本文選題：鼻咽癌 + EMT　； 參考：《南方醫(yī)科大學(xué)》2010年碩士論文

【摘要】： 研究背景和目的 鼻咽癌(NasoPharyngeal Carcinoma,NPC)是一種主要發(fā)生在我國南方地區(qū)的鼻咽部惡性腫瘤,由于NPC發(fā)生的部位比較隱蔽,早期癥狀常不明顯而容易被忽略,因此確診的患者60%以上都是中、晚期病例,常伴有轉(zhuǎn)移發(fā)生。尋找鼻咽癌發(fā)生發(fā)展及轉(zhuǎn)移的機(jī)制,是我們當(dāng)前研究的主要方向。 腫瘤的形成和侵襲轉(zhuǎn)移是一個(gè)多步驟、多階段、多因子參與的復(fù)雜而又連續(xù)的過程,涉及了一些關(guān)鍵的瘤基因和抑瘤基因。在本研究中,我們從公共基因芯片數(shù)據(jù)庫GEO(Gene expression omnibus)中尋找并下載鼻咽癌的相關(guān)基因芯片數(shù)據(jù),并使用Genclip軟件對其進(jìn)行分析,找到鼻咽癌公共基因芯片數(shù)據(jù)中與上皮間充質(zhì)轉(zhuǎn)化(Epithelial——mesenchymal transition, EMT)相關(guān)的基因35個(gè),其中包括本課題所研究的ID2,它在鼻咽癌組織和細(xì)胞中表達(dá)明顯上調(diào),提示該基因可能正向參與促進(jìn)了鼻咽癌的發(fā)病過程。 ID蛋白家族成員共有四個(gè)ID1, ID2, ID3, ID4,它們最初被發(fā)現(xiàn)在負(fù)性調(diào)節(jié)細(xì)胞分化方面起了重要作用,后來越來越多的研究證明它們在調(diào)節(jié)譜系定型,基因表達(dá),細(xì)胞命運(yùn),細(xì)胞增殖,以及在神經(jīng)發(fā)生,淋巴組織形成,新生血管形成中細(xì)胞的分化時(shí)間也起了關(guān)鍵作用。ID蛋白家族成員被發(fā)現(xiàn)在很多腫瘤中過表達(dá),比如大腸癌,膠質(zhì)母細(xì)胞瘤,髓母細(xì)胞瘤,神經(jīng)細(xì)胞瘤,胰腺癌,甲狀腺癌,鱗狀細(xì)胞癌,前列腺癌,乳腺癌,子宮內(nèi)膜癌,宮頸癌和黑色素瘤等。 為了闡明ID2基因在鼻咽癌發(fā)病中的作用,我們利用RNAi技術(shù)高效、特異的靶向沉默機(jī)制干擾鼻咽癌細(xì)胞SUNE1中ID2表達(dá),建立穩(wěn)定靶向干擾ID2表達(dá)的siRNA鼻咽癌細(xì)胞,以觀察干擾ID2后鼻咽癌細(xì)胞生物學(xué)功能改變,并探尋其與EMT的關(guān)系,為鼻咽癌的發(fā)病機(jī)制和治療提供新的思路。 方法 1.鼻咽癌EMT相關(guān)基因的篩選 從公共基因芯片數(shù)據(jù)庫GEO (Gene expression omnibus)中尋找并下載鼻咽癌的相關(guān)基因芯片數(shù)據(jù),并使用Genclip軟件對下載的數(shù)據(jù)進(jìn)行分析,尋找鼻咽癌公共基因芯片數(shù)據(jù)中與上皮間充質(zhì)轉(zhuǎn)化(Epithelial——mesenchymal transition, EMT)相關(guān)的基因；并用生物信息學(xué)方法對篩選出來的基因進(jìn)一步分析。 2. ID2在鼻咽癌中的表達(dá)特性鑒定 免疫組化SP法從蛋白水平檢測ID2在非癌鼻咽組織和鼻咽癌中的表達(dá)水平,初步探討ID2在組織水平與鼻咽癌發(fā)生發(fā)展的關(guān)系。 熒光定量PCR法從mRNA水平檢測ID2在永生化鼻咽上皮細(xì)胞NP69和鼻咽癌細(xì)胞SUNE1、5-8F、6-10B、CNE2、HNE1、CNE1、C666-1、HONE1中的表達(dá)水平,初步探討ID2在永生化鼻咽上皮細(xì)胞和鼻咽癌細(xì)胞中的表達(dá)差異,并找到高表達(dá)ID2的鼻咽癌細(xì)胞作為下一步干擾對象。 3. ID2表達(dá)沉默對鼻咽癌細(xì)胞生物學(xué)影響及部分與EMT相關(guān)基因表達(dá)水平的檢測 構(gòu)建ID2慢病毒干擾載體,包裝成成熟的慢病毒顆粒感染高表達(dá)ID2的SUNE1細(xì)胞,有限稀釋法篩選出穩(wěn)定的陽性和空載克隆,熒光定量PCR檢測各干擾克隆細(xì)胞中ID2干擾效率,篩選干擾效率最高的細(xì)胞克隆并將該細(xì)胞克隆作為實(shí)驗(yàn)對象被進(jìn)一步研究。MTT法、平板克隆形成實(shí)驗(yàn)檢測ID2沉默后對細(xì)胞體外增殖的影響；Transwell檢測ID2沉默后細(xì)胞遷移運(yùn)動(dòng)能力的改變。 熒光定量PCR法檢測與ID2相關(guān)的TGF-beta以及與EMT相關(guān)的轉(zhuǎn)錄因子Slug, SIP1, Twist, Snail,上皮標(biāo)志物E-cadherin,間質(zhì)標(biāo)志物Vimentin在四株細(xì)胞株SUNE1/plv-ID2-1, SUNE1/plv-ID2-2, SUNE1/plv, SUNE1中mRNA的表達(dá)水平。 4.統(tǒng)計(jì)學(xué)方法 采用SPSS 13.0統(tǒng)計(jì)軟件包進(jìn)行統(tǒng)計(jì)學(xué)處理,第二章中因免疫組化各指標(biāo)均為等級資料,故其組間的比較采用非參數(shù)秩和檢驗(yàn),ID2的表達(dá)在非癌鼻咽組織和鼻咽癌比較采用Mann-Whitney U檢驗(yàn),ID2的表達(dá)與鼻咽癌臨床分期的關(guān)系檢驗(yàn)用Kruskal Wallis Test,檢驗(yàn)水準(zhǔn)均取雙側(cè)α=0.05；熒光定量PCR法檢測鼻咽癌細(xì)胞株ID2表達(dá)特性結(jié)果比較采用單因素方差分析,多重比較采用SNK檢驗(yàn)。第三章中熒光定量PCR、運(yùn)動(dòng)、平板克隆形成實(shí)驗(yàn)采用單因素方差分析；MTT采用析因設(shè)計(jì)的方差分析；多重比較采用SNK或LSD檢驗(yàn)。 結(jié)果 1.鼻咽癌EMT相關(guān)基因的篩選 在公共的鼻咽癌芯片數(shù)據(jù)中找到35個(gè)與EMT相關(guān)的差異表達(dá)基因,而且這些基因功能大致與細(xì)胞組分、細(xì)胞粘附、通信、信號(hào)轉(zhuǎn)導(dǎo)、分化、運(yùn)動(dòng)、遷移以及細(xì)胞表面受體相關(guān)的信號(hào)轉(zhuǎn)導(dǎo)等有關(guān),這些功能往往都被認(rèn)為與腫瘤的侵襲和轉(zhuǎn)移有關(guān)。 2.ID2在鼻咽癌中的表達(dá)特性鑒定 1、共收集鼻咽炎組18例、鼻咽癌組52例臨床標(biāo)本。SP免疫組化結(jié)果表明,ID2表達(dá)主要定位在細(xì)胞核和細(xì)胞漿。