本文選題：上皮性卵巢癌 + 叉頭框轉(zhuǎn)錄因子FOXC1��； 參考：《鄭州大學(xué)》2017年碩士論文

【摘要】：上皮性卵巢癌(Epithelial ovarian cancer,EOC)是女性最常見的生殖系統(tǒng)惡性腫瘤之一。目前,EOC在發(fā)達(dá)國家的病死率已居?jì)D科腫瘤之首。對惡性腫瘤而言,腫瘤細(xì)胞除了呈現(xiàn)活躍的增殖狀態(tài)外,受到威脅最嚴(yán)重的是腫瘤細(xì)胞所表現(xiàn)出來的侵襲遷移特性。目前,國內(nèi)外對影響腫瘤細(xì)胞的生物學(xué)功能的部分基因已進(jìn)行了相關(guān)靶點(diǎn)實(shí)驗(yàn)及探索,對其靶點(diǎn)進(jìn)行干預(yù)的同時(shí)也促進(jìn)了腫瘤治療的發(fā)展,為靶向治療提供了更多的參考。對于EOC而言,通過明確某些基因的異常表達(dá)是否能夠引起上皮性卵巢癌細(xì)胞生物學(xué)行為的改變,進(jìn)而探討其調(diào)控機(jī)制,對EOC病因機(jī)制的深入研究及長遠(yuǎn)靶向治療具有重要意義。轉(zhuǎn)錄因子FOXC1(forkhead box C1)是叉頭框轉(zhuǎn)錄因子基因家族(FOX家族)的一員,是通過自身的叉頭區(qū)DNA結(jié)合域結(jié)合目的基因片段從而啟動(dòng)相關(guān)基因轉(zhuǎn)錄。FOXC1除了參與細(xì)胞或器官分化及代謝等生物學(xué)過程外,目前證實(shí)FOXC1還可以調(diào)控多種腫瘤細(xì)胞信號(hào)傳導(dǎo)途徑,如NF-κB、Wnt/β-Catenin等。這些細(xì)胞信號(hào)通路與細(xì)胞增殖、侵襲、遷移、凋亡等密切相關(guān),因此,FOXC1已成為腫瘤發(fā)病機(jī)制研究的熱點(diǎn)。微小染色體維持蛋白2(minichromosomemai n-tenance proteins 2,MCM2)是細(xì)胞增殖活性判斷的新指標(biāo),用來反映細(xì)胞增殖狀態(tài)時(shí)能表現(xiàn)出更強(qiáng)的特異性及敏感性�；|(zhì)金屬蛋白酶9(matrix metallopro teinase,MMP9)作為細(xì)胞外基質(zhì)降解的主要蛋白水解酶,與腫瘤細(xì)胞侵襲、轉(zhuǎn)移相關(guān)的細(xì)胞外基質(zhì)降解密切相關(guān)。因此當(dāng)EOC中的腫瘤細(xì)胞發(fā)生增殖及侵襲等生物學(xué)行為時(shí)在分子水平常常能夠檢測到MCM2、MMP9的改變。近年來有報(bào)道稱,在卵巢腫瘤組織中,FOXC1在良性上皮性卵巢腫瘤的表達(dá)率為84%,在上皮性卵巢癌中的表達(dá)率為37.5%。本課題組前期研究也發(fā)現(xiàn),上皮性卵巢癌組織中的FOXC1 mRNA表達(dá)量較交界性卵巢上皮性腫瘤組織及良性卵巢上皮性腫瘤組織中減少,且FOXC1在組織中的mRNA表達(dá)量與淋巴結(jié)轉(zhuǎn)移相關(guān),提示FOXC1在組織中表達(dá)的缺失可能對上皮性卵巢癌的發(fā)生發(fā)展有重要意義。然而,FOXC1的異常表達(dá)能否引起上皮性卵巢癌細(xì)胞生物學(xué)功能的改變,如何參與EOC的發(fā)生發(fā)展尚不清楚。另外,大量研究顯示,在EOC中NF-κB信號(hào)傳導(dǎo)通路可以參與MCM2、MMP9的調(diào)控。因此,本課題將對FOXC1是否參與了上皮性卵巢癌細(xì)胞的惡性生物學(xué)行為,是否能通過NF-κB信號(hào)通路對其調(diào)控進(jìn)行初步探討。目的通過慢病毒感染方式在上皮性卵巢癌細(xì)胞SKOV3中構(gòu)建FOXC1過表達(dá)及干擾穩(wěn)定細(xì)胞株后,探討FOXC1對SKOV3細(xì)胞增殖及侵襲能力的影響,并初步判斷FOXC1是否可以通過激活NF-κB信號(hào)通路對其進(jìn)行調(diào)控,分析EOC中FOXC1異常表達(dá)所扮演的角色。材料和方法1研究對象及分組本研究選用人上皮性卵巢癌細(xì)胞系SKOV3細(xì)胞(第四軍醫(yī)大學(xué)病原生物學(xué)教研室趙亞教授饋贈(zèng)),應(yīng)用RPMI-1640完全培養(yǎng)基,將細(xì)胞置于37℃、5%CO2的培養(yǎng)箱中進(jìn)行培養(yǎng)。實(shí)驗(yàn)分組:實(shí)驗(yàn)組(FOXC1 Overexpress組、FOXC1shRNA組),載體對照組(Overexpress Control組、shRNA Control組)及空白對照組(Control組)。2實(shí)驗(yàn)方法在上皮性卵巢癌SKOV3細(xì)胞中分別感染慢病毒FOXC1 shRNA、FOXC1慢病毒載體過表達(dá)質(zhì)粒,構(gòu)建穩(wěn)定細(xì)胞株后分別在mRNA和蛋白水平進(jìn)行驗(yàn)證。應(yīng)用CCK-8實(shí)驗(yàn)、Transwell實(shí)驗(yàn),分別觀察SKOV3細(xì)胞的增殖、侵襲能力的變化;通過qRT-PCR法檢測比較各組MCM2、MMP9的mRNA水平的變化;采用Western blot法檢測各組MCM2、MMP9、NF-κB p65、NF-κB p-p65的蛋白表達(dá)水平情況。3統(tǒng)計(jì)學(xué)處理采用SPSS21.0軟件進(jìn)行統(tǒng)計(jì)學(xué)分析。實(shí)驗(yàn)數(shù)據(jù)均以x±s表示,各組間數(shù)據(jù)的比較,正態(tài)分布的采用單因素方差分析和獨(dú)立樣本的t檢驗(yàn)。偏態(tài)分布的計(jì)量資料各組間比較采用Kruskal-Wallis檢驗(yàn)和秩和檢驗(yàn)。檢驗(yàn)水準(zhǔn)α=0.05。結(jié)果1穩(wěn)定株構(gòu)建及鑒定情況經(jīng)qRT-PCR篩選鑒定3條FOXC1干擾序列,FOXC1 shRNA1抑制效果最佳,選取該序列,通過感染及嘌呤霉素篩選后,應(yīng)用Western blot驗(yàn)證,結(jié)果顯示實(shí)驗(yàn)組FOXC1蛋白表達(dá)量較載體對照組及空白對照組明顯減少,差異具有統(tǒng)計(jì)學(xué)意義(P0.05)。在SKOV3細(xì)胞中成功構(gòu)建了FOXC1干擾穩(wěn)定株。應(yīng)用FOXC1慢病毒載體過表達(dá)質(zhì)粒成功感染SKOV3細(xì)胞,經(jīng)嘌呤霉素篩選,通過qRT-PCR和Western blot驗(yàn)證,實(shí)驗(yàn)組中FOXC1在mRNA的表達(dá)水平及蛋白水平均明顯高于2組對照組,且差異有統(tǒng)計(jì)學(xué)意義(P0.05)。