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| 1 | α-平滑肌肌动蛋白在PVR增生膜中的表达以及PDGF对其在人RPE细胞中表达的影响显示文摘目的探讨α-平滑肌肌动蛋白(α-SMA)在增生性玻璃体视网膜病变(proliferative vitreoretinopathy,PVR)增生膜中的表达以及血小板源性生长因子(PDGF)对人视网膜色素上皮(RPE)细胞表达α-SMA的影响。方法通过免疫荧光实验和免疫组化法对14例PVR患者视网膜表面增生膜(PRM)中α-SMA的表达进行定性及定量分析;用外源性PDGF-BB处理体外培养的人RPE细胞,并通过免疫荧光实验检测PDGF-BB对RPE细胞表达α-SMA的影响。结果免疫组织化学结果显示:α-SMA在14例不同级别的PRM中均有表达,主要分布在胞浆中,但其表达的程度有差异。α-SMA阳性细胞在PVR/C级PRM膜中比率为35/80,在PVR/D级PRM膜中的比率为50/60。免疫荧光定量分析结果显示:α-SMA在C级PRM膜和D级PRM膜中的平均荧光强度分别为12.31和23.09,二者差异有统计学意义(P<0.01)。外源性的PDGF-BB(50μg.L-1)能显著促进人RPE细胞中α-SMA的表达(50μg.L-1PDGF-BB处理前后平均荧光强度分别为10.08和17.23),差异有统计学意义(P<0.05),这种促进作用在培养基中有血清存在时明显增强。结论α-SMA在PVR增生膜中广泛表达,其表达量与PVR病变程度有关,提示α-SMA可作为检测PVR病变程度的一个潜在因子;PDGF促进α-SMA的表达,这提示PDGF在PVR发病中有重要作用,为临床上PVR的预防和治疗提出新的思路。 | 司艳芳 王君 关娟 韩泉洪 惠延年 | 2012 | 眼科新进展2012，32，11： | 4 |
| 2 | EpCAM和CA_(125)在子宫内膜腺癌及子宫癌前病变患者血清中的表达水平与意义显示文摘目的:探讨上皮细胞黏附分子(Ep CAM)和CA125水平变化与子宫内膜样腺癌(EAC)及子宫癌前病变发生、发展的关系和在诊断、监测EAC及子宫癌前病变方面的临床价值。方法:抽取26份EAC患者术前血清标本及其中17份术后血清标本;抽取6例子宫内膜不典型增生(EIN)患者及17例对照组患者手术前后血清标本(增生性子宫内膜5例、分泌性子宫内膜6例、萎缩性子宫内膜6例)。采用ELISA测定Ep CAM及CA125在上述血清标本中的表达水平。结果:术前,Ep CAM和CA125在对照组、EIN组及EAC组血清中的表达水平递次增加(P<0.05);术后,3组血清Ep CAM和CA125水平较术前均有所降低。在EAC组及对照组中,无绝经史者术前血清Ep CAM水平显著低于有绝经史者(P<0.05),CA125水平则相反(P<0.05)。在诊断EAC及EIN的敏感度、特异度、准确度和阳性预测值方面,血清Ep CAM水平均高于血清CA125水平,二者联合检测提高了诊断的敏感度和准确度;在EAC组及EIN组中,有绝经史者血清CA125诊断的敏感度高于血清Ep CAM,但无绝经史者则相反,二者联合检测提高了诊断敏感度。结论:血清Ep CAM和CA125水平可能与子宫内膜癌的发生、发展有关;二者联合检测可能成为诊断EAC更便捷、有效、互补的方法;分泌性子宫内膜患者的血清Ep CAM水平明显低于其他患者,提示其可能对判定非EAC状态及监测孕激素治疗效果具有指导意义。 | 罗丽丽 张易欣 倪惠杰 马晓艳 | 2014 | 中国妇幼保健2014，29，33： | 3 |
| 3 | Is there a genetic signature for liver metastasis in colorectal cancer?显示文摘Even though liver metastasis accounts for the vast majority of cancer deaths in patients with colorectal cancer (CRC), fundamental questions about the molecular and cellular mechanisms of liver metastasis still remain unanswered. Determination of gene expression profiles by microarray technology has improved our knowledge of CRC molecular pathways. However, defined gene signatures are highly variable among studies. Expression profiles and molecular markers have been specifically linked to liver metastases mechanistic paths in CRC. However, to date, none of the identified signatures or molecular markers has been successfully validated as a diagnostic or prognostic tool applicable to routine clinical practice. To obtain a genetic signature for liver metastasis in CRC, measures to improve reproducibility, to increase consistency, and to validate results need to be implemented. Alternatives to expression profiling with microarray technology are continuing to be used. In the recent past, many genes codifying for proteins that are directly or indirectly involved in adhesion, invasion, angiogenesis, survival and cell growth have been linked to mechanisms of liver metastases in CRC. | Cristina Nadal Joan Maurel Pere Gascon | 2007 | World Journal of Gastroenterology2007，13，44： | 1 |
| 4 | Aberrant methylation of Glutathione S-transferase P1 and E-cadherin in invasive ductal breast carcinoma and fibroadenoma显示文摘Objective To investigate the hypermethylation status of glutathione transferase P1(GSTP1)and E-cadherin(ECAD),TSGs(tumor suppressor genes)in our breast cancer samples and explore their correlation with clinicopathological features of corresponding cancer patients.Methods One hundred and thirty-six IDC(invasive ductal carcinoma)patients were recruited for analysis and 16 fibroadenoma patients acted as control.DNA extraction and methylation-specific PCR(MSP)were subsequently performed preceded by pathological examination.Results The percentage of hypermethylated GSTP1 in carcinoma and fibroadenoma groups was 34.92% and 