ID2在鼻咽癌和非癌鼻咽組織中的表達(dá)具有統(tǒng)計(jì)學(xué)差異(Z=-5.553, P=0.000), ID2的表達(dá)情況與臨床分期沒有統(tǒng)計(jì)學(xué)差異(χ2=0.963,P=0.810) 2、熒光定量PCR法檢測ID2在永生化鼻咽上皮細(xì)胞NP69和鼻咽癌細(xì)胞SUNE1、5-8F、6-10B、CNE2、HNE1、CNE1、C666-1、HONE1 mRNA水平表達(dá)具有統(tǒng)計(jì)學(xué)差異(F=2.980, P=0.002), SUNE1表達(dá)最高,表達(dá)量為NP69 ID2表達(dá)量的78倍,作為下一步干擾對象。 3.ID2表達(dá)沉默對鼻咽癌細(xì)胞生物學(xué)影響及部分與EMT相關(guān)基因表達(dá)水平的檢測 1、構(gòu)建ID2慢病毒干擾載體,包裝慢病毒后感染SUNE1細(xì)胞,有限稀釋法篩選GFP+單克隆,熒光定量PCR檢測各克隆的ID2表達(dá)情況,篩選出干擾效率最高的2個(gè)單克隆為下一步實(shí)驗(yàn)的研究對象。陽性克隆的干擾效率與SUNE1和陰性對照細(xì)胞表達(dá)具有統(tǒng)計(jì)學(xué)差異(F=48.693,P=0.000),同時(shí)檢測ID2在陰性對照中的表達(dá)相對于SUNE1強(qiáng)度較一致(0.933±0.006)。陽性干擾克隆命名為SUNE1/plv-ID2-1和SUNE1/plv-ID2-2,陰性對照克隆為SUNE1/plv。 2、MTT法檢測細(xì)胞增殖情況,與陰性對照SUNE1/Plv和SUNE1細(xì)胞相比,干擾克隆細(xì)胞SUNE1/plv-ID2-1和SUNE1/plv-ID2-2的增殖速度明顯減慢并且呈時(shí)間依賴關(guān)系,具有統(tǒng)計(jì)學(xué)差異(F=3.301,P=0.000)；平板克隆形成實(shí)驗(yàn)顯示四組細(xì)胞的克隆形成率具有統(tǒng)計(jì)學(xué)差異(F=253.434,P=0.000), SUNE1/plv-ID2細(xì)胞克隆形成減少,SUNE1和陰性對照組不具有統(tǒng)計(jì)學(xué)差異(P=0.866)。綜合表明ID2表達(dá)干擾后,SUNE1細(xì)胞體外生長被顯著抑制。 3、Transwell小室檢測結(jié)果顯示,與SUNE1和SUNE1/plv細(xì)胞相比,SUNE1 /plv-ID2細(xì)胞穿過聚碳酸酯膜的細(xì)胞數(shù)沒有明顯變化,差異不具有顯著性(F=0.624,P=0.610)。 4、熒光定量PCR法檢測結(jié)果顯示TGF-beta, E-cadherin, Slug, SIP1, Vimentin在4組細(xì)胞間的mRNA表達(dá)不具有統(tǒng)計(jì)學(xué)差異(F=0.405,P=0.754；F=0.571,P=0.650; F=0.541,P=0.668; F=0.456,P=0.721; F=1.058,P=0.419),而Twist, Snail在4組細(xì)胞間的表達(dá)具有統(tǒng)計(jì)學(xué)差異(F=94.627,P=0.000;F=155.295,P=0.000)。 結(jié)論 1、生物信息學(xué)方法篩選出35個(gè)與鼻咽癌EMT相關(guān)的基因 2、免疫組化SP法證實(shí)ID2的表達(dá)與鼻咽癌的發(fā)生發(fā)展有關(guān)系。 3、熒光定量PCR法檢測ID2在永生化鼻咽上皮細(xì)胞NP69和鼻咽癌細(xì)胞SUNE1、5-8F、6-10B、CNE2、HNE1、CNE1、C666-1、HONE1中的表達(dá)具有統(tǒng)計(jì)學(xué)差異,SUNE1表達(dá)最高。 4、ID2干擾后部分細(xì)胞體外生物學(xué)功能發(fā)生改變。 5、ID2干擾后部分與EMT相關(guān)的基因1nRNA表達(dá)水平出現(xiàn)改變。
[Abstract]:Background and purpose of research
NasoPharyngeal Carcinoma (NPC) is a malignant tumor of nasopharynx, which mainly occurs in the southern part of China. Because the location of NPC is more concealed, the early symptoms are often not obvious and easy to be ignored. Therefore, more than 60% of the confirmed patients are in the middle and late cases, often accompanied by metastasis. The mechanism is the main direction of our current research.
The formation and invasion of tumor is a complex and continuous process involving multiple steps, multistages and multiple factors. It involves some key tumor genes and tumor suppressor genes. In this study, we find and download the related gene chip data of nasopharyngeal carcinoma from the public gene chip database GEO (Gene Expression Omnibus) and use G The enclip software analyzed it to find 35 genes related to Epithelial - mesenchymal transition (EMT) in the common gene chip data of nasopharyngeal carcinoma, including ID2, which was studied in this subject. It was expressed clearly in the tissues and cells of nasopharyngeal carcinoma, suggesting that the gene may be positively involved in promoting the nose. The process of the cancer of the pharynx.
