SOX4與EZH2在乳腺癌組織中的表達(dá)及其臨床病理意義
[Abstract]:Background: breast cancer is one of the most common malignant tumors in women worldwide. Both SOX4 and EZH2 can promote tumor metastasis by inducing epithelial-interstitial transition (epithelial-mesenchymal transition,EMT), but it is still unclear whether there is a certain correlation between them in breast cancer. As an important auxiliary method for pathological diagnosis, immunohistochemical method can detect the expression of protein in tumor tissue in a simple, direct and specific way, which is not only helpful to the diagnosis of tumor patients, including breast cancer patients, but also helpful to the diagnosis of breast cancer. It can also evaluate the prognosis of tumor to a certain extent and guide the clinical treatment. Objective: to observe the expression and correlation of SOX4 and EZH2 in breast cancer and to explore their clinicopathological significance. Methods: immunohistochemical method was used to detect the expression of SOX4,EZH2 in 241 cases of breast cancer and 126 cases of adjacent non-tumor breast tissue, and the expression of EMT marker E-cadherin and vimentin was detected in 129 cases of breast cancer. The correlation between the expression of SOX4 and EZH2 and the clinicopathological features of breast cancer was observed and analyzed under microscope. The correlation between the expression of VEGF and Vimentin and the expression of E-cadherin and vimentin were also analyzed. Results: the expression of 1.SOX4 was localized in the cytoplasm and / or nucleus of breast epithelial cells and cancer cells. The high expression rate was 82.2% (198 / 241) in breast cancer nests. The high expression rate in non-tumor breast tissues was significantly higher than that in non-tumor breast tissues (72.1%, 72.1%) (P0.05). The expression of 2.EZH2 was localized in the nuclei of breast epithelial cells and cancer cells, and showed diffuse homogenous expression in breast cancer nests, with a high expression rate of 80.1% (1931 / 241). The high expression rate of non-tumor breast tissue was 47.6% (60 / 126) (P0.05). The high expression of 3.SOX4 was correlated with lymph node metastasis, TNM stage and HER-2 expression (P0.05). With the increase of TNM stage, the expression of SOX4 increased (P0.008). The high expression of 4.EZH2 was correlated with high histological grade, lymph node metastasis, ER negative, EGFR positive and high Ki-67 proliferation index (P0.05). At the same time, the high expression of EZH2 was also correlated with molecular typing of breast cancer (P0.05), and the high expression rate of EZH2 was significantly higher than that of Luminal A in the over-expression of HER-2 (P0.05), and the difference was statistically significant (P0.008). The expression of 5.E-cadherin was heterogeneous in breast cancer nests. The loss of 5.E-cadherin expression was based on the loss of cell membrane expression in breast cancer cells, spindle-shaped, and E-cadherin was frequently lost in tumor cells with obvious dysplasia, with a loss of expression rate of 50.4% (65 / 129). The expression of vimentin was localized in the cytoplasm of tumor cells and showed heterogeneous staining in the nests of breast cancer, and the expression was higher in the central part of the nests of breast cancer. The positive rate was 73.6% (95 / 129), and the positive rate was 73.6% (95 / 129). In breast cancer, the expression of E-cadherin was negatively correlated with the expression of vimentin (rs=-0.357,P0.05), and the expression of SOX4,EZH2 was negatively correlated with the expression of E-cadherin (rs=-0.246,P0.05;). Rs=-0.357,P0.05 was positively correlated with the expression of vimentin (rs=0.310,P0.05;rs=0.268,P0.05), 7. There was a positive correlation (rs=0.256,P0.05) between the expression of SOX4 and EZH2 in breast cancer. Conclusion: the expression of SOX4 and EZH2 is up-regulated in breast cancer tissues, both of them may be involved in EMT process and promote lymph node metastasis. Combined detection of SOX4 and EZH2, may be a potential biomarker for predicting breast cancer metastasis.