15.79% respectively and the percentage of hypermethylated ECAD in carcinomas and fibroadenomas was 18.00% and 0.00% respectively.Carcinoma had the highest percentage of c-erbB2 overexpression being 54.55% among the clinicopathological parameters.Conclusion Hypermethylation patterns are frequent in IDC and seem to relate to c-erbB2 overexpression,and such epigenetic change should not be neglected in fibroadenoma.Tumor methylation status in cancer patients can be determined at early stage and it may be a reference for better treatment planning. | Wings Tjing Yung Loo Mary Ngan Bing Cheung Louis Wing Cheong Chow | 2010 | 中华乳腺病杂志(电子版)2010，4，5： | 1 |
| 5 | 抗IFITM1单克隆抗体的制备及检测显示文摘目的:制备抗干扰素诱导的跨膜蛋白-1(interferon-induced transmembrane protein 1,IFITM1)的单克隆抗体,为检测IFITM1及进一步研究其在结肠肿瘤发生过程中的作用提供实验基础。方法:以结肠癌患者的癌组织为材料,提取总RNA,以RT-PCR扩增得到IFITM1 cDNA序列,经EcoRⅠ和HindⅢ双酶切后,克隆入pGEX-4T-3进行原核表达并纯化得IFITM1-GST;以该融合蛋白免疫BALB/c小鼠,淋巴细胞杂交瘤法制备单克隆抗体;采用ELISA、Western-blot及免疫组织化学法以制备的抗体检测结肠癌患者结肠癌组织中的IFITM1。结果:成功构建了IFITM1原核表达载体,获得了IFITM1-GST重组蛋白;制备得到了1株抗IFITM1单克隆抗体,腹水ELISA效价为1:30000,抗体亚类为IgG1,可用于ELISA、Western-blot及免疫组织化学法检测结肠癌患者结肠癌组织中的IFITM1。结论:获得了1株可用于ELISA、Western-blot及免疫组织化学法的抗IFITM1单克隆抗体2F-1,为进一步研究IFITM1在结肠肿瘤发生过程中的作用提供了实验基础。 | 刘灏 林智琪 符方勇 周忠信 刘正军 | 2014 | 现代生物医学进展2014，14，9： | 1 |
| 6 | 抗GPNMB单克隆抗体的制备及双抗体夹心ELISA方法的建立显示文摘目的:制备抗GPNMB单克隆抗体,建立双抗体夹心ELISA检测GPNMB在胶质母细胞瘤中的表达情况。方法:以新鲜胶质母细胞瘤组织为材料,提取总RNA,通过RT-PCR扩增得到GPNMB cDNA序列,经NcoI和XhoI双酶切后,克隆入PET-28a(+)进行原核表达,经蛋白纯化得GPNMB-6×His融合蛋白;以该融合蛋白免疫BALB/c小鼠,淋巴细胞杂交瘤法制备单克隆抗体;采用Western-blot、双抗体夹心ELISA以制备所得的抗GPNMB抗体检测胶质母细胞瘤细胞系U251、U373、SHG44和星形胶质细胞系SVG12中GPNMB的表达。结果:成功构建了GPNMB原核表达载体,获得了GPNMB-6×His重组蛋白;制备得到了G203、F105和M306共3株抗GPNMB的单克隆抗体,腹水ELISA效价分别为1:8000、1:8000、1:5000,抗体亚类分别为IgG2、IgG1和IgG1,进一步实验证实单克隆抗体G203和M306可用于双抗体夹心ELISA检测不同胶质细胞瘤细胞系中GPNMB的表达。结论:成功制备出抗GPNMB单克隆抗体,效价及特异性良好,并证实GPNMB在胶质母细胞瘤细胞系中高表达,为进一步研究GPNMB在胶质母细胞瘤中的作用奠定了基础。 | 张健民 张凡喜 黄晓龙 周玉峰 | 2013 | 现代生物医学进展2013，13，18： | 0 |
| 7 | Could gastrointestinal tumor-initiating cells originate from cell-cell fusion in vivo?显示文摘Tumor-initiating cells(TICs)or cancer stem cells are believed to be responsible for gastrointestinal tumor initiation,progression,metastasis,and drug resistance.It is hypothesized that gastrointestinal TICs(giTICs)might originate from cell-cell fusion.Here,we systemically evaluate the evidence that supports or opposes the hypothesis of giTIC generation from cell-cell fusion both in vitro and in vivo.We review giTICs that are capable of initiating tumors in vivo with 5000 or fewer in vivo fused cells.Under this restriction,there is currently little evidence demonstrating that giTICs originate from cell-cell fusion in vivo.However,there are many reports showing that tumor generation in vitro occurs with more than 5000 fused cells.In addition,the mechanisms of giTIC generation via cell-cell fusion are poorly understood,and thus,we propose its potential mechanisms of action.We suggest that future research should focus on giTIC origination from cell-cell fusion in vivo,isolation or enrichment of giTICs that have tumor-initiating capabilities with 5000 or less in vivo fused cells,and further clarification of the underlying mechanisms.Our review of the current advances in our understanding of giTIC origination from cell-cell fusion may have significant implications for the understanding of carcinogenesis and future cancer therapeutic strategies targeting giTICs. | Yang Zhou Jun-Ting Cheng Zi-Xian Feng Ying-Ying Wang Ying Zhang Wen-Qi Cai Zi-Wen Han Xian-Wang Wang Ying Xiang Hui-Yu Yang Bing-Rong Liu Xiao-Chun Peng Shu-Zhong Cui Hong-Wu Xin | 2021 | World Journal of Gastrointestinal Oncology2021，13，2： | 0 |
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