Objective: To screen and validate cancer testis antigens (CTAs) as potential biomarkers and explore their molecular mechanisms in glioblastoma (GBM). Methods: Ribonucleic acid sequencing (RNA-seq) and bioinformatics analyses were utilized to screen the highly expressed CTAs in GBM. Correlation analysis was used to identify poten-tial biomarkers associated with tumor purity and prognosis. Immunohistochemistry was applied for detection of pro-tein expression. Protein-protein interaction (PPI) network construction, functional enrichment analysis, and binding domain prediction were performed to investigate the underlying molecular mechanisms of GBM. Results: A total of 8 highly expressed CTAs were identified in GBM. One of them was PDZ-binding kinase (PBK). PBK messenger RNA (mRNA) was most highly expressed in GBM and associated with tumor purity and prognosis, PBK protein expression was also significantly increased in GBM tissues and correlated with p53 expression. Functional enrichment analysis revealed that the PBK related genes were predominantly enriched in cell cycle pathway with 38 genes enriched. The proteins encoding by these 38 genes were performed by binding domain prediction analysis, which demonstrated 15 proteins interacting with PBK. Most of these proteins were up regulated in GBM. Conclusion: PBK is highly ex-pressed in GBM. It may serve as a potential biomarker for GBM targeting therapy and the cell cycle modulator by interacting with certain key molecules of cell cycle in GBM.

OY-TES-1 is reportedly involved in carcinogenesis and spermatogenesis. However, the tissue distribution of OY-TES-1 in the normal human body remains elusive. This study detected OY-TES-1 expression in human fetal and adult normal tissues by immunohistochemistry. We identified a general principle of OY-TES-1 expression. The expression of OY-TES-1 was found in neurons, smooth muscle cells, and cardiac muscle cells from both fetuses and adults. The connective tissue showed no specific staining throughout the fetal and adult samples. With OY-TES-1-positive staining of the epithelium irregular, OY-TES-1 was strongly expressed in the epithelium of the skin and bladder, as well as hepatocytes, pancreatic islets, and acinous cells during the fetal stage but was not detected in the postnatal period. In contrast to the epithelium of blood vessels, the fetal and adult central hepatic vein and glomeruli showed negative expression of the OY-TES-1 protein. Sex-dimorphism was observed in the distribution of OY-TES-1 in male and female germ cells. Collectively, our results indicate that OY-TES-1 is a member of the cancer-testis antigen and autoantigen, with tissue-specific and period-specific expression patterns, revealing potential contributions of OY-TES-1 to the diagnosis and therapeutic treatment for neoplasms and infertility.

OBJECTIVE:Glioblastoma multiforme (GBM), the most malignant intracranial neoplasm, is associated with a high mortality and recurrence rate due to the aggressive nature and heterogeneity of the tumor. Some of the molecular markers involved in the tumorigenesis of GBM are essential in prognosis, diagnosis, and treatment. Due to the limitations of therapeutic effects, this study aims to explore novel biomarkers with prognostic value and to provide new insights into therapeutic targets.METHODS:The expression profile of mRNAs in GBM was detected by RNA-sequencing, and differentially expressed genes were identified by integrating the data from RNA-seq results and the GEPIA2 database. Of the total 40 hub genes, FN1, P4HB, and PPIB showed prognostic significance based on both GEPIA2 and CGGA databases. The validation of FN1, P4HB, and PPIB expression by qPCR and correlation analysis with clinicopathological features were performed in 41 GBM tissues from our institution.RESULTS:Kaplan-Meier analysis revealed that FN1 and P4HB expressions levels were related to the overall survival (OS) of GBM patients (P<0.05). Multivariate analysis showed that FN1 overexpression (HR=9.199, P=0.002) was an independent and unfavorable prognostic factor for GBM patients. The median survival time was 8.5 months and 21 months for high and low expressions of FN1, respectively.CONCLUSION:It was suggested that FN1 could be an ideal target for prognosis and a potential therapeutic target in GBM.

