枸杞多糖对肝癌患者血清AFP、PHCA、VEGF及CTGF水平的影响

目的:探讨枸杞多糖对原发性肝癌患者血清中甲胎蛋白(AFP)、人肝癌抗原(PHCA)、血管内皮生长因子(VEGF)及结缔组织生长因子(CTGF)水平的影响。方法:选取我院诊治的原发性肝癌患者84例为研究对象,根据治疗方案分为两组,其中对照组41例给予肝动脉化疔栓塞术(TACE)治疗,实验组43例在对照组基础上给予枸杞多糖治疗。用酶联免疫吸附法对两组患者治疗前后血清中VEGF、CTGF及PHCA水平进行检测,应用电化学发光法对AFP进行检测,并比较两组患者的临床疗效。结果:干预前,两组的AFP以及PHCA水平无显著差异(P0.05);干预后,实验组AFP及PHCA水平显著低于对照组,差异具有统计学意义(P0.05);干预后,实验组患者VEGF和CTGF下降幅度显著明显高于对照组,差异具有统计学意义(P0.05);干预后,实验组治疗有效率(76.74%)显著高于对照组(60.98%),差异具有统计学意义(P0.05)。与同期对照组比较,实验组生存率较高,不良反应发生率较低,差异具有统计学意义,P0.05。结论:枸杞多糖能够降低原发性肝癌患者的血清AFP、PHCA、VEG以及CTGF水平,提高原发性肝癌治疗效果。     

AFP、AFU、β2-MG、CA199联合检测对原发性肝癌的早期诊断价值

目的:探讨原发性肝癌患者血清甲胎蛋白(AFP)、а-L岩藻糖苷酶(AFU)、β2-微球蛋白(β2-MG)、糖类抗原-199(CA199)的含量及其联合检测对原发性肝癌的早期诊断价值。方法:选择56例原发性肝癌患者、60名肝炎肝硬化患者和60名健康对照作为研究对象,分别应用比值法和化学发光法、生化法检测其血清AFP、AFU、β2-MG、CA199的含量。结果:原发性肝癌患者血清AFP、AFU、β2-MG、CA199含量均显着高于肝炎肝硬化组及健康对照组,差异均有统计学意义(P均<0.05);联合检测AFP、AFU、β2-MG、CA199四种肿瘤标志物,其阳性率达(85.7%)明显高于AFP(53.6%)、AFU(55.4%)、β2-MG(48.2%)和CA199(42.9%)单项检测组(P均<0.05);且AFP、AFU、β2-MG、CA199四种肿瘤标志物联合检测的敏感性均高于单一检测指标,差异有统计学意义(P<0.05),但其特异性显著低于AFU、β2-MG单项检测(P<0.05)。结论:联合检测血清AFP、AFU、β2-MG、CA199含量可以提高对原发性肝癌的阳性诊断率,对诊断及鉴别诊断原发性肝癌具有重要意义。     

肝动脉导管化疗栓塞序贯经皮微波消融治疗原发性肝癌的临床应用

目的:探讨肝动脉导管化疗栓塞(TACE)序贯B超/CT精准引导下经皮微波消融(MWA)在原发性肝癌中的治疗应用,分析比较疗效。方法:回顾性分析2016年1月至2018年7月在上海交通大学附属第一人民医院接受治疗的96例原发性肝癌患者,42例行TACE序贯联合B超/CT精准引导下MWA治疗(联合组),另54例仅行单纯TACE治疗(TACE组)。术后1月、3月、6月、1年、2年复查增强CT/MRI、AFP、肝功能,随访2年比较两组患者肿瘤坏死、复发、进展和生存情况,评价两组疗效。结果:联合组肿瘤坏死率92.9%,TACE组肿瘤坏死率48.1%,差异有统计学意义(P0.05);联合组肿瘤复发率7.1%,TACE组肿瘤复发率24.1%,差异有统计学意义(P0.05);联合组肿瘤进展率19.1%,TACE组肿瘤进展率27.8%,差异无统计学意义(P0.05);联合组肿瘤进展时间13.2个月,TACE组肿瘤进展时间7.6个月,差异有统计学差异(P0.05);联合组1年生存率83.3%,TACE组1年生存率57.4%,差异有统计学意义(P0.05);联合组2年生存率62%,TACE组2年生存率31.5%,差异有统计学意义(P0.05);联合组中位生存时间28.9个月,TACE组中位生存时间16.9个月,差异有统计学意义(P0.05)。结论:TACE序贯MWA治疗肝癌安全有效,互补增益,是肝癌综合治疗的新模式。     