【學(xué)位授予單位】:安徽醫(yī)科大學(xué)
【學(xué)位級(jí)別】:碩士
【學(xué)位授予年份】:2017
【分類號(hào)】:R737.9
【相似文獻(xiàn)】
相關(guān)期刊論文 前10條
1 ;鈣粘素E水平低提示乳腺癌細(xì)胞轉(zhuǎn)移[J];中國腫瘤;2000年08期
2 黃嘯原;用“印度閱兵”形容乳腺癌合適嗎?[J];診斷病理學(xué)雜志;2001年02期
3 張嘉慶,王殊,喬新民;乳腺癌的現(xiàn)狀和遠(yuǎn)景[J];中華外科雜志;2002年03期
4 張維彬,汪波,石靈春;中醫(yī)藥在現(xiàn)代乳腺癌治療中的運(yùn)用[J];中國中西醫(yī)結(jié)合急救雜志;2002年01期
5 薛志勇;食物與乳腺癌[J];山東食品科技;2002年04期
6 王旬果,王建軍,鄭國華;乳腺癌相關(guān)標(biāo)志物的研究進(jìn)展[J];山東醫(yī)藥;2002年33期
7 陸尚聞;;男人也患乳腺癌[J];環(huán)境;2003年12期
8 ;新技術(shù)清晰拍攝早期乳腺癌細(xì)胞[J];上海生物醫(yī)學(xué)工程;2005年04期
9 田富國;郭向陽;張華一;;乳腺癌診治研究新進(jìn)展[J];腫瘤研究與臨床;2005年S1期
10 馬濤,谷俊朝;血管內(nèi)皮生長因子與乳腺癌的臨床研究進(jìn)展[J];國外醫(yī)學(xué)(外科學(xué)分冊);2005年01期
相關(guān)會(huì)議論文 前10條
1 于永利;;抗乳腺癌免疫治療融合蛋白[A];中國免疫學(xué)會(huì)第四屆學(xué)術(shù)大會(huì)會(huì)議議程及論文摘要集[C];2002年
2 郭紅飛;;中醫(yī)治療乳腺癌的策略[A];江西省中醫(yī)、中西醫(yī)結(jié)合腫瘤學(xué)術(shù)交流會(huì)論文集[C];2012年
3 龐朋沙;伍會(huì)健;;乳腺癌治療靶標(biāo)的研究進(jìn)展[A];北方遺傳資源的保護(hù)與利用研討會(huì)論文匯編[C];2010年
4 陸勁松;邵志敏;吳炅;韓企夏;沈鎮(zhèn)宙;;新型維甲酸抑制乳腺癌細(xì)胞的生長及誘導(dǎo)凋亡的機(jī)制研究[A];2000全國腫瘤學(xué)術(shù)大會(huì)論文集[C];2000年
5 劉愛國;胡冰;;乳腺癌臨床治療進(jìn)展[A];安徽省抗癌協(xié)會(huì)第四次代表大會(huì)暨乳腺癌、肺癌專業(yè)委員會(huì)成立會(huì)議、安徽省腫瘤防治進(jìn)展學(xué)術(shù)研討會(huì)論文匯編[C];2001年
6 張嘉慶;王殊;喬新民;;乳腺癌的現(xiàn)狀和遠(yuǎn)景[A];第一屆全國中西醫(yī)結(jié)合乳腺疾病學(xué)術(shù)會(huì)議論文匯編[C];2002年
7 劉清俊;;乳腺癌綜合治療的新進(jìn)展[A];山西省抗癌協(xié)會(huì)第六屆腫瘤學(xué)術(shù)交流會(huì)論文匯編[C];2003年
8 邵志敏;;21世紀(jì)乳腺癌治療的展望[A];第三屆中國腫瘤學(xué)術(shù)大會(huì)教育論文集[C];2004年
9 陳松旺;張明;;乳腺癌治療的回顧與展望[A];西部地區(qū)腫瘤學(xué)學(xué)術(shù)會(huì)議論文匯編[C];2004年
10 白霞;傅建新;丁凱陽;王兆鉞;阮長耿;;組織因子途徑抑制物-2在乳腺癌細(xì)胞中的表達(dá)研究[A];第10屆全國實(shí)驗(yàn)血液學(xué)會(huì)議論文摘要匯編[C];2005年
相關(guān)重要報(bào)紙文章 前10條
1 ;血檢有望揭示乳腺癌治療效果[N];醫(yī)藥經(jīng)濟(jì)報(bào);2004年