OY-TES-1 is reportedly involved in carcinogenesis and spermatogenesis. However, the tissue distribution of OY-TES-1 in the normal human body remains elusive. This study detected OY-TES-1 expression in human fetal and adult normal tissues by immunohistochemistry. We identified a general principle of OY-TES-1 expression. The expression of OY-TES-1 was found in neurons, smooth muscle cells, and cardiac muscle cells from both fetuses and adults. The connective tissue showed no specific staining throughout the fetal and adult samples. With OY-TES-1-positive staining of the epithelium irregular, OY-TES-1 was strongly expressed in the epithelium of the skin and bladder, as well as hepatocytes, pancreatic islets, and acinous cells during the fetal stage but was not detected in the postnatal period. In contrast to the epithelium of blood vessels, the fetal and adult central hepatic vein and glomeruli showed negative expression of the OY-TES-1 protein. Sex-dimorphism was observed in the distribution of OY-TES-1 in male and female germ cells. Collectively, our results indicate that OY-TES-1 is a member of the cancer-testis antigen and autoantigen, with tissue-specific and period-specific expression patterns, revealing potential contributions of OY-TES-1 to the diagnosis and therapeutic treatment for neoplasms and infertility.

Objective Cancer/testis antigen FMR1NB is aberrantly expressed in various types of cancer, but not in normal tissues except for testis. This study aimed to investigate the expression and functional role of FMR1NB in glioma. Methods The expression of FMR1NB mRNA and protein was determined using RT-PCR and immunohistochemistry, respectively, in glioma specimens from 83 patients at follow-up. The effects of siRNA-mediated FMR1NB silencing on malignant biological behaviors were evaluated in glioma cell lines A172 and U251. Results FMR1NB mRNA and protein expression was detected in 58.8% (77/131) and 46.34% (57/123) of glioma tissues, respectively. FMR1NB protein was positively correlated with World Health Organization grade and found to be an independent prognostic marker for poor outcome. Knockdown of FMR1NB induced apoptosis and suppressed proliferation, adhesion, migration, and invasion by modulating the expression of cyclin A, CDK2, caspase-3, E-cadherin, and N-cadherin in A172 and U251 cells. Conclusion Our findings suggest that FMR1NB contributes to the tumorigenesis of glioma cells and may represent a potential prognostic biomarker and an attractive therapeutic target in glioma.

Glioma is the most common malignant brain tumor in central nervous system. Despite advances in the treatment of glioma such as surgery and chemoradiotherapy, most patients are easy to relapse, resulting in adverse clinical outcomes. Hence, effective molecular-targeting treatment may be one of attractive strategies for glioma therapy. The dysregulated microRNAs (miRNAs), one of the candidates of therapeutic targets, are believed to play an important role in the progression of glioma. In this study, we aimed to examine the expression profile of miRNAs in glioma and provide a reference for glioma therapy. Firstly, expression profile of miRNAs in 5 normal brain tissues, 5 low-grade glioma (LGG) tissues and 5 glioblastoma (GBM) tissues was detected by RNA sequencing (RNA-seq). Next, the target genes of differentially expressed miRNAs (DEmiRNAs) were predicted and then GO enrichment and KEGG pathway analysis performed by bioinformatics. Finally, 10 miRNAs which were significantly up- or down-regulated both in GBM and LGG were validated by real-time quantitative PCR (qRT-PCR). RNA-seq results indicated a number of DEmiRNAs in glioma. There were 64 up-regulated miRNAs and 17 down-regulated miRNAs in LGG, and 181 up-regulated miRNAs and 124 down-regulated miRNAs in GBM, respectively. Bioinformatics analysis showed that the target genes of these DEmiRNAs were enriched in various biological processes and signaling pathways such as cell metabolic and developmental process. Selected DEmiRNAs were further confirmed by qRT-PCR. miRNA-10b-5p, miRNA-92b-3p and miRNA-455-5p were significantly up-regulated in both GBM and LGG; while miRNA-542-3p was significantly up-regulated in LGG; miRNA-184 and miRNA-206 were significantly down-regulated in both GBM and LGG; miRNA-766-5p and miRNA-1-3p were significantly down-regulated in GBM. The subject of our study demonstrated several dysregulated miRNAs may serve as a potential therapeutic target for glioma.

