非小细胞肺癌患者ＸＲＣＣ１基因多态性对ｐ５３基因突变发生的影响

目的：观察非小细胞肺癌（ＮＳＣＬＣ）患者ＸＲＣＣ１基因３９９位点多态性以及吸烟对ｐ５３基因突变发生的影响。方法：运用不对称ＰＣＲ技术扩增ｐ５３基因的第５～８外显子,用聚合酶链反应 单链构象多态性分析法（ＰＣＲ-ＳＳＣＰ）检测ｐ５３基因突变,并对有差异的结果测序验证;运用ＰＣＲ技术扩增ＸＲＣＣ１基因的第１０外显子,从正反两个方向对扩增片段进行ＤＮＡ测序分析其多态性;同时了解吸烟与它们的关系。结果：３８例可手术的ＮＳＣＬＣ患者中发现１６例有ｐ５３基因的突变,发生突变的１６例中６例至少携带１个ＸＲＣＣ１-３９９Ｇｌｎ等位基因,１０例为野生基因型ＸＲＣＣ１-３９９Ａｒｇ／Ａｒｇ,用二项分类Ｌｏｇｉｓｔｉｃ回归模型分析ＸＲＣＣ１-３９９Ｇｌｎ多态性与ｐ５３基因突变两者的关系,优势比（ＯＲ）为１.５３６（９５％ＣＩ：０.３７６～６.２８０）;该模型中吸烟与ｐ５３基因突变的ＯＲ为１.５２４（９５％ＣＩ：０.２５０～９.２９５）。结论：ＮＳＣＬＣ患者中,ＸＲＣＣ１基因３９９位点多态性和吸烟情况对ｐ５３基因突变发生无明显影响。     

结直肠癌ＣＯＸ-２蛋白表达水平及其与临床关系的Ｍｅｔａ分析

目的　系统评价环氧化酶 ２（ＣＯＸ ２）在结直肠癌中表达水平及其与临床病理特征的关系。方法　计算机检索ＣｏｃｈｒａｎｅＬｉｂｒａｒｙ、ＰｕｂＭｅｄ、ＣＮＫＩ等数据库,按照纳入与排除标准选择研究文献,评价质量及提取资料后采用Ｓｔａｔａ１１.０软件对数据库进行系统评价。结果　共纳入１４项研究,其中结直肠癌患者１２００例,正常对照２７６例。Ｍｅｔａ分析结果显示：（１）ＣＯＸ-２在结直肠癌组及正常对照组中的表达差异有统计学意义（ＯＲ＝２４.４９,９５％ＣＩ＝１５.９５～３７.６０,Ｐ＝０.０００）;（２）ＣＯＸ-２表达水平与结直肠癌临床病理特征的关系为：男性与女性（ＯＲ＝１.７７,９５％ＣＩ＝０.７９～３.９４,Ｐ＝０.１６５）,年龄＜５０岁与≥５０岁（ＯＲ＝０.５２,９５％ＣＩ＝０.２４～１.１１,Ｐ＝０.０８９）,结肠癌与直肠癌（ＯＲ＝０.９８,９５％ＣＩ＝０.７０～１.３９,Ｐ＝０.９２４）,Ｔ１＋Ｔ２与Ｔ３＋Ｔ４（ＯＲ＝２.３７,９５％ＣＩ＝０.９６～５.８９,Ｐ＝０.０６３）,肿瘤直径≥５ｃｍ与＜５ｃｍ（ＯＲ＝３.０７,９５％ＣＩ＝１.９４～４.８６,Ｐ＝０.０００）,淋巴结转移与无淋巴结转移（ＯＲ＝３.０８,９５％ＣＩ＝１.７３～５.４８,Ｐ＝０.０００）,Ｄｕｋｅｓ分期中Ｃ＋Ｄ期与Ａ＋Ｂ期（ＯＲ＝３.０８,９５％ＣＩ＝１.２５～７.６１,Ｐ＝０.００２）,低分化与高、中分化（ＯＲ＝１.７０,９５％ＣＩ＝１.０６～２.７３,Ｐ＝０.０２７）。结论　ＣＯＸ-２在结直肠癌中表达增高,且其高表达增加了结直肠癌恶性行为发生的危险。     