The ID family members have four ID1, ID2, ID3, ID4. They were initially found to play an important role in the differentiation of negative regulatory cells. More and more studies have shown that they are regulating lineage stereotypes, gene expression, cell fate, cell proliferation, and cell differentiation in the generation of the divine, lymphatic tissue, and neovascularization. Time also plays a key role in the.ID protein family that has been found to be overexpressed in many tumors, such as colorectal cancer, glioblastoma, medulloblastoma, neurocytoma, pancreatic cancer, thyroid cancer, squamous cell carcinoma, prostate cancer, breast cancer, endometrial cancer, cervical cancer and melanoma.
In order to elucidate the role of ID2 gene in the pathogenesis of nasopharyngeal carcinoma, we use RNAi technology to interfere with the expression of ID2 in nasopharyngeal carcinoma cell SUNE1 by efficient and specific targeting silencing mechanism, to establish a siRNA nasopharyngeal carcinoma cell with stable target interference ID2 expression, in order to observe the biological function changes of the nasopharyngeal carcinoma cells after interference and explore the relationship between the nasopharyngeal carcinoma cells and the nasopharyngeal carcinoma cells, and to make the nasopharynx to be nasopharynx. The pathogenesis and treatment of cancer provide a new way of thinking.
Method
Screening of EMT related genes in 1. nasopharyngeal carcinoma
The related gene chip data of nasopharyngeal carcinoma were searched and downloaded from the public gene chip database GEO (Gene Expression Omnibus), and the data were analyzed by Genclip software to find the genes associated with the epithelial mesenchymal transition (Epithelial -- mesenchymal transition, EMT) in the common gene chip data of nasopharyngeal carcinoma. The selected genes were further analyzed by bioinformatics.
Identification of expression characteristics of 2. ID2 in nasopharyngeal carcinoma
The expression level of ID2 in noncancerous nasopharyngeal tissue and nasopharyngeal carcinoma was detected by immunohistochemical SP method, and the relationship between the level of ID2 and the development of nasopharyngeal carcinoma was preliminarily discussed.
The expression level of ID2 in the immortalized nasopharyngeal epithelial cells NP69 and nasopharyngeal carcinoma cells SUNE1,5-8F, 6-10B, CNE2, HNE1, CNE1, C666-1, HONE1 in the immortalized nasopharyngeal epithelial cells, NP69 and nasopharyngeal carcinoma cells was detected by fluorescence quantitative PCR, and the difference in the expression of ID2 in the immortalized nasopharyngeal epithelial cells and nasopharyngeal carcinoma cells was preliminarily discussed, and the nasopharyngeal carcinoma cells with high expression were found as the next interference. Object.
3. the effect of ID2 silencing on the biological effects of nasopharyngeal carcinoma cells and the detection of some EMT related gene expression levels
