bladder cancer. However, the recurrence rate and death rate of bladder cancer are still high because of the high metastasis of bladder cancer. Therefore, it is necessary to study the metastasis mechanism of bladder cancer in recent years, and it has been reported that.MTDH is in the evil. The expression of epithelial mesenchymal transition (EMT) is the characteristic of epithelial cells obtaining interstitial phenotypes and prone to invasion and metastasis. The classical epithelial markers of E-cadherin. have reported that MTDH can promote the occurrence of EMT in malignant tumors, and EMT is an important reason for the invasion and metastasis of bladder cancer. At present, there is no MTDH and EMT in bladder cancer. The purpose of this study is to analyze the relationship between MTDH and E-cadherin in bladder cancer tissues and cells, to explore the relationship between MTDH and EMT, and then to use gene silencing and overexpression technology to study the effect of MTDH on EMT, and the mechanism of MTDH to promote the invasion and metastasis of bladder cancer cells. The first part MTDH and E-cadherin Expression and clinical significance in bladder cancer tissues and cells objective to detect the expression of MTDH, E-cadherin in bladder cancer tissues and cells, to explore the relationship between MTDH, E-cadherin and clinicopathological features, and the correlation between MTDH and E-cadherin expression. Method 1. the SP method of immunohistochemistry (IHC) was used to detect MTD in bladder cancer tissues. The expression level of H and EMT epithelial marker E-cadherin. Analysis of the relationship between MTDH, E-cadherin protein expression and clinicopathological features, Spearman 's method to analyze the possible correlation between MTDH and E-cadherin expression and.2.Real-time PCR method to detect the expression level of MTDH in bladder cancer cell lines and urinary tract epithelial cells. .Western blot method was used to detect the expression level of MTDH and E-cadherin protein in bladder cancer cell line and urinary tract epithelial cell line. Results 1. compared with para cancer tissue, the protein expression level of MTDH in cancer tissue was significantly higher, the expression level of E-cadherin decreased obviously, and the expression of E-cadherin was not related to age, sex, size and quantity of the patient, and the swelling of E-cadherin. Tumor distant metastasis, clinical staging, pathological grade related to the protein expression of.MTDH and E-cadherin was negatively correlated (r=-0.722, P0.05).2. bladder cancer cell line 5637, MTDH m RNA expression level in T24 was significantly higher in T24 than in human urinary tract epithelial cell strain SV-HUC-1; E-cadherin m (E-cadherin m) expression level in bladder cancer cell line 5637, relative to human The urinary tract epithelial cell line SV-HUC-1 significantly reduced the.3. bladder cancer cell line 5637, and the expression level of MTDH protein in T24 was significantly higher than that in human urinary tract epithelial cell strain SV-HUC-1; the protein expression level of E-cadherin was significantly lower in bladder cancer cell line 5637 and in T24 than in human urinary tract epithelial cell strain SV-HUC-1. Conclusion MTDH is in bladder. High expression of E-cadherin in cystocarcinoma tissue and cells, high expression of.MTDH in para cancer tissues and normal cells is closely related to the clinicopathological features of tumor. It can be a negative correlation between.MTDH and E-cadherin as a molecular marker of tumor clinicopathology, and there is a negative regulation between each other. Second part of MTDH gene silencing on the function of bladder cancer cells Effect and mechanism study to investigate the effect of inhibition of MTDH expression on the proliferation, apoptosis, migration, invasion of bladder cancer cells and the effect of MTDH silence on epithelial mesenchymal transition related markers. 1.Real-time PCR detection of MTDH m RNA changes after Si RNA-MTDH transfection of 5637 and T24 cells, Western blot method After 24 cells, the expression of MTDH protein was expressed and the inhibition efficiency of Si RNA was analyzed. Finally, the Si RNA.2. with the highest silence efficiency was selected to detect the proliferation of 5637 and T24 after MTDH gene silencing by CCK8 method. The effect of MTDH gene silencing on the apoptosis of 5637 and T24 cells was detected by flow cytometry, and the cell scratch test was used to detect the MTDH gene silencing of 563 7, the effect of T24 cell migration, Transwell test detected the influence of MTDH gene silencing on the invasiveness of 5637, T24 cells,.3.Real-time PCR method was used to detect Si RNA2-MTDH transfection 5637, T24 cell epithelial mesenchymal transition related markers E-cadherin, N-cadherin. The expression of epithelial mesenchymal transition related markers E-cadherin, N-cadherin, Vimentin protein expression after T24 cells. Cell immunofluorescence technique was used to detect Si RNA2-MTDH transfection 5637, E-cadherin, N-cadherin, Vimentin fluorescent expression of epithelial mesenchymal transition markers after T24 cells, and 1. from gene and protein level to verify Si RNA2-MTDH precipitation. The effect of Si RNA2 was more than 70%. The results of the screening and determination of Si RNA2 for subsequent experiment showed that compared with the control group, the proliferation ability of bladder cancer cells was 5637 and T24 was significantly reduced after the silence of the control group. The results of flow cytometry showed that the MTDH gene was 5637, and the apoptosis rate of T24 was significantly higher than that of the control group, and the cell scratch test