肝动脉插管栓塞化疗后原发性肝癌血清AFP变化与疗效的关系

目的探讨肝动脉插管栓塞化疗(TACE)后原发性肝癌患者血清AFP变化与疗效的关系。方法对TACE治疗的64例原发性肝癌患者,于介入前、介入后1月,行上腹部CT检查以及测定患者血清AFP水平,观察其疗效和AFP值变化。结果有效组(包括PR组和SD组)44例介入前后AFP值比较差异具有显著性(P0.05),PD组20例介入前后AFP值比较差异有显著性(P0.05)。PR组(22例)和SD组(22例)介入前后AFP差值比较,差异无显著性(P0.50)。结论原发性肝癌患者血清AFP水平的变化对评价TACE疗效具有重要的临床价值。     

血清PIVKA-Ⅱ与AFP检测在原发性肝细胞癌诊断中的应用

为探究血清PIVKA-Ⅱ与AFP检测在原发性肝细胞癌诊断中的优劣性,对237例患者的血清PIVKA-Ⅱ与AFP进行检测,其中乙肝病毒相关性原发性肝细胞癌(hepatocellular carcinoma, HCC)患者115例、乙肝携带者(asymptomatic carrier, As C) 55例、乙肝病毒相关肝硬化(liver cirrhosis, LC)患者47例、非肝癌肿瘤患者20例。检测结果显示:肝癌组PIVKA-Ⅱ的中位表达量高于非肝癌组(包括As C组、LC组、非肝癌肿瘤组), P均小于0.05;使用AFP、PIVKA-Ⅱ和AFP+PIVKA-Ⅱ诊断肝癌的灵敏度分别为67.8%、81.7%和90.4%,对应的ROC曲线下面积为0.881、0.945和0.962, PIVKA-Ⅱ检测肝癌的cut-off值为32 m AU/m L。已有研究报道以40 m AU/m L为PIVKA-Ⅱ的cut-off值,本研究根据PIVKA-Ⅱ是否≥40 m AU/m L将HCC组分为PIVKA-Ⅱ≥40组、PIVKA-Ⅱ40组,对两组患者的性别、年龄、病毒载量、肿瘤分期、癌结节数目、肿块直径和是否抗病毒治疗进行比较,采用logistic回归分析两组患者的差异性指标,结果显示病毒载量[OR=1.150, 95%CI (1.022, 1.295), P=0.02]为PIVKA-Ⅱ检测肝癌的独立影响因素。相关分析表明PIVKA-Ⅱ与肝癌肿块直径呈正相关。此外, AFP、PIVKA-Ⅱ的cut-off值分组结果表明, PIVKA-Ⅱ≥32且AFP20组的肝癌肿块直径大于PIVKA-Ⅱ32且AFP≥20组(P=0.035)。因此, PIVKA-Ⅱ是优于AFP筛查肝细胞癌的血清学肿瘤标志物,其表达量与肿瘤肿块直径呈正相关。     

miR-224在原发性肝癌患者血清中的表达及意义

目的：原发性肝癌（primary hepatocellular carcinoma,PHC）作为常见的恶性程度极高的肿瘤,严重威胁着人类的生命。miR-224是近年来发现的一个肿瘤相关miRNA分子,在肿瘤的发生及发展过程中发挥着重要的作用。本研究通过测定原发性肝癌患者血清中miR-224的表达水平,探讨血清miR．224与原发性肝癌预后的关系。方法：采用实时荧光定量RT-PCR（Real-timeRT．PCR）方法。分别检测40例原发性肝癌患者,20例慢性肝炎患者,20例慢性肝硬化患者及20例正常人的血清标本中miR-224的表达水平。分析血清miR-224的表达水平与AFP和MMP-9的相关性。结果：原发性肝癌患者血清miR-224的表达水平明显高于正常人、慢性肝炎和慢性肝硬化患者（P〈0．05）。皮尔森相关分析结果显示原发性肝癌患者血清miR-224的表达与AFP和MMP．9呈正相关。血清miR-224低表达组术后复发／转移率显著低于高表达组,术后生存率则高于高表达组（P〈0．01）。结论：miR-224在原发性肝癌患者的血清中呈高表达,其血清表达水平与原发性肝癌的临床预后密切相关。这提示我们,miR-224可能成为新的原发性肝癌检测标记物和潜在的原发性肝癌预后分子标志物。     