The ID2 lentivirus interference carrier was constructed and packaged into mature lentivirus particles infected with SUNE1 cells with high expression of ID2. The stable positive and unloaded clones were screened by the finite dilution method. The ID2 interference efficiency in the interference cloned cells was detected by fluorescence quantitative PCR, and the cell clones with the highest interference efficiency were screened and the cell clone was used as the experimental object. One step was to study the.MTT method. The effect of ID2 silencing on the proliferation of cells in vitro was detected by a flat clone formation test, and Transwell was used to detect the change of cell migration and movement after ID2 silencing.
ID2 related TGF-beta and EMT related transcription factors Slug, SIP1, Twist, Snail, epithelial markers E-cadherin, and interstitial marker Vimentin were detected in the expression level of four cell lines in four cell lines.
4. statistical method
SPSS 13 statistical software package was used for statistical processing, and the second chapters were classified as grade data due to immunohistochemistry, so the comparison between the groups was compared with the non parametric rank sum test. The expression of ID2 was compared with Mann-Whitney U test in non cancer nasopharyngeal tissue and nasopharyngeal carcinoma. The relationship between the expression of ID2 and the clinical stage of nasopharyngeal carcinoma was tested by Kruskal Wal. Lis Test, the test level was both bilateral alpha =0.05; fluorescence quantitative PCR method was used to detect the expression characteristics of ID2 in nasopharyngeal carcinoma cell lines by single factor variance analysis and multiple comparison using SNK test. The third chapter fluorescence quantitative PCR, exercise, flat clone formation experiment using single factor difference analysis; MTT using analysis of variance analysis of factorial design; The SNK or LSD test is used for the re comparison.
Result
Screening of EMT related genes in 1. nasopharyngeal carcinoma
35 differentially expressed genes associated with EMT are found in the common nasopharyngeal carcinoma chip data, and the functions of these genes are related to cell components, cell adhesion, communication, signal transduction, differentiation, movement, migration, and cell surface receptor related signal transduction. These functions are often considered to be associated with tumor invasion and metastasis.
Identification of 2.ID2 expression in nasopharyngeal carcinoma
1, a total of 18 cases of nasopharyngitis group were collected. The results of.SP immunohistochemical staining in 52 cases of nasopharyngeal carcinoma group showed that the expression of ID2 expression in the nucleus and cytoplasm.ID2 in nasopharyngeal carcinoma and non cancer nasopharynx tissues was statistically different (Z=-5.553, P=0.000), and there was no statistical difference between the expression of ID2 and the clinical stage (x 2=0.963, P=0.810).
2, the fluorescence quantitative PCR method was used to detect ID2 in the immortalized nasopharyngeal epithelial cells NP69 and nasopharyngeal carcinoma cells SUNE1,5-8F, 6-10B, CNE2, HNE1, CNE1, C666-1, HONE1 mRNA, and the expression was the highest, and the expression amount was 78 times as the next step.