成功獲得穩(wěn)定過表達(dá)FOXC1的SKOV3細(xì)胞株。2 FOXC1對SKOV3細(xì)胞增殖、侵襲能力的影響情況2.1 FOXC1對各組SKOV3細(xì)胞增殖的影響情況通過CCK-8檢測SKOV3細(xì)胞增殖能力結(jié)果顯示:0h各組細(xì)胞吸光度值無差異。下調(diào)FOXC1組SKOV3細(xì)胞的增殖活性高于2組對照組,尤其48h后增殖活性明顯增高,經(jīng)統(tǒng)計(jì)學(xué)分析,差異均有統(tǒng)計(jì)學(xué)意義(P0.05)。當(dāng)上調(diào)FOXC1后,SKOV3細(xì)胞的增殖活性較2組對照組降低,且差異具有統(tǒng)計(jì)學(xué)意義(P0.05)。2.2 FOXC1對各組SKOV3細(xì)胞侵襲能力的影響情況各組SKOV3細(xì)胞種板24h后,在光鏡下計(jì)數(shù)各組細(xì)胞穿膜數(shù),下調(diào)FOXC1組穿膜數(shù)較2組對照組相比明顯增多,差異具有統(tǒng)計(jì)學(xué)意義(P0.05)。上調(diào)FOXC1組與2組對照組相比細(xì)胞穿膜數(shù)明顯減少,且差異具有統(tǒng)計(jì)學(xué)意義(P0.001)。3 FOXC1各組細(xì)胞MMP9、MCM2的mRNA和蛋白的表達(dá)情況3.1干擾FOXC1后SKOV3細(xì)胞中MMP9、MCM2的mRNA及蛋白水平變化情況經(jīng)qRT-PCR檢測,結(jié)果顯示:下調(diào)FOXC1組的SKOV3細(xì)胞與2組對照組相比,MMP9、MCM2的mRNA表達(dá)量明顯增加,差異有統(tǒng)計(jì)學(xué)意義(P0.05)。應(yīng)用Western blot檢測顯示:下調(diào)FOXC1組的SKOV3細(xì)胞與2組對照組相比,MCM2的蛋白水平表達(dá)量增加,差異具有統(tǒng)計(jì)學(xué)意義(P0.05)。3.2過表達(dá)FOXC1后SKOV3細(xì)胞中MMP9、MCM2的mRNA及蛋白水平變化情況經(jīng)qRT-PCR檢測,上調(diào)FOXC1組的SKOV3細(xì)胞較2組對照組相比MMP9、MCM2的mRNA表達(dá)量減少,差異均有統(tǒng)計(jì)學(xué)意義(P0.05)。經(jīng)Western blot檢測,結(jié)果顯示:上調(diào)FOXC1組的SKOV3細(xì)胞中MMP9、MCM2的蛋白表達(dá)量較2組對照組相比明顯降低,差異有統(tǒng)計(jì)學(xué)意義(P0.05)。4 FOXC1各組細(xì)胞p65、p-p65的蛋白表達(dá)情況4.1干擾FOXC1后SKOV3細(xì)胞中p65、p-p65蛋白水平變化情況經(jīng)Western blot檢測,結(jié)果顯示,下調(diào)FOXC1組的SKOV3細(xì)胞中p65的蛋白表達(dá)量較2組對照組相比有所增多,但差異無統(tǒng)計(jì)學(xué)意義(P0.05)。下調(diào)FOXC1組中p-p65的蛋白表達(dá)量較2組對照組明顯增加,差異具有統(tǒng)計(jì)學(xué)意義(P0.05)。4.2過表達(dá)FOXC1后SKOV3細(xì)胞中p65、p-p65蛋白水平變化情況經(jīng)Western blot檢測,結(jié)果顯示:SKOV3細(xì)胞中上調(diào)FOXC1組p65的蛋白表達(dá)量較2組對照組降低,但差異無統(tǒng)計(jì)學(xué)意義(P0.05)。上調(diào)FOXC1組p-p65的蛋白表達(dá)量較2組對照組明顯降低,差異具有統(tǒng)計(jì)學(xué)意義(P0.05)。結(jié)論分別成功構(gòu)建了FOXC1干擾及過表達(dá)SKOV3細(xì)胞穩(wěn)定株。在上皮性卵巢癌SKOV3細(xì)胞中,下調(diào)FOXC1能夠促進(jìn)腫瘤細(xì)胞的增殖侵襲能力,上調(diào)FOX C1能夠抑制腫瘤細(xì)胞的增殖侵襲能力。FOXC1可能是通過激活NF-κB信號(hào)傳導(dǎo)通路實(shí)現(xiàn)對上皮性卵巢腫瘤細(xì)胞生物學(xué)功能的調(diào)控,在一定程度上參與卵巢癌的發(fā)生發(fā)展。
[Abstract]:Epithelial ovarian cancer (EOC) is one of the most common malignant tumor of reproductive system in women. At present, the mortality rate of EOC in developed countries is the first in gynecologic tumors. For malignant tumors, tumor cells are most threatened by the invasion of tumor cells in addition to active proliferation. At present, some target experiments and exploration of some genes affecting the biological function of tumor cells have been carried out at home and abroad. Intervention on its targets also promotes the development of tumor therapy and provides more reference for targeted therapy. For EOC, it is clear whether the abnormal expression of some genes can be expressed. The changes in biological behavior of epithelial ovarian cancer cells and further study of its regulatory mechanism are of great significance for the in-depth study of the etiological mechanism of EOC and long-term targeting therapy. The transcription factor FOXC1 (forkhead box C1) is a member of the forkhead transcription factor gene family (FOX family), which combines