T－LYMPHOCYTE MEDIATED TUMOR CELL DESTRUCTIONIN VIVO ASSOCIATING WITH A SPECIFICFEATURE OF APOPTOSIS

Ｔ－ＬＹＭＰＨＯＣＹＴＥＭＥＤＩＡＴＥＤＴＵＭＯＲＣＥＬＬＤＥＳＴＲＵＣＴＩＯＮＩＮＶＩＶＯＡＳＳＯＣＩＡＴＩＮＧＷＩＴＨＡＳＰＥＣＩＦＩＣＦＥＡＴＵＲＥ　ＯＦ　ＡＰＯＰＴＯＳＩＳＹｕＤａ鱼达；ＹａｎｇＨｕａ杨骅；ＺｈｅｎｇＳｈｕ郑树；ＷａｎｇＸｉａ...     

THE IN VITRO POTENTIATION OF LAK CELL CYTOTOXICITY IN CANCER AND AIDS PATIENTS INDUCED BY F3—A FRACTIONATED EXTRACT OF ASTRAG

ＴＨＥＩＮＶＩＴＲＯＰＯＴＥＮＴＩＡＴＩＯＮＯＦＬＡＫＣＥＬＬＣＹＴＯＴＯＸＩＣＩＴＹＩＮＣＡＮＣＥＲＡＮＤＡＩＤＳＰＡＴＩＥＮＴＳＩＮＤＵＣＥＤＢＹＦ３—ＡＦＲＡＣＴＩＯＮＡＴＥＤＥＸＴＲＡＣＴＯＦＡＳＴＲＡＧＡＬＵＳＭＥＭＢＲＡＮＡＣＥＵＳＣｈｕ...     

THE EXPRESSION OF C－MYC AND N－RAS ONCOGENES IN HUMAN HEPATOCELLULAR CARCINOMA－AN IN SITU HYBRIDIZATION STUDY ON PARAFFIN EMBE

ＴＨＥＥＸＰＲＥＳＳＩＯＮＯＦＣ－ＭＹＣＡＮＤＮ－ＲＡＳＯＮＣＯＧＥＮＥＳＩＮＨＵＭＡＮＨＥＰＡＴＯＣＥＬＬＵＬＡＲＣＡＲＣＩＮＯＭＡ－ＡＮＩＮＳＩＴＵＨＹＢＲＩＤＩＺＡＴＩＯＮＳＴＵＤＹＯＮＰＡＲＡＦＦＩＮＥＭＢＥＤＤＥＤＴＩＳＳＵＥＳＥＣＴＩＯＮ...     