Biological effects of 3.ID2 silencing on nasopharyngeal carcinoma cells and detection of partial EMT related gene expression
1, the ID2 lentivirus interference carrier was constructed, SUNE1 cells were infected after the lentivirus was packaged, the GFP+ monoclonal was screened by the finite dilution method, and the ID2 expression of each clone was detected by the fluorescence quantitative PCR, and the 2 monoclonal antibodies with the highest interference efficiency were selected for the next experiment. The interference efficiency of the positive clones was expressed with the SUNE1 and negative control cells. The statistical difference (F=48.693, P=0.000), and the expression of ID2 in negative control was the same as that of SUNE1 (0.933 + 0.006). The positive clones were named SUNE1/plv-ID2-1 and SUNE1/plv-ID2-2, and the negative control clones were SUNE1/plv.
2, MTT assay was used to detect cell proliferation. Compared with negative control SUNE1/Plv and SUNE1 cells, the proliferation rate of interference cloned cells, SUNE1/plv-ID2-1 and SUNE1/plv-ID2-2, was significantly slower and time dependent, with statistical differences (F=3.301, P=0.000). The clone formation rate of the four groups was statistically significant. F=253.434 (P=0.000), SUNE1/plv-ID2 cell clone formation decreased, SUNE1 and negative control group did not have statistical difference (P=0.866). The growth of SUNE1 cells in vitro was significantly inhibited after ID2 expression interference.
3, the results of Transwell cell detection showed that compared with SUNE1 and SUNE1/plv cells, the number of cells passing through the polycarbonate membrane of SUNE1 /plv-ID2 cells did not change significantly, and the difference was not significant (F=0.624, P=0.610).
4, the results of fluorescence quantitative PCR assay showed that the expression of TGF-beta, E-cadherin, Slug, SIP1, Vimentin did not have statistical differences between the 4 groups of cells (F=0.405, P=0.754; F=0.571, P=0.650), but there were statistical differences between the 4 groups of cells. F=155.295, P=0.000).
conclusion
1, bioinformatics methods screened 35 genes related to nasopharyngeal carcinoma (EMT).
2, immunohistochemical SP method confirmed that the expression of ID2 was related to the occurrence and development of nasopharyngeal carcinoma.
3, the expression of ID2 in the immortalized nasopharyngeal epithelial cells NP69 and nasopharyngeal carcinoma cells SUNE1,5-8F, 6-10B, CNE2, HNE1, CNE1, C666-1, HONE1 in the immortalized nasopharyngeal epithelial cells NP69 and nasopharyngeal carcinoma cells were statistically different, and the SUNE1 expression was the highest.
4, the biological function of some cells changed after ID2 interference.
5, the expression level of 1nRNA related to EMT after ID2 interference was changed.
【學(xué)位授予單位】：南方醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2010
【分類號(hào)】：R739.63