RNA剪接过程受到多种调节因子作用,以保证前体mRNA剪接的准确性.但是大量研究发现,在人类肿瘤中经常发生选择性剪接的异常或者来自特定癌症基因的剪接调控元件的突变.因此,RN A剪接调节剂作为一类新的癌蛋白和肿瘤抑制因子而逐渐受到关注,并有望通过调节参与致癌基因的RN A而达到治疗肿瘤的效果.改变RN A的异常剪接是治疗相关癌症的基础,这也为靶向治疗提供了更加丰富的靶点.本文综述了新发现的和预测的不同的剪接事件导致癌症的相关基因,并且对它们如何促成疾病的发病机制进行讨论.最后,我们总结了最新的针对可变剪接而发展的癌症诊断和治疗方法,包括使用小分子的剪接抑制剂来阻断剪接体或转录因子修饰酶,以调节特异性剪接导致的癌症.

目的 构建肾嫌色细胞癌(CRCC)的内源竞争性RNA(ceRNA)调控网络,筛选出与CRCC预后相关的信使RNA(mRNA)、长非编码RNA(lncRNA)和微小RNA(miRNA),为CRCC的诊断和预后提供理论依据.方法 提取TCGA数据库中CRCC样本(65例)和正常肾样本(24例)的转录组数据,以错误发现率(FDR)<0.05,差异倍数的对数绝对值(log2|FC|)>2为条件筛选差异表达(DE)的lncRNA、miRNA和mRNA,据此构建ceRNA调控网络.应用Kaplan-Meier法探讨与CRCC患者预后相关的因子,据此进一步构建蛋白-蛋白互作(PPI)网络,并进行GO与KEGG富集分析.结果 共筛选出3679个DElncRNA,297个DEmiRNA和5914个DEmRNA.mRNA下调的ceRNA网络包含DEmiRNA 95个、DEmRNA 268个、DElncRNA 737个;mRNA上调的ceRNA网络包含DEmiRNA 85个、DEmRNA 234个、DElncRNA 924个.Kaplan-Meier分析筛选出3个DEmRNA(DEPDC1、SLC7A11和E2F7)和1个DEmiRNA(miR-26b-5p)与CRCC预后存在关联(P<0.05).以DEPDC1、SLC7A11和E2F7构建的PPI网络中共含有8个mRNA(TOP2A、DEPDC1、SLC3A2、E2F8、SLC7A11、E2F1、TP53和E2F7)参与蛋白互作,GO和KEGG富集分析显示,这些互作蛋白功能主要富集于DNA损伤反应、p53介导的细胞组织与启动子特异结合、铁死亡,以及肿癌疾病相关信号通路.结论 该研究通过构建CRCC的ceRNA调控网络筛选出与其预后相关的关键RNAs,为CRCC的诊断和治疗提供了理论依据.

Objective: This work was designed to explore whether the combination of Tanshinone IIA (T-IIA) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has a direct anti-cancer effect in glioblastoma (GBM) and the possible mechanisms. Methods: GBM cells (U-87 and U-251 MG) were treated with T-IIA or/and TRAIL, or the expression of death receptors (DRs), DR4 and DR5, was suppressed in GBM cells. The activity of GBM cells was determined by MTT, and the apoptosis was assessed by Hoechst33342 staining and flow cytometry. The expression levels of cleaved caspase-3/8/9, phosphorylated (p)-STAT3 as well as DR4 and DR5 in GBM cells were assessed by Western blotting. A nude mouse xenograft model was constructed to evaluate the effects of T-IIA and TRAIL cotreatment on tumor growth and apoptosis in vivo. Results: After T-IIA treatment, GBM cells resumed the sensitivity to TRAIL-induced apoptosis dependent on inhibition of p-STAT3 and activation of DR4, DR5 and caspases. DR4 or/and DR5 knockdown significantly abated the co-effect of T-IIA and TRAIL on GBM cell apoptosis and proliferation. Furthermore, T-IIA and TRAIL cotreatment markedly inhibited the growth of transplanted tumor and activated U87 cell apoptosis in nude mice. Conclusion: T-IIA increases TRAIL-induced apoptosis by downregulating STAT3 and upregulating DR4 and DR5, indicating T-IIA therapy as a novel treatment strategy for TRAIL-resistant GBM.