晚期非小细胞肺癌ＧＳＴＰ１、ＸＲＣＣ１基因多态性与铂类药物疗效的关系

目的　探讨谷胱甘肽Ｓ转移酶Ｐ１（ＧＳＴＰ１）和Ｘ线修复交叉互补基因１（ＸＲＣＣ１）基因多态性与晚期非小细胞肺癌（ＮＳＣＬＣ）患者化疗疗效的关系。方法　经病理学确诊的晚期ＮＳＣＬＣ患者９４例,化疗前取静脉血采用ＤＮＡ测序法检测ＧＳＴＰ１和ＸＲＣＣ１基因多态性,给予铂类为主方案化疗（顺铂７５ｍｇ／ｍ２,ｄ１）,２～３周期后评价疗效,记录疾病进展时间（ＴＴＰ）,分析ＧＳＴＰ１和ＸＲＣＣ１基因多态性与化疗疗效的关系。结果　在９４例晚期ＮＳＣＬＣ患者中,携带ＧＳＴＰ１Ａ／Ａ基因４９例,Ｇ／Ａ基因３４例,Ｇ／Ｇ基因１１例;携带ＸＲＣＣ１Ｇ／Ｇ基因５２例,Ｇ／Ａ基因３５例,Ａ／Ａ基因７例,均符合Ｈａｒｄｙ Ｗｅｉｎｂｅｒｇ遗传平衡规律。携带ＧＳＴＰ１Ｇ／Ａ＋Ｇ／Ｇ基因型的有效率为４４.４４％,显著高于Ａ／Ａ基因型的２０.４１％（Ｐ＜０.０５）;携带ＸＲＣＣ１Ｇ／Ｇ基因型与Ｇ／Ａ＋Ａ／Ａ基因型的有效率差异无统计学意义（Ｐ＞０.０５）;两基因多态性的联合分析显示,同时携带ＧＳＴＰ１Ｇ／Ａ＋Ｇ／Ｇ和ＸＲＣＣ１Ｇ／Ａ＋Ａ／Ａ基因型的有效率最高,为６６.６７％,但未见统计学意义（Ｐ＞０.０５）。９４例患者中有５例失访,８９例患者的中位ＴＴＰ为６.５个月,携带ＧＳＴＰ１Ｇ／Ａ＋Ｇ／Ｇ基因型的中位ＴＴＰ为８.０个月,Ａ／Ａ基因型为６.０个月,两者差异有统计学意义（Ｐ＜０.０１）;携带ＸＲＣＣ１Ｇ／Ｇ基因型的中位ＴＴＰ为７.０个月,Ｇ／Ａ＋Ａ／Ａ基因型为６.５个月,两者差异无统计学意义（Ｐ＞０.０５）;联合分析显示同时携带ＧＳＴＰ１Ｇ／Ａ＋Ｇ／Ｇ和ＸＲＣＣ１Ｇ／Ａ＋Ａ／Ａ基因型的中位ＴＴＰ最长,为９.５个月,各组间差异有统计学意义（Ｐ＜０.０１）。结论　ＧＳＴＰ１基因多态性与晚期ＮＳＣＬＣ患者接受铂类为主化疗方案的疗效及预后有关,同时携带ＧＳＴＰ１Ｇ／Ａ＋Ｇ／Ｇ和ＸＲＣＣ１Ｇ／Ａ＋Ａ／Ａ基因型患者的化疗有效率高,预后好,但因样本量较小,需要扩大样本进一步验证。     

A MOLECULAR EPIDEMIOLOGIC MARKER OF HEPATOCELLULAR CARCINOMA FROM AFLATOXIN B1 CONTAMINATED AREA IN THE SOUTHWEST OF GUANGXI

ＡＭＯＬＥＣＵＬＡＲＥＰＩＤＥＭＩＯＬＯＧＩＣＭＡＲＫＥＲＯＦＨＥＰＡＴＯＣＥＬＬＵＬＡＲＣＡＲＣＩＮＯＭＡＦＲＯＭＡＦＬＡＴＯＸＩＮＢ１ＣＯＮＴＡＭＩＮＡＴＥＤＡＲＥＡＩＮＴＨＥＳＯＵＴＨＷＥＳＴＯＦＧＵＡＮＧＸＩＤｅｎｇＺｈｕｏｌｉｎ邓卓霖ＭａＹ...     

THE EFFECT OF ACTIVE COMPONENTS OF LYCIUM BARBARUM AND GARLIC（LB－GO）ON THE SYNTHESIS OF DNA AND ULTRASTRUCTURE OF U_（14） CERV

ＴＨＥＥＦＦＥＣＴＯＦＡＣＴＩＶＥＣＯＭＰＯＮＥＮＴＳＯＦＬＹＣＩＵＭＢＡＲＢＡＲＵＭＡＮＤＧＡＲＬＩＣ（ＬＢ－ＧＯ）ＯＮＴＨＥＳＹＮＴＨＥＳＩＳＯＦＤＮＡＡＮＤＵＬＴＲＡＳＴＲＵＣＴＵＲＥＯＦＵ_（１４）ＣＥＲＶＩＸＣＡＮＣＥＲＣＥＬＬＳＩＮＭＩＣ?..     