and Transwell were real. The results suggested that after MTDH gene silencing, 5637, T24 cell migration and invasion ability significantly decreased.3.Real-time PCR, Western blot experiment suggested that Si RNA2-MTDH transfected 5637, E-cadherin m RNA and protein expression was significantly increased after T24 cell, and the interstitial marker and protein expression decreased significantly. The immunofluorescence technique showed that the transfection of Si RNA2-MTDH was 5637, the fluorescent expression of E-cadherin was enhanced and the number of positive cells increased, while N-cadherin, Vimentin fluorescent expression decreased, and the number of positive cells decreased. Conclusion MTDH gene silencing inhibits the proliferation of bladder cancer cells, promotes its apoptosis and inhibits the migration and invasion of bladder cancer cells. Promote the expression of epithelial markers, inhibit the expression of interstitial markers, inhibit epithelial mesenchymal transition. Third the effect of MTDH overexpression on the function of bladder cancer cells and its mechanism research to explore the effect of MTDH overexpression on the proliferation, apoptosis, migration, invasion of bladder cancer cells and the effect of MTDH overexpression on epithelial mesenchymal transition markers Methods 1. MTDH overexpressed lentivirus vectors, GV341-MTDH and GV341-NC, were constructed to prepare the lentivirus concentrate LV-MTDH, LV-NC, infection 5637, T24 cells, and the LV-MTDH McAb of MTDH was established and the LV-NC cell line of the negative control group was detected 5637 and the T24 cells were detected. After the overexpression of MTDH in 5637 and T24 cells, the expression of MTDH protein was detected by.2.. The proliferation ability of 5637 and T24 cells was detected by CCK8, and the effect of MTDH gene overexpression on the apoptosis of 5637 and T24 cells was detected by flow cytometry. The cell scratch test was used to detect the effect of MTDH gene over the migration ability of 5637 and T24 cells. The influence of the overexpression of MTDH gene on the invasiveness of 5637, T24 cells;.3.Real-time PCR method was used to detect the expression of E-cadherin, N-cadherin, Vimentin m RNA, after the overexpression of MTDH in 5637, T24 cell MTDH Cadherin, N-cadherin, Vimentin protein expression changes. Cell immunofluorescence technology detected 5637, T24 cell MTDH overexpression E-cadherin, N-cadherin, Vimentin fluorescence expression changes. Results 1.MTDH overexpression lentivirus vector construction successfully, from gene and protein level confirmed the successful establishment of LV-MTDH monoclonal cell lines and negative expression MTDH negative and negative The results of.2.CCK8 assay in the control group LV-NC showed that the proliferation ability of bladder cancer cells 5637 and T24 increased significantly after MTDH overexpression compared with the control group. The results of flow cytometry showed that after MTDH overexpression was 5637, the apoptosis rate of T24 was significantly lower than that of the control group, the cell scratch test, and the result of Transwell test suggested that the MTDH gene was overexpressed 56. 37, the migration and invasion ability of T24 cells significantly enhanced.3.Real-time PCR. Western blot experiments suggested that the expression of E-cadherin m RNA and protein expression of epithelial mesenchymal transition was significantly weakened after the overexpression of MTDH gene in T24 cells, while N-cadherin, Vimentin and protein expression was enhanced. Cell immunofluorescence technique detection suggested 5637. After the overexpression of MTDH gene, the fluorescence expression of E-cadherin decreased, the number of positive cells decreased, while the expression of N-cadherin, Vimentin increased and the number of positive cells increased. Conclusion MTDH gene overexpression promotes the proliferation of bladder cancer cells, inhibits its apoptosis, enhances the migration and invasion ability of bladder cancer cells, inhibits the expression of epithelial markers, and improves the standard of interstitial markers. Fourth part MTDH overexpression on T245637 cell Wnt/ beta -catenin signaling pathway and its downstream target genes regulation of MTDH overexpression on T245637 cells Wnt/ beta -catenin signaling pathway and its downstream target gene regulation, 1.Western blot detection MTDH overexpression of 5637, T24 cells The influence of tenin signaling pathway, downstream target gene and matrix metalloproteinase MMP9 protein expression 2. immunofluorescence detection of MTDH overexpression 5637 and T24 cells on the expression of beta -catenin fluorescent expression results 1.Western blot experiment 5637, T24 cell MTDH overexpression Wnt pathway is activated, intracellular beta -catenin total protein expression increased, the nucleus of the cell nucleus The expression of beta -catenin protein was significantly increased, while the expression of cytoplasmic beta -catenin protein was significantly reduced, and the expression of c-Myc and MMP9 protein was significantly increased by.2. immunofluorescence experiment: 5637, after the MTDH gene was overexpressed in T24 cells, the expression of beta -catenin protein increased, the number of positive cells increased, and the expression of the cell nucleus increased significantly. Conclusion lentivirus vector mediated M Over expression of TDH gene promotes epithelial mesenchymal transition and enhances invasion ability of bladder cancer cells through Wnt/ beta -catenin signaling pathway.

【學(xué)位授予單位】：重慶醫(yī)科大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2016
【分類號(hào)】：R737.14

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