目的 探讨肿瘤相关抗原MAGE-D4在肝细胞癌(HCC)中的表达情况,并分析其临床意义.方法 基于癌症基因组图谱(TCGA)数据库,获取371例HCC组织和50例正常肝组织的转录数据.应用数据挖掘工具UALCAN分析HCC组织中MAGE-D4 mRNA的表达情况,并筛选与其表达相关的基因.应用Kaplan-Meier Plotter分析MAGE-D4 mRNA表达水平与患者生存预后的关系.另收集于广西医科大学第一附属医院2009年6月至2011年8月经手术获取的HCC标本70例,癌旁组织标本30例,采用免疫组织化学法(IHC)检测MAGE-D4蛋白的表达情况,并分析其与患者临床指标的关联性.结果 基于TCGA数据库数据的分析结果显示,MAGE-D4 mRNA在HCC组织中的表达水平显著高于正常肝组织(P<0.05),且与甲胎蛋白(AFP)mRNA表达呈正相关(r=0.556,P=0.000).生存分析结果显示,MAGE-D4 mRNA高表达与黄种人HCC患者不良生存预后具有显著关联(HR=1.860,P=0.037).基于临床获取标本的分析结果显示,MAGE-D4蛋白主要定位于细胞质和细胞核,HCC组织的MAGE-D4高表达率显著大于癌旁组织(48.57％vs 23.33％;χ2=5.530,P=0.019).MAGE-D4高表达组HCC患者血清AFP浓度≥400μg/L的人数比例显著大于低表达组(P<0.05),但两组在性别、年龄、肿瘤级别、肿瘤分期、肿瘤直径、癌栓和乙型肝炎病毒(HBV)感染等方面比较差异无统计学意义(P>0.05).结论 MAGE-D4在HCC组织中高表达,其可能在HCC的发生和发展过程中发挥重要作用,有望成为HCC的潜在治疗靶点和预后标志物.

BACKGROUND The family of MAGE genes is well known due to the majority of MAGE genes expressing specifically in tumor tissues while restrictedly in normal tissues. MAGE-D4 is one of the MAGE family and considered as a promising target for glioma immunotherapy because of its overexpression in glioma and restricted expression in normal tissues. Whereas the mechanism of MAGE-D4 heterogeneous expression in glioma has not yet been elucidated. In this study, the transcriptional regulation mechanism of MAGE-D4 in glioma is focused from the perspectives of promoter methylation and SP1. METHODS Dual-luciferase reporter assay was performed to identify the core promoter of MAGE-D4 gene. Mass spectrometry was applied to quantify the methylation status of MAGE-D4 promoter in 50 glioma and 9 normal brain tissues. The influence of methylation and SP1 on MAGE-D4 transcriptional activity was evaluated by dual-luciferase reporter assay, qRT-PCR, western blot and ChIP-qPCR. Decitabine, an epigenetic drug, was used to treat the glioma cells. Then the treated cells were evaluated the influence of demethylation on SP1 binding to MAGE-D4 promoter. RESULTS The -358 to +172 bp region was identified as the core promoter of MAGE-D4 gene which demonstrated hypomethylated and negative correlation between methylation level and MAGE-D4 mRNA expression in glioma tissues. For single CpG unit analysis, 8 CpG units (CpG unit 1, 2, 3, 4, 5, 6, 9 and 12) in MAGE-D4 core promoter showed hypomethylated in glioma and the methylation level of CpG unit 6 was positively associated with the prognosis of glioma patients. Furthermore, the methylation level of CpG unit 1 and 6 was negative negatively correlated with MAGE-D4 mRNA expression. Then, the results demonstrated that the promoter activity of MAGE-D4 was decreased by methylation in glioma cell lines. In addition, SP1 can binds directly to the MAGE-D4 promoter leading to up-regulation of MAGE-D4 mRNA through activation of its promoter. Finally, demethylation of MAGE-D4 promoter could benefit the SP1 binding and resulting co-activation of MAGE-D4 promoter by demethylation and SP1 in glioma cell lines. CONCLUSION These findings indicate that the synergies of promoter hypomethylation and SP1 up-regulated MAGE-D4 transcription in glioma, which implies a potential approach to resolve the heterogeneous expression of MAGE-D4 in order to establish foundation for the MAGE-D4 based glioma therapy.