EXPRESSION OF EBV LATENT MEMBRANE PROTEIN IN ESOPHAGEAL CARCINOMA AND PARA-CANCEROUS MUCOSA

ＥＸＰＲＥＳＳＩＯＮＯＦＥＢＶＬＡＴＥＮＴＭＥＭＢＲＡＮＥＰＲＯＴＥＩＮＩＮＥＳＯＰＨＡＧＥＡＬＣＡＲＣＩＮＯＭＡＡＮＤＰＡＲＡＣＡＮＣＥＲＯＵＳＭＵＣＯＳＡＷｕＭｉｎｇｙａｏ吴名耀ＬｉａｎｇＹｉｎｇｒｕｉ梁英锐ＷｕＸｉａｎｙｉｎｇ吴贤英Ｄｅｐａｒ...     

A MICROCOMPUTER PROGRAM FOR CALCULATINGTHE CONFIDENCE INTERVALS OF SURVIVAL PROBABILITY IN MEDICAL FOLLOW－UP STUDIES

ＡＭＩＣＲＯＣＯＭＰＵＴＥＲＰＲＯＧＲＡＭＦＯＲＣＡＬＣＵＬＡＴＩＮＧＴＨＥＣＯＮＦＩＤＥＮＣＥＩＮＴＥＲＶＡＬＳＯＦＳＵＲＶＩＶＡＬＰＲＯＢＡＢＩＬＩＴＹＩＮＭＥＤＩＣＡＬＦＯＬＬＯＷ－ＵＰＳＴＵＤＩＥＳＸｉａｎｇｙｏｎｇｂｉｎｇ项永兵；Ｇａｏｙｕ...     

P21^WAF-1和cyclinD1蛋白在食管鳞癌组织中表达的研究

目的研究P21^WAF-1和cyclinD1在食管鳞状细胞癌组织中的表达及与临床病理的相关性。方法用免疫组化方法检测80例食管鳞癌标本和80例正常食管组织中P21和cyclinD1蛋白的表达水平。结果P21蛋白和cyclinD1蛋白在食管鳞癌组织中的表达均明显增加,与癌细胞的分化程度、肿瘤的TNM分期密切相关。P21在正常食管黏膜生发层细胞中也有少量的表达。结论1921与cyclinD1参于调节细胞的生长周期,P21可以作为临床预测食管鳞癌预后的潜在的指标。     

p21cip1和p27kip1基因遗传多态与食管癌及贲门癌发病风险的关联

背景与目的：有研究表明p21^cip1和p27^kip1的基因多态性与乳腺癌、肺癌、前列腺癌等肿瘤易感性有关。本研究分析中国北方高发区人群食管鳞状细胞癌（ESCC）和贲门腺癌（GCA）与勺p21^cip1和p27^kip1基因多态性之间的关系。方法：应用聚合酶链反应-限制性片段长度多态性（PCR—RFLP）方法检测299例ESCC患者、256例GCA患者及437名健康对照人群p21^cip1 3’非翻译区和p27^kip1第109位密码子基因多态性分布情况。结果：ESCC患者组p21^cip1 T等位基因型频率（42．8％）显著高于健康对照组（36．7％）（P=0．02）,ESCC和GCA患者组p27^kip1等位基因型频率（分别为96．8％和96．1％）均显著高于健康对照组（92．9％）（P值分别为0．00和0．02）。ESCC患者组p21^cip1基因型频率分布与健康对照组相比有显著性差异（P=0．04）,与C／C和C／T基因型相比,T／T基因型可显著增加ESCC的发病风险（校正OR=1．93,95％CI=1．12～3．94）ESCC和GCA患者细p27^kip1基因型频率分布与健康对照组相比均有显著性差异（P分别为0．00和0．01）,与V／G和G／G基因型相比,V／V基因型可显著增加ESCC和GCA的发病风险（校正OR分别为2．44和2．01,95％CI分别为1．2l～4．02和1.12～3．68）。当按吸烟和上消化道肿瘤家族史状况进行分层分析时发现,与V／G和G／G基因型相比,V／V基因型可显著增加吸烟人群患ESCC和GCA（校正OR分别为2．24和2．61,95％C1分别为1.14～4．03和1．25～3．82）以及有家族史人群患ESCC的发病风险（校正OR=2．04,95%CI=1．04～3．43）．两基因联合分析显示,携带p21^cip1T／T和p27^kip1V／V基因型可显著增加患食管癌和贲门癌的发病风险（校正OR分别为3．78和2．56,95?分别为1．46～5．89和1．06～4．78）。结论：在中国北方人群中,p21^cip1基因多态性可能与食管癌的易感性有关,p27^kip1基因多态性可能与食管癌和贲门癌的易感性有关．而且这两个基因的多念性可能存食管癌和贲门癌发病中起联合作用．     