the binding domain of the DNA binding domain of the forked region of the DNA. In addition to participating in biological processes such as cell or organ differentiation and metabolism, the gene fragment, in addition to the biological processes such as cell or organ differentiation and metabolism, has shown that FOXC1 can also regulate the signal transduction pathways of various tumor cells, such as NF- kappa B, Wnt/ beta -Catenin, and so on. These cell signaling pathways are closely related to cell proliferation, invasion, migration, and apoptosis, thus, FOXC1, FOXC1 The micro chromosome maintenance protein 2 (minichromosomemai n-tenance proteins 2, MCM2) is a new indicator of cell proliferation activity, which is more specific and sensitive when it is used to reflect cell proliferation. Matrix metal egg white enzyme 9 (matrix metallopro teinase, MMP9) is used as a cell. The main protein hydrolase degrading of the external matrix is closely related to the invasion of tumor cells and the degradation of extracellular matrix related to metastasis. Therefore, MCM2, MMP9 changes are often detected at the molecular level when the proliferation and invasion of tumor cells in EOC are at the molecular level. In recent years, it has been reported that FOXC1 is benign in ovarian tumor tissues. The expression rate of epithelial ovarian tumor was 84%. The expression rate in epithelial ovarian cancer was 37.5%. in the previous study group. The expression of FOXC1 mRNA in epithelial ovarian cancer tissue was less than that of borderline ovarian epithelial tumor tissue and benign ovarian epithelial tumor tissue, and the mRNA expression of FOXC1 in the tissues and lymph nodes The deletion of FOXC1 expression in the tissue may be of great significance to the development of epithelial ovarian cancer. However, it is not clear whether the abnormal expression of FOXC1 can cause the biological function of epithelial ovarian cancer cells and how to participate in the development of EOC. In addition, a large number of studies have shown that the NF- kappa B signal transduction pathway in EOC has been shown. The road can be involved in the regulation of MCM2 and MMP9. Therefore, this topic will discuss whether FOXC1 is involved in the malignant biological behavior of epithelial ovarian cancer cells and whether it can be regulated by the NF- kappa B signaling pathway. The purpose of this study is to construct FOXC1 overexpression and interfere with stable cells in the SKOV3 of epithelial ovarian cancer cells by the way of lentivirus infection. After the study, the effects of FOXC1 on the proliferation and invasion of SKOV3 cells were investigated, and whether FOXC1 could be regulated by activating NF- kappa B signaling pathway and analyzing the role of abnormal FOXC1 expression in EOC. Materials and methods 1 research subjects and groups selected human epithelial ovarian cancer cell line SKOV3 cells (Fourth Military Medical doctors) Professor Zhao Ya, Professor Kui Zeng of the Institute