目的 检测肿瘤相关抗原M AGE-D4剪接变体ab和c在胶质瘤和非肿瘤脑组织中的表达情况,分析其临床意义,探讨M AGE-D4选择性剪接与胶质瘤的相关性.方法 采用RT-PCR技术进行检测,首先以Primer premier 5.0和O lig o 6.0软件设计和评价引物,对引物进行特异性检测和扩增产物测序验证,然后检测89例不同病理类型胶质瘤组织和24例非肿瘤脑组织中M AGE-D4ab和M AGE-D4c的表达,并结合胶质瘤患者临床病理参数进行统计分析.结果 所设计的引物可特异性扩增M AGE-D4ab和M AGE-D4c.所检测的组织中,M AGE-D4ab的表达普遍较M AGE-D4c丰富,其中胶质瘤组织中MAGE-D4ab的表达率明显高于非肿瘤脑组织(P<0.05),而MAGE-D4c的表达率与非肿瘤脑组织比较差异无统计学意义(P>0.05);胶质瘤组织和非肿瘤脑组织中均存在MAGE-D4ab-c和MAGE-D4ab+c两种表达形式,其中胶质瘤中MAGE-D4ab-c的表达率高于非肿瘤脑组织(P<0.05),而MAGE-D4ab+c的表达率则与非肿瘤脑组织差异无统计学意义(P>0.05);此外,MAGE-D4ab、MAGE-D4c、MAGE-D4ab-c和MAGE-D4ab+c的表达率均与性别、年龄、肿瘤直径和W HO分级等胶质瘤临床资料无显著性关联.结论 M AGE-D4ab及M AGE-D4ab-c形式在胶质瘤中异常表达,可能与胶质瘤的发生相关.

目的:研究黑色素瘤相关抗原基因-D4 (MAGE-D4)和细胞分裂周期蛋白25A(CDC25A)在人脑胶质瘤(胶质瘤)中的表达水平和临床意义,并探究二者的关系.方法:利用GEPIA在线数据库分析胶质瘤组织中MAGE-D4和CDC25A的表达情况,然后收集47例胶质瘤组织,逆转录实时荧光定量聚合酶链反应(PT-qPCR)验证MAGE-D4和CDC25A的表达,并进一步统计分析其与临床病理指标的关系及二者表达相关性.结果:GEPIA数据库显示MAGE-D4与CDC25A在胶质瘤组织中均高表达(P＜0.05);PT-qPCR结果显示所检测的胶质瘤组织MAGE-D4 mRNA和CDC25A mRNA的表达水平均明显高于正常脑组织,且二者表达呈明显正相关关系(r=0.3174,P＜0.05);此外,MAGE-D4 mRNA的表达与WHO分级和Ki-67表达相关,而CDC25A mRNA表达仅与WHO分级相关(P＜0.05).结论:CDC25A与MAGE-D4在胶质瘤组织中呈正相关关系,提示二者可能共同在胶质瘤的发生发展中发挥重要作用,可能成为胶质瘤生物治疗的潜在靶点.