Hypermethylation-associated inactivation of retinoic acid receptor beta in human esophageal squamous cell carcinoma.

PURPOSE: The purpose of this study was to investigate the mechanism of altered retinoic acid receptor beta (RARbeta) expression during esophageal squamous carcinogenesis. EXPERIMENTAL DESIGN: Samples were collected from Linzhou, China. The hypermethylation of CpG islands in the promoter region of the RARbeta gene was examined by methylation-specific PCR in human esophageal squamous cell carcinoma (ESCC) samples, as well as in neighboring tissues with normal epithelium, basal cell hyperplasia, and dysplasia. RARbeta mRNA expression was determined by in situ hybridization. The DNA methyltransferase inhibitor 2'-deoxy-5-azacytidine was used to treat the ESCC cell line, and the DNA hypermethylation status and mRNA expression level were examined. RESULTS: Two of 17 (12%) normal, 9 of 21 basal cell hyperplasia (43%), 7 of 12 dysplasia (58%), and 14 of 20 ESCC (70%) samples had hypermethylation of the RARbeta promoter region. The loss of RARbeta mRNA expression was highly concordant with RARbeta promoter CpG island hypermethylation when individual samples were considered in the correlation analysis. Good statistical correlation between hypermethylation and loss of RARbeta expression was revealed. Frequencies of hypermethylation appeared to increase with the progression of carcinogenesis. In samples from the same patients, if hypermethylation was detected in earlier lesions, it was usually observed in more severe lesions. In the ESCC cell line KYSE 510, 2'-deoxy-5-azacytidine partially reversed CpG island hypermethylation and restored RARbeta mRNA expression. CONCLUSIONS: The results suggest that hypermethylation of RARbeta promoter region is an important mechanism for RARbeta gene silencing in esophageal squamous carcinogenesis.     

Inactivation of DNA repair gene O6-methylguanine-DNA methyltransferase by promoter hypermethylation and its relation to p53 mutations in esophageal squamous cell carcinoma