【相似文獻(xiàn)】

相關(guān)期刊論文 前10條

1 楊利霞;李淼;李鄉(xiāng)南;方長清;李建華;;多效蛋白PTN在肺腺癌血清、組織和胸水細(xì)胞中的表達(dá)及意義[J];中國組織化學(xué)與細(xì)胞化學(xué)雜志;2011年03期

2 徐國萍;高不郎;姜巍;許祖德;;TGF-β1與EGF對肺泡Ⅱ型上皮細(xì)胞表型及功能的影響[J];大理學(xué)院學(xué)報(bào);2011年06期

3 ;[J];;年期

4 ;[J];;年期

5 ;[J];;年期

6 ;[J];;年期

7 ;[J];;年期

8 ;[J];;年期

9 ;[J];;年期

10 ;[J];;年期

相關(guān)會(huì)議論文 前10條

1 周庚寅;蓋志博;白艷花;劉志艷;覺道建一;村垣泰光;;上皮-間葉轉(zhuǎn)化(EMT)的研究及進(jìn)展[A];中華醫(yī)學(xué)會(huì)病理學(xué)分會(huì)2010年學(xué)術(shù)年會(huì)日程及論文匯編[C];2010年

2 張棟棟;詹啟敏;;EMT相關(guān)分子標(biāo)志物的篩選[A];全國腫瘤流行病學(xué)和腫瘤病因?qū)W學(xué)術(shù)會(huì)議論文集[C];2011年

3 徐向明;林建江;;EMT和腫瘤進(jìn)展[A];2011年浙江省肛腸外科學(xué)術(shù)大會(huì)暨結(jié)直腸肛門疾病診治新進(jìn)展學(xué)習(xí)班論文匯編[C];2011年