BACKGROUND:Cancer/testis antigens (CTAs) are attractive therapeutic targets for tumor immunotherapy due to their restrictive expression in normal testis but excessive in majority of tumor types. ACTL8, CTCFL, OIP5 and XAGE3 are members of the CTAs family. Currently, the data of ACTL8, CTCFL, OIP5 and XAGE3 expression in glioma is limited. Methods: ACTL8, CTCFL, OIP5 and XAGE3 mRAN and protein expressions were detected in 108 glioma samples by Reverse Transcriptase-PCR (RT-PCR) and immunohistochemistry and the correlations between their expressions and clinical indexes were analyzed. Furthermore, their clinical significance on glioma prognosis was determined by follow-up data. Results: The mRNA positive rate of ACTL8, CTCFL, OIP5 and XAGE3 was 15.74% (17/108), 22.22% (24/108), 13.89% (15/108) and 37.96% (41/108), respectively. At least one CTA mRNA was expressed by 61.11% of glioma tissues, while 2 or more by 29.63%. For protein expression, the positive rate of them was 21.30% (23/108), 34.26% (37/108), 19.44% (21/108) and 23.15% (25/108), respectively. At least one CTA protein was expressed by 58.33% of glioma tissues and 2 or more by 29.63%. Although there were no correlations between their mRNA expressions and clinicopathological parameters, the protein expression of ACTL8, OIP5 and XAGE3 was positively correlated with KPS; while the ACTL8 protein was correlated with gender, and OIP5 protein with gender and WHO grade. Kaplan-Meier analysis revealed a significant negative correlation between the CTCFL protein expression, combined ACTL8 and/or CTCFL protein expression and survival. Conclusions: The results suggest that the cohort of glioma does express ACTL8, CTCFL, OIP5 and XAGE3 at both mRNA and protein levels indicating glioma is CTAs-rich tumors. CTCFL protein and the combined ACTL8 and/or CTCFL protein might act as poor prognostic markers for glioma and as potential ideal combined antigens for glioma immunotherapy.

目的 检测和明确癌-睾丸相关抗原(CTA)CT23基因在人脑肿瘤中的表达情况,评估该基因潜在的临床价值.方法 收集广西医科大学第一附属医院神经外科14例颅脑肿瘤病理标本,包括星形细胞瘤5例,髓母细胞瘤4例,胶质母细胞瘤5例,使用RT-PCR技术检测CT23基因在不同病理类型的脑肿瘤中的表达情况,比较其在不同类型脑肿瘤中的表达差异.结果 14例脑肿瘤样本中13例CT23表达阳性,其中星形细胞瘤4例,胶质母细胞瘤5例,髓母细胞瘤4例,CT23基因在三类脑肿瘤样本中的表达比较,差异无统计学意义(P>0.05).结论 CT23基因作为一种肿瘤相关的基因,可表达于多种类型的人类脑肿瘤中,另外该基因的表达与脑肿瘤的发生、发展可能有关.

Cancer testis antigens (CTAs) are attractive targets for tumor immunotherapy because of their tumor-specific expression. Since more than half of confirmed CTAs are located on the X-chromosome, we asked whether there is a link between CTA expression and X-chromosomes. Recent reports have shown that reactivation of the inactive X-chromosome, known as X-chromosome reactivation (XCR), a unique phenomenon that exists in many high-risk tumors in women, can transform the expression of many X-linked genes from monoallelic to biallelic. In this review, we discuss the link between CTA and XCR with the hopes of providing some novel insights into tumor biology.