The development of esophageal squamous cell carcinoma (ESCC) has been linked to exposure to carcinogens such as nitrosamines that cause various alkyl DNA damages and O6-methylguanine-DNA methyltransferase (MGMT) is a primary defence against alkylation-induced mutagenesis and carcinogenesis. This study was to investigate the role of inactivation of MGMT by promoter hypermethylation and its relation to p53 mutations in ESCC. Methylation of MGMT promoter was determined by methylation-specific polymerase chain reaction in 119 ESCC specimens, 22 corresponding tissue samples adjacent to the tumors, and 21 normal epithelial specimens of the esophagus. The levels of MGMT protein in ESCC with methylated or unmethylated MGMT were analyzed by quantitative immunohistochemistry. Mutations of p53 in 119 ESCC were detected by denaturing high-performance liquid chromatography and sequencing. We found that all 21 normal esophageal tissues had unmethylated MGMT; however, among 119 ESCC, 46 (38.7%) had hypermethylated MGMT. This epigenetic change also occurred in some normal tissues adjacent to the tumors. The level of MGMT protein in MGMT-methylated ESCC was significantly lower than that in MGMT-unmethylated ESCC, whereas great inter-individual variation and poor expression was also observed among MGMT-unmethylated ESCC. Fifty-one percent (61/119) ESCC showed p53 mutations but the distribution of the mutations did not differ significantly between MGMT-methylated ESCC (44%) and MGMT-unmethylated ESCC (56.2%; P = 0.18). MGMT promoter hypermethylation was neither associated with overall G:C to A:T mutations nor associated with this type of mutations in non-CpG dinucleotides in p53. Our results demonstrate that inactivation of MGMT by aberrant promoter methylation is a frequent molecular event in ESCC. This epigenetic alteration is an important, but may not be the sole, mechanism leading to the impaired expression of MGMT. Aberrant MGMT methylation seemed not to be associated with overall frequency and spectrum of p53 mutations in ESCC.     

Clinical impact of serum exosomal microRNA‐21 as a clinical biomarker in human esophageal squamous cell carcinoma

BACKGROUND:

Exosomes are 40‐nm to 100‐nm membrane vesicles that are secreted by various cells, and they play a major role in cell‐cell communication. The objective of this study was to clarify the significance of the levels of microRNA in exosomes extracted from the sera of patients with esophageal squamous cell cancer (ESCC).

METHODS:

The authors isolated exosomes in serum samples from patients who had ESCC and from patients who had benign diseases without systemic inflammation. Total RNA was purified from the exosomes, and expression levels of microRNA‐21 (miR‐21) were analyzed by quantitative real‐time polymerase chain reaction.

RESULTS:

Serum exosomes from patients with ESCC induced the proliferation of ESCC cells in vitro. The expression levels of exosomal miR‐21 were significantly higher in patients with ESCC than those with benign diseases with and without (C‐reactive protein <0.3 mg/dL) systemic inflammation. MiR‐21 was not detected in serum that remained after exosome extraction. Exosomal miR‐21 expression was correlated with advanced tumor classification, positive lymph node status, and the presence of metastasis with inflammation or and clinical stage without inflammation (C‐reactive protein <0.3 mg/dL).

CONCLUSIONS:

The current results confirmed that exosomal miR‐21 expression is up‐regulated in serum from patients with ESCC versus serum from patients who have benign diseases without systemic inflammation. Exosomal miR‐21 was positively correlated with tumor progression and aggressiveness, suggesting that it may be a useful target for cancer therapy. Cancer 2013. © 2012 American Cancer Society.     

Overexpression of human pituitary tumor transforming gene (hPTTG), is regulated by beta-catenin /TCF pathway in human esophageal squamous cell carcinoma

Overexpression of human pituitary tumor transforming gene (PTTG) is wildly detected in many tumors, including esophageal cancer. Besides overexpression of PTTG in esophageal squamous cell carcinoma (ESCC) tissues and cells, we detected accumulation of cytoplasmic beta-catenin in ESCC. In our study, a putative TCF4-binding element (TBE) was identified in PTTG promoter region. The activity of PTTG promoter containing the TBE was activated by S37Abeta-catenin and inhibited by dominant-negative TCF. Furthermore, the activation by S37Abeta-catenin was mostly abrogated among PTTG promoter region without the TBE or with a mutant one. By using biotin-streptavidin pull-down assay, we also found that the TBE among PTTG promoter bound to TCF-4 protein. Moreover, levels of PTTG mRNA and protein were increased by S37Abeta-catenin. Finally, it is noticeable that we detected a correlation between beta-catenin localization and PTTG expression in 69 primary ESCC (p<0.01). In brief, our study shows that overexpression of PTTG in ESCC is likely due to the activation of beta-catenin/WNT signaling. As a target gene of beta-catenin/TCF pathway, PTTG may play an important role in tumorigenesis of human ESCC.     