4 林森;陳崇喜;王春雷;李先輝;陳小奉;;琥珀酸脫氫酶和丙酮酸脫氫酶激酶1在鼻咽癌癌變過程中的表達(dá)變化[A];浙江省醫(yī)學(xué)會(huì)耳鼻咽喉科學(xué)分會(huì)成立60周年慶典暨2011年浙江省醫(yī)學(xué)會(huì)耳鼻咽喉頭頸外科學(xué)學(xué)術(shù)年會(huì)論文匯編[C];2011年

5 林少俊;宗井鳳;;鼻咽癌的治療進(jìn)展[A];第十三屆中國科協(xié)年會(huì)第18分會(huì)場-癌癥流行病趨勢和防控策略研討會(huì)論文集[C];2011年

6 周小軍;田道法;王士貞;阮巖;邱寶珊;張麗娟;;鼻咽癌高癌家系成員基因組穩(wěn)定與修復(fù)基因表達(dá)研究[A];中華中醫(yī)藥學(xué)會(huì)耳鼻喉科分會(huì)第15屆學(xué)術(shù)交流會(huì)論文集[C];2009年

7 項(xiàng)光早;;微血管密度與鼻咽癌生長、浸潤、轉(zhuǎn)移和預(yù)后關(guān)系的研究[A];浙江省醫(yī)學(xué)會(huì)耳鼻咽喉科學(xué)分會(huì)成立60周年慶典暨2011年浙江省醫(yī)學(xué)會(huì)耳鼻咽喉頭頸外科學(xué)學(xué)術(shù)年會(huì)論文匯編[C];2011年

8 李美香;石金鳳;謝元杰;趙國軍;龍治峰;黃欣瓊;;間質(zhì)蛋白Periostin促進(jìn)鼻咽癌轉(zhuǎn)移的機(jī)制研究[A];中國解剖學(xué)會(huì)2011年年會(huì)論文文摘匯編[C];2011年

9 楊凌;馬禮欽;孔祥泉;潘建基;鄭雄偉;蔡曉文;;ERCC1等基因在鼻咽癌組織中的表達(dá)及其臨床意義[A];第六屆全國鼻咽癌學(xué)術(shù)大會(huì)論文匯編[C];2010年

10 王琳琳;蔣捍東;;肺癌化療耐藥性與上皮細(xì)胞間質(zhì)轉(zhuǎn)型(EMT)的相關(guān)性研究[A];中華醫(yī)學(xué)會(huì)呼吸病學(xué)年會(huì)——2011（第十二次全國呼吸病學(xué)學(xué)術(shù)會(huì)議）論文匯編[C];2011年

相關(guān)重要報(bào)紙文章 前10條

1 本報(bào)記者 謝明霞;從蛋白質(zhì)組學(xué)入手 探究鼻咽癌[N];健康報(bào);2011年

2 記者 馬曉芳;揭秘華為架構(gòu)變動(dòng)：與EMT并行 董事會(huì)走向臺(tái)前[N];第一財(cái)經(jīng)日報(bào);2011年

3 記者 馬曉芳;董事會(huì)取代EMT 華為向公眾公司邁進(jìn)[N];第一財(cái)經(jīng)日報(bào);2011年

4 劉葳漪;上海通用前5月銷量突破40萬[N];中國質(zhì)量報(bào);2010年

5 劉海英;上皮間質(zhì)轉(zhuǎn)化基因可用于檢測循環(huán)腫瘤細(xì)胞[N];科技日報(bào);2009年

6 丘慧慧;華為海外員工本地化率近60%[N];中國企業(yè)報(bào);2009年

7 本報(bào)記者 王雪敏;肝癌干細(xì)胞及其分化治療[N];醫(yī)藥經(jīng)濟(jì)報(bào);2010年

8 證券時(shí)報(bào)記者 范彪;華為澄清人事震蕩 接班問題再成焦點(diǎn)[N];證券時(shí)報(bào);2010年

9 鐘良;孫亞芳離職與否,華為接班人問題都很現(xiàn)實(shí)[N];21世紀(jì)經(jīng)濟(jì)報(bào)道;2010年

10 本報(bào)記者 丘慧慧;華為改選董事會(huì) 厘定新四大業(yè)務(wù)[N];21世紀(jì)經(jīng)濟(jì)報(bào)道;2011年