of pathogenic biology of the University, used the RPMI-1640 complete culture medium to place cells in the incubator of 37 C and 5%CO2. Experimental groups: experimental group (group FOXC1 Overexpress, FOXC1shRNA group), carrier control group (Overexpress Control group, shRNA Control group) and.2 control group (Control group).2 experiment method in The SKOV3 cells of epithelial ovarian cancer were infected with lentivirus FOXC1 shRNA, FOXC1 lentivirus vector overexpressed plasmids, and the stable cell lines were constructed to verify the level of mRNA and protein respectively. CCK-8 experiment and Transwell experiment were used to observe the proliferation of SKOV3 cells and the changes of invasion ability. MCM2, MMP9 of each group were detected by qRT-PCR method. Western blot method was used to detect the protein expression level of MCM2, MMP9, NF- kappa B p65 and NF- kappa B p-p65 in each group. The statistical analysis of.3 statistical processing was carried out by mRNA software. The experimental data were compared with each other, and the normal distribution was analyzed by single factor analysis of variance and independent sample test. Kruskal-Wallis test and rank sum test were used in the measurement data of partial distribution. Test level alpha =0.05. results 1 stable strain construction and identification of 3 FOXC1 interference sequences by qRT-PCR screening, FOXC1 shRNA1 inhibition effect is the best, select the sequence, through infection and purinomycin screening, Western blot validation, knot The results showed that the expression of FOXC1 protein in the experimental group was significantly lower than that in the vector control group and the blank control group. The difference was statistically significant (P0.05). The FOXC1 interference stable strain was successfully constructed in the SKOV3 cells. The SKOV3 cells were successfully infected with the FOXC1 lentivirus vector overexpression plasmid, and it was screened by purinicamycin and verified by qRT-PCR and Western blot. In the experimental group, the expression level and protein level of FOXC1 in mRNA were significantly higher than those in the 2 groups, and the difference was statistically significant (P0.05). The effect of.2 FOXC1 on the proliferation of SKOV3 cells and the invasiveness of SKOV3 cells were successfully obtained. 2.1 FOXC1 on the proliferation of SKOV3 cells in each group by CCK-8 detection of SKOV3 thin. The results of cell proliferation showed that the cell absorbency of 0h groups was not different. The proliferation activity of SKOV3 cells in the FOXC1 group was higher than that of the 2 groups, especially after 48h, the proliferation activity was significantly higher, and the difference was statistically significant (P0.05). The proliferation activity of SKOV3 cells was lower than that of the control group of the 2 groups after the up regulation of FOXC1, and the difference was found. The effect of statistical significance (P0.05).2.2 FOXC1 on the invasive ability of