食管鳞状细胞癌118例肿瘤标志物HSP90α联合Cyfra21-1和CEA检测临床意义

目的目前食管鳞状细胞癌(esophageal squamous cell carcinoma,ESCC)尚缺乏灵敏度高的诊断标志物,大多数患者确诊时已到中晚期且预后不良。本研究探讨热休克蛋白90α(heat shock protein 90α,HSP90α)、细胞角蛋白片段19抗原21-1(cytokeratin fragment 19antigen 21-1,Cyfra21-1)和癌胚抗原(carcinoembryonic antigen,CEA)联合检测对ESCC患者的诊断价值及其临床意义。方法选取2016-01-06-2018-12-10山东省肿瘤医院血液采集时未接受放化疗及手术治疗的118例ESCC患者为研究对象并采集血样,同期收集33名健康体检者血液标本。采用酶联免疫吸附测定法检测血浆HSP90α表达水平,采用电化学发光法检测血清Cyfra21-1和CEA表达水平。ROC曲线评估3个指标单独或联合检测对ESCC的诊断效能,各指标表达与食管癌患者临床病理因素的关联分析采用χ^2检验。结果 ESCC患者中HSP90α、Cyfra21-1和CEA中位数(四分位间距)分别为62.535(45.190~107.708)、3.365(2.038~4.633)和3.545(2.190~5.000)ng/mL,均高于对照组的48.882(36.190~64.033)、1.970(1.590~2.380)和1.990(1.990~2.635)ng/mL,差异有统计学意义,Z值分别为-3.566、-4.131和-4.829,均P=0。ESCC患者中HSP90α、Cyfra21-1和CEA阳性表达与患者的肿瘤大小、远端转移及TNM分期,差异均有统计学意义,P<0.05。ESCCⅣ期患者HSP90α、Cyfra21-1及CEA表达水平高于Ⅲ期患者,差异有统计学意义,P<0.05。ESCC患者中HSP90α与Cyfra21-1、CEA联合检测双阳性率分别为31.36%和34.75%,表达呈正相关(r=0.23,P=0.012;r=0.397,P=0)。HSP90α与Cyfra21-1、CEA联合检测对ESCC患者的诊断灵敏度为78.0%,特异性为72.8%,曲线下面积为0.862。结论肿瘤标志物HSP90α和Cyfra21-1、CEA在ESCC患者中呈现高表达状况,联合检测能够提高ESCC患者的诊断灵敏性和特异性,3种肿瘤标志物联合检测对于ESCC早期诊断与评估分期有一定价值。     

Serum miR-21 expression in human esophageal squamous cell carcinomas

To investigate the relationship between serum miRNA-21 (miR-21) expression in esophageal squamous cell carcinomas (ESCCs) and their clinicopathologic features, a 1:1 matched case-control study including 21 patients with ESCC and 21 age- and gender-matched healthy controls was carried out. Serum specimens were taken from all subjects. Total RNA was extracted and the stem-loop real time polymerase chain reaction was used to measure serum miR-21 in both groups. Clinical parameters were assessed to determine associations with serum miR-21 concentrations. Serum miR-21 expression in ESCC samples was significantly higher than in paired cancer-free samples (P <0.05). Metastasis was associated with mir-21 expression in serum (P <0.05), ESCC patients with metastasis having 8.4-fold higher serum miR-21 concentrations than healthy controls. There were no statistically significant associations between miR-21 expression and clinicopathologic parameters, such as gender (P >0.05), age (P >0.05), tumor location (P >0.05), cell differentiation (P >0.05), TNM staging (P >0.05), whether chemo/radiotherapy had been administered (P >0.05), or whether surgery had been performed (P >0.05). These findings suggest that the detection of microRNA-21 in serum might serve as a new tumor biomarker in diagnosis and assessment of prognosis of ESCCs.