相關(guān)博士學(xué)位論文 前10條

1 姜漢國;PI3K/AKT信號(hào)傳導(dǎo)通路與鼻咽癌侵襲轉(zhuǎn)移關(guān)系的研究[D];山東大學(xué);2010年

2 王路;EBNA1在鼻咽癌轉(zhuǎn)移中的作用及分子機(jī)制研究[D];南方醫(yī)科大學(xué);2011年

3 周文;鼻咽癌染色體12p12-11區(qū)段擴(kuò)增基因的篩選及其功能研究[D];中南大學(xué);2010年

4 陳舒華;鼻咽癌高癌家系體質(zhì)證型的蛋白質(zhì)組學(xué)研究[D];湖南中醫(yī)藥大學(xué);2008年

5 李萍;鼻咽癌雞胚絨毛尿囊膜移植瘤模型的建立及其在腫瘤生物學(xué)行為研究上的應(yīng)用[D];廣西醫(yī)科大學(xué);2010年

6 樓建軍;抑癌基因單核苷酸多態(tài)性與鼻咽癌遺傳易感性研究[D];廣西醫(yī)科大學(xué);2012年

7 蘇波;鼻咽癌臨床進(jìn)展過程中轉(zhuǎn)錄因子活性譜動(dòng)態(tài)變化規(guī)律研究[D];中南大學(xué);2010年

8 肖哲鋒;不同分化程度的鼻咽癌組織定量蛋白質(zhì)組學(xué)研究[D];中南大學(xué);2010年

9 阮林;鼻咽癌表皮生長因子受體信號(hào)通路的磷酸化蛋白質(zhì)組學(xué)研究[D];中南大學(xué);2010年

10 何本夫;瞬時(shí)受體電位通道TRPC1在人鼻咽癌CNE2細(xì)胞增殖和侵襲作用的初步研究[D];南方醫(yī)科大學(xué);2011年

相關(guān)碩士學(xué)位論文 前10條

1 陳靖;鼻咽癌相關(guān)基因ID2與EMT關(guān)系的初步探討[D];南方醫(yī)科大學(xué);2010年

2 李錫清;鼻咽癌新生脈管及其臨床病理意義[D];桂林醫(yī)學(xué)院;2010年

3 張麗煌;Survivin,Bcl-2,Pml mRNA的表達(dá)及其與鼻咽癌臨床分期及預(yù)后的關(guān)系[D];昆明醫(yī)學(xué)院;2011年

4 鄧玲;角蛋白19表達(dá)與鼻咽癌臨床病理特征的關(guān)系研究[D];南華大學(xué);2010年

5 鄧澤鋒;鼻咽癌頸椎破壞的臨床特征及預(yù)后分析[D];南昌大學(xué);2011年

6 侯吉光;影響鼻咽癌預(yù)后因素分析[D];吉林大學(xué);2011年

7 張鋒;己糖激酶2在鼻咽癌組織中的表達(dá)[D];華中科技大學(xué);2011年

8 張曉靜;影響鼻咽癌放射治療預(yù)后因素分析[D];廣西醫(yī)科大學(xué);2012年

9 劉彬;整合素α_v、β_3和bFGF與鼻咽癌浸潤轉(zhuǎn)移的相關(guān)性研究[D];廣西醫(yī)科大學(xué);2010年

10 劉新強(qiáng);噬菌體隨機(jī)肽庫篩選鼻咽癌患者血清腫瘤標(biāo)記物的實(shí)驗(yàn)研究[D];廣西醫(yī)科大學(xué);2011年

，

本文編號(hào)：2106866