SKOV3 cells in each group, after 24h of SKOV3 cells, the number of membranes in each group was counted under light microscope, and the number of membrane in the FOXC1 group was significantly increased compared with the control group in the 2 groups, the difference was statistically significant (P0.05). The number of cell transmissions compared with the 2 group was significantly higher than that of the control group. The difference was statistically significant (P0.001).3 FOXC1 cells MMP9, mRNA and protein expression of MCM2 3.1 interfered MMP9 in SKOV3 cells after FOXC1, mRNA and protein levels of MCM2 were detected by qRT-PCR detection. The difference was statistically significant (P0.05). The application of Western blot detection showed that the protein level expression of MCM2 was increased in the SKOV3 cells of the down-regulation group compared with the 2 groups, and the difference was statistically significant (P0.05).3.2 overexpressed FOXC1 in SKOV3 cells. 3 cells were compared with the control group of the 2 group MMP9, and the expression of mRNA in MCM2 decreased, the difference was statistically significant (P0.05). The results showed that the expression of MMP9 in SKOV3 cells of the FOXC1 group was higher than that of the control group of the 2 groups. The difference was statistically significant compared with the control group, and the difference was statistically significant (P0.05). The changes of p65 and p-p65 protein in SKOV3 cells after FOXC1 interference after FOXC1 were detected by Western blot. The results showed that the protein expression of p65 in SKOV3 cells of the down regulated FOXC1 group increased compared with those of the control group, but the difference was not statistically significant (P0.05). The protein expression of p-p65 in the FOXC1 group was significantly higher than that of the control group of 2 groups. The variation of p65 and p-p65 protein levels in SKOV3 cells after FOXC1 was statistically significant (P0.05).4.2 was detected by Western blot. The results showed that the protein expression of p65 in the up regulation of FOXC1 group in SKOV3 cells was lower than that of the control group, but the difference was not statistically significant (P0.05). The amount of protein expression in the up regulation group was compared with the control group of the 2 group. The difference was statistically significant (P0.05). Conclusion FOXC1 interference and overexpression of SKOV3 cell stable strain were successfully constructed. In the SKOV3 cells of epithelial ovarian cancer, the down regulation of FOXC1 could promote the proliferation and invasion of tumor cells, and the up regulation of FOX C1 to inhibit the proliferation and invasion of tumor cells may be by activating NF- kappa B. Signal transduction pathway can regulate the biological function of epithelial ovarian tumor cells and participate in the development of ovarian cancer to some extent.
【學(xué)位授予單位】：鄭州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R737.31