Objective To investigate the approaches,techniques and efficacies ofmicrosurgical resection ofpetroclival meningiomas.Methods A total of 59 patients with petroclival meningiomas,admitted to our hospital from January 2003 to January 2016,were chosen in our study;single microscopic resection was performed in 55 patients (93.2％) and re-operation was performed in 4 patients (6.8％);29 times (46.0％) via retrosigmoid approach,17 times (27.0％) via tranpetrosal approach,and 17 time via subtemporal approach (27.0％) were chosen.The clinical data,radiological findings,surgical records and outcomes of patients were retrospectively analyzed,and the prognostic factors was analyzed.Results Complete resection was achieved in 31 patients (52.5％),subtotal resection in 19 (21.7％) and partial resection in 9 (15.3％).There was no death in perioperative period.Follow-up were obtained in 55 patients,and median follow-up was 42.6 months (ranged 3-131 months).Permanent neurological damage occurred in 16 patients (27％).Tumor recurred in 11 patients:6 had gamma knife radiosurgery,one had routine radiotherapy,and 4 required re-operation.Two patients died of tumor recurrence/progression reoperation.In these 55 patients,42 enjoyed good prognosis and 13 had poor prognosis.The tumor sizes,brainstem edema and preoperative Kamofsky performance scale scores were unfavorable prognostic factors.Conclusion By using appropriate approaches,surgical strategies and techniques,the petroclival meningiomas can be removed with relatively favorable outcome.

Glioblastoma(GBM) is a highly malignant tumor. Despite various treatment modalities, such as surgery, radiotherapy and chemotherapy, most patients with GBM are still dying of its recurrence. The prognosis of patients with GBM is extremely poor, which is related to not only tumor cell invasion and proliferation, but also immature tumor monitoring methods. For a long time, many studies have found that circulating tumor cells(CTCs) can be detected in patients' blood. It plays an extremely important role in the recurrence of GBM. Therefore, the CTCs detection technology of glioblastoma and its clinical significance have been a hotspot in the present research.

The aim of the present study was to evaluate the clinical importance of melanoma-associated antigen D4 (MAGE-D4) expression in glioma, and to identify it as a valuable prognostic biomarker and therapeutic target. To achieve this, the expression of MAGE-D4 protein in 124 tumor tissues from patients with glioma was measured using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry (IHC), and the associations between MAGE-D4expression and clinicopathological factors were evaluated. The survival analysis demonstrated the significant prognostic value of MAGE-D4 in glioma using follow-up data. RT-qPCR and IHC analysis confirmed that MAGE-D4 mRNA and protein expression levels were significantly increased in glioma tissues compared with those in normal brain tissues. The present study demonstrated that the percentage of glioma tissues with high expression of MAGE-D4 mRNA was 67.74%, and the percentage positive for MAGE-D4 protein expression was 78.23%. All patients with high MAGE-D4 expression in cancerous tissues experienced significantly reduced median overall survival (OS; 18.00 vs. 33.29 months; P<0.001) and recurrence-free survival (RFS; 12.7 vs. 28.3 months; P<0.001) times compared with those with low MAGE-D4 expression. In the patients with lower grade glioma [World Health Organization (WHO), I-II], similar results were obtained for the OS (26.11 vs. 57.85 months; P=0.013) and RFS (22.7 vs. 55.3 months; P=0.010) times; however, in patients with high-grade glioma (WHO, III-IV), there were no significant differences between high and low MAGE-D4 expression levels with regard to OS and RFS times (P>0.05). Multivariate analysis indicated that high MAGE-D4 protein expression was an important independent prognostic factor for patients with glioma (hazard ratio, 2.384; P=0.005), and was significantly associated with higher grade glioma (P<0.001). These results indicated that MAGE-D4 may be a potential biomarker for glioma and an important prognostic factor for patients with new or recurring glioma.

目的 探讨miR-200a在肝细胞癌(HCC)组织及癌旁组织中的表达及其临床意义.方法 采用实时荧光定量PCR检测HCC组织和癌旁组织中miR-200a的表达水平,并结合患者临床资料进行分析.结果 miR-200a在HCC组织中的表达水平明显低于癌旁组织,两者比较差异有统计学意义(P<0.05);miR-200a在HCC组织中的表达水平与患者病理分级有关(P<0.05),但与其他临床病理指标均无关(P>0.05).结论 miR-200a在HCC组织中表达下调,可能与肝癌发生有关,有望成为HCC早期诊治的靶标.