2 記者 鄭曉春;乳腺癌細(xì)胞擴(kuò)散基因被找到[N];科技日?qǐng)?bào);2007年
3 中國軍事醫(yī)學(xué)科學(xué)院腫瘤中心主任 宋三泰;乳腺癌有了新療法[N];中國婦女報(bào);2002年
4 王艷紅;抑制DNA修補(bǔ)可消滅乳腺癌細(xì)胞[N];醫(yī)藥經(jīng)濟(jì)報(bào);2005年
5 詹建;乳腺癌飲食 兩個(gè)時(shí)期不一樣[N];中國中醫(yī)藥報(bào);2006年
6 辛君;乳腺癌擴(kuò)散基因“浮出水面”[N];大眾衛(wèi)生報(bào);2009年
7 記者 毛黎;美發(fā)現(xiàn)有效抑制乳腺癌細(xì)胞生長的分子[N];科技日?qǐng)?bào);2010年
8 記者 吳春燕 通訊員 王麗霞;乳腺癌治療將有新途徑[N];光明日?qǐng)?bào);2011年
9 王樂 沈基飛;我科學(xué)家發(fā)現(xiàn)導(dǎo)致乳腺癌耐藥的新標(biāo)志物[N];科技日?qǐng)?bào);2011年
10 劉霞;一種天然分子能阻止乳腺癌惡化[N];科技日?qǐng)?bào);2011年
相關(guān)博士學(xué)位論文 前10條
1 柴紅燕;疾病狀態(tài)下CYP4Z1和4A的生物學(xué)行為及其藥物干預(yù)研究[D];武漢大學(xué);2012年
2 李凱;ID(inhibitor of DNA binding)家族蛋白調(diào)控乳腺細(xì)胞的分化并影響乳腺癌的預(yù)后[D];復(fù)旦大學(xué);2014年
3 江一舟;乳腺癌新輔助化療前后基因變異檢測及其功能論證[D];復(fù)旦大學(xué);2014年
4 馬邵;酪氨酸去磷酸化增強(qiáng)表皮生長因子受體在乳腺癌治療中靶向性的研究[D];山東大學(xué);2015年
5 姚若斯;精氨酸甲基轉(zhuǎn)移酶PRMT7誘導(dǎo)乳腺癌細(xì)胞發(fā)生表皮—間質(zhì)轉(zhuǎn)換及轉(zhuǎn)移的作用機(jī)制研究[D];東北師范大學(xué);2015年
6 侯培鋒;α-酮戊二酸二甲酯(DM-2KG)上調(diào)缺氧誘導(dǎo)因子-1α(HIF-1α)誘發(fā)高致瘤性干細(xì)胞樣乳腺癌細(xì)胞機(jī)制研究[D];福建醫(yī)科大學(xué);2014年
7 李麗麗;分泌蛋白SHON調(diào)控乳腺癌細(xì)胞EMT的分子機(jī)制研究[D];東北師范大學(xué);2015年
8 陳麗艷;PI3K抑制劑聯(lián)合組蛋白去乙;敢种苿⿲(duì)乳腺癌協(xié)同殺傷作用的分子機(jī)制研究[D];延邊大學(xué);2015年
9 樸俊杰;乳腺癌差異基因篩選及PAIP1對(duì)其生物學(xué)行為的影響[D];延邊大學(xué);2015年
10 汪[?如;染色體6q25.1區(qū)域基因多態(tài)性與乳腺癌遺傳易感性的關(guān)聯(lián)研究[D];南方醫(yī)科大學(xué);2015年
相關(guān)碩士學(xué)位論文 前10條
1 杜文英;乳腺癌分子亞型的臨床與病理特點(diǎn)[D];鄭州大學(xué);2011年
2 賈曉菲;彩色多普勒超聲與乳腺癌病理及免疫組化指標(biāo)的相關(guān)性研究[D];內(nèi)蒙古大學(xué);2015年
3 靳文;乳腺癌全基因組DNA甲基化修飾的研究[D];內(nèi)蒙古大學(xué);2015年
4 吳坤琳;TLR4/MyD88信號(hào)通路對(duì)乳腺癌侵襲性影響的實(shí)驗(yàn)研究[D];福建醫(yī)科大學(xué);2015年
5 葛廣哲;樹,
本文編號(hào):2447849
本文鏈接:http://sikaile.net/yixuelunwen/zlx/2447849.html