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3 王常玉,顧美皎,王世宣,馬丁;三種化療方案治療晚期上皮性卵巢癌的療效比較[J];實(shí)用婦產(chǎn)科雜志;2002年04期

4 李雙弟,萬小平,楊兆瑞,胡宏慧,席曉薇,徐先明;血管內(nèi)皮生長因子及其受體與上皮性卵巢癌發(fā)展[J];腫瘤;2003年03期

5 袁令芹;上皮性卵巢癌226例臨床病理分析[J];腫瘤防治雜志;2003年08期

6 周曉亮 ,陳軼群;血小板計(jì)數(shù)與晚期上皮性卵巢癌患者二探結(jié)果及疾病進(jìn)展的關(guān)系[J];國外醫(yī)學(xué).婦產(chǎn)科學(xué)分冊;2004年06期

7 趙玲軍;術(shù)中即時(shí)化療在上皮性卵巢癌治療中的應(yīng)用[J];中國基層醫(yī)藥;2005年10期

8 Hopkins L.;Fung Kee Fung M.;王穎;;上皮性卵巢癌進(jìn)展期輔助和補(bǔ)救化療過程中患者生活質(zhì)量評估[J];世界核心醫(yī)學(xué)期刊文摘(婦產(chǎn)科學(xué)分冊);2005年11期

9 王鑫;呂杰強(qiáng);朱雪瓊;;胰島素樣生長因子系統(tǒng)在上皮性卵巢癌中的研究進(jìn)展[J];國外醫(yī)學(xué).婦產(chǎn)科學(xué)分冊;2006年04期

10 李海玲;任慕蘭;錢惠勤;;上皮性卵巢癌血管內(nèi)皮生長因子表達(dá)及微血管密度[J];江蘇醫(yī)藥;2007年01期

相關(guān)會(huì)議論文 前10條

1 程蓓;郭軼男;呂衛(wèi)國;萬小云;陳亞俠;謝幸;;上皮性卵巢癌患者保留生育功能13例分析[A];第四屆長三角婦產(chǎn)科學(xué)術(shù)論壇暨浙江省2009年婦產(chǎn)科學(xué)術(shù)年會(huì)論文匯編[C];2009年

2 許紅;;Ⅲ期上皮性卵巢癌的治療與預(yù)后分析[A];中國抗癌協(xié)會(huì)婦科腫瘤專業(yè)委員會(huì)第六次全國學(xué)術(shù)會(huì)議論文匯編[C];2001年

3 周慧梅;黃惠芳;潘凌亞;沈鏗;吳鳴;楊佳欣;;血清CA125值的變化對判斷上皮性卵巢癌預(yù)后的臨床價(jià)值[A];中華醫(yī)學(xué)會(huì)第九次全國婦科腫瘤學(xué)術(shù)會(huì)議論文匯編[C];2006年

4 葉海燕;陳建國;徐嘉文;陳志紅;;has-miRNA let-7a在上皮性卵巢癌中的表達(dá)及其臨床意義[A];中華醫(yī)學(xué)會(huì)第十次全國婦產(chǎn)科學(xué)術(shù)會(huì)議婦科腫瘤會(huì)場（婦科腫瘤學(xué)組、婦科病理學(xué)組）論文匯編[C];2012年

5 謝敏;李藝;崔恒;;復(fù)發(fā)性上皮性卵巢癌的手術(shù)治療[A];中華醫(yī)學(xué)會(huì)第十次全國婦產(chǎn)科學(xué)術(shù)會(huì)議婦科腫瘤會(huì)場（婦科腫瘤學(xué)組、婦科病理學(xué)組）論文匯編[C];2012年

6 許紅;王中彌;左馨;;Ⅲ期上皮性卵巢癌58例臨床分析[A];中國抗癌協(xié)會(huì)婦科腫瘤專業(yè)委員會(huì)第七次全國學(xué)術(shù)會(huì)議論文匯編[C];2003年

7 郄明蓉;楊小蕓;張崇淑;;28例Ⅳ期及復(fù)發(fā)上皮性卵巢癌的治療選擇與預(yù)后分析[A];中國抗癌協(xié)會(huì)婦科腫瘤專業(yè)委員會(huì)第七次全國學(xué)術(shù)會(huì)議論文匯編[C];2003年

8 郄明蓉;鄭艾;楊小蕓;張崇淑;;28例Ⅳ期及復(fù)發(fā)上皮性卵巢癌的治療選擇與預(yù)后分析[A];第八次全國婦產(chǎn)科學(xué)學(xué)術(shù)會(huì)議論文匯編[C];2004年

9 郄明蓉;張崇淑;鄭艾;楊小蕓;;28例Ⅳ期及復(fù)發(fā)上皮性卵巢癌的治療選擇與預(yù)后分析[A];第八次全國婦產(chǎn)科學(xué)學(xué)術(shù)會(huì)議論文匯編[C];2004年

10 彭素蓉;王金華;陳小祥;;上皮性卵巢癌系統(tǒng)性腹膜后淋巴結(jié)切除術(shù)及臨床意義——附102例報(bào)告[A];江蘇省抗癌協(xié)會(huì)婦科腫瘤專業(yè)委員會(huì)第四次腫瘤學(xué)術(shù)研討會(huì)暨無錫市婦產(chǎn)科年會(huì)論文匯編[C];2005年

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1 王宇;FoxM1剪接異構(gòu)體在上皮性卵巢癌中的表達(dá)及相關(guān)功能研究[D];第四軍醫(yī)大學(xué);2013年

2 金佟;CA125/T ELISA法用于CA125升高的良惡性鑒別及其臨床應(yīng)用[D];復(fù)旦大學(xué);2014年

3 嚴(yán)春曉;水通道蛋白亞型AQP5及AQP9在上皮性卵巢癌細(xì)胞增殖與遷移中的功能研究[D];浙江大學(xué);2015年

4 黃宇婷;基于定量多色熒光原位雜交技術(shù)的卵巢癌多基因拷貝數(shù)異常的研究[D];天津醫(yī)科大學(xué);2015年

5 冷若冰;Rac1在上皮性卵巢癌上皮間質(zhì)轉(zhuǎn)化中的作用及機(jī)制的初步研究[D];重慶醫(yī)科大學(xué);2015年

6 梁軍;腫瘤干細(xì)胞樣細(xì)胞在上皮性卵巢癌血管生成擬態(tài)中作用的研究[D];河北醫(yī)科大學(xué);2016年

7 胡建國;MARCH7促進(jìn)上皮性卵巢癌惡性進(jìn)展及機(jī)制的研究[D];重慶醫(yī)科大學(xué);2016年

8 陸萌;FKBP14對上皮性卵巢癌細(xì)胞增殖和遷移能力的影響[D];南京醫(yī)科大學(xué);2016年

9 牛海英;PPA1通過促進(jìn)上皮—間質(zhì)轉(zhuǎn)化影響上皮性卵巢癌的轉(zhuǎn)移[D];天津醫(yī)科大學(xué);2016年

10 郭立麗;靶向谷氨酰胺代謝逆轉(zhuǎn)上皮性卵巢癌鉑類及m-TOR抑制劑耐藥的機(jī)制研究[D];華中科技大學(xué);2016年

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1 楊一鳴;血小板增多癥在上皮性卵巢癌中的診斷意義及預(yù)后評估[D];大連醫(yī)科大學(xué);2013年

2 邱章燦;Ⅲc期上皮性卵巢癌預(yù)后危險(xiǎn)因素與無進(jìn)展生存期關(guān)系探討[D];廣西醫(yī)科大學(xué);2015年

3 秦凱云;上皮性卵巢癌患者血漿化療耐藥相關(guān)蛋白質(zhì)分析及臨床意義[D];河北醫(yī)科大學(xué);2015年

4 董杰;上皮性卵巢癌中TGF-β1的表達(dá)與耐藥相關(guān)基因的關(guān)系[D];河北醫(yī)科大學(xué);2015年

5 齊新穎;LRP、GST-π表達(dá)與上皮性卵巢癌鉑類化療耐藥及預(yù)后的關(guān)系[D];河北醫(yī)科大學(xué);2015年

6 田美玲;ERCC1基因多態(tài)性及蛋白表達(dá)與上皮性卵巢癌鉑類化療敏感性及預(yù)后關(guān)系的研究[D];河北醫(yī)科大學(xué);2015年

7 賈亞靜;子宮內(nèi)膜癌、上皮性卵巢癌、早期宮頸癌預(yù)后因素分析[D];河北醫(yī)科大學(xué);2015年

8 楊晗;77例上皮性卵巢癌預(yù)后相關(guān)因素分析[D];河北醫(yī)科大學(xué);2015年

9 張根豪;阿司匹林對人上皮性卵巢癌SKOV3細(xì)胞SOX7表達(dá)和Wnt/β-catenin信號(hào)通路的影響[D];鄭州大學(xué);2015年

10 肖喜云;HER2蛋白在上皮性卵巢癌中的表達(dá)及曲妥珠單抗對卵巢癌SKOV3細(xì)胞的影響[D];河北醫(yī)科大學(xué);2015年

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