HER-2/neu基因高表达及靶向治疗

HER-2/neu癌基因在许多肿瘤,如乳腺癌、卵巢癌、非小细胞肺癌等肿瘤中高表达,在肿瘤的发生与发展中起重要作用,与肿瘤的转化、转移、复发、预后差、患者生存期缩短有关。HER-2/neu在乳腺癌过度表达率约为20%～30%,编码蛋白P185HER2属生长因子受体家族,抗P185HER2单克隆抗体(Herceptin)作为靶向药物已临床应用治疗HER2/neu高表达乳腺癌。     

血清AFP,CEA,CA125单独或联合检测对原发性肝癌早期诊断的临床价值研究

目的:探讨血清中甲胎蛋白(AFP)、癌胚抗原(CEA)、糖类抗原125(CA125)单独以及联合检测对于原发性肝癌的早期诊断临床价值。方法:选择2012年1月~2016年6月在我院检验科确诊的120例原发性肝癌患者作为观察组,并以80例健康志愿者作为对照组,检测和比较两组的AFP、CEA和CA125水平,分析血清AFP、CEA、CA125单项及联合检测检出原发性肝癌的阳性率和约登指数。结果:观察组血清AFP(319.53±35.78 ng/mL)、CEA(81.4±27.8 ng/mL)、CA125(20.67±4.61 ng/mL)水平均明显高于健康对照组(P0.05)。血清AFP、CEA、CA125在单独检测时诊断原发性肝癌的敏感性分别为65%(78/120)、75%(90/120)和60%(72/120),而三者的联合检测能够使检测的敏感性达到92%(112/120),显著高于单独检测时的敏感度(P0.05)。血清AFP、CEA、CA125单项检测约登指数均显著低于联合检测(P0.05)。结论:相较于血清AFP、CEA、CA125的单独检测,三者联合检测可明显提高原发性肝癌的检出率。     

MRI扫描联合血清4项肿瘤标志物诊断原发性肝癌的临床价值研究

目的:探究磁共振成像(MRI)扫描联合血清4项肿瘤标志物诊断原发性肝癌(PHC)的临床价值。方法:将我院从2017年9月~2019年8月收治的65例PHC患者(肝癌组)纳入研究,另选取同期我院收治的60例良性肝病患者作为对照组。比较两组MRI图像特征。此外,检测并比较两组血清甲胎蛋白(AFP)和甲胎蛋白异质体(AFP-L3)、高尔基体蛋白73(GP73)、磷脂酰肌醇蛋白聚糖-3(GPC-3)水平。以病理诊断为金标准,分析不同诊断方式应用于PHC患者诊断中的效能。结果:PHC患者的MRI图像表现为边界清晰,呈类圆形或不规则分叶状,肝癌组T1WI呈低或稍低信号人数占比高于对照组,且T2WI、DWI呈高信号强度人数占比高于对照组(均P<0.05)。肝癌组血清AFP、AFP-L3、GP73、GPC-3水平均高于对照组(均P<0.05)。以病理诊断为金标准,MRI联合血清AFP、AFP-L3、GP73、GPC-3诊断PHC的灵敏度、特异度以及准确度分别为95.24%(40/42)、95.65%(22/23)、95.38%(62/65),均高于MRI诊断的73.81%(31/42)、69.57%(16/23)、72.31%(47/65)(P<0.05),以及血清4项肿瘤标志物联合诊断的80.95%(34/42)、73.91%(17/23)、78.46%(51/65)(P<0.05)。结论:PHC患者血清AFP、AFP-L3、GP73、GPC-3水平升高,MRI扫描联合血清AFP、AFP-L3、GP73、GPC-3检测可作为诊断PHC的有效手段。     

AFU, AFP, GP73和GPC3联合检测对原发性肝癌的诊断价值

目的:研究α-L-岩藻糖苷酶(AFU)、甲种胎儿球蛋白(AFP)、高尔基体蛋白73(GP73)和磷脂酰肌醇蛋白聚糖3(GPC3)联合检测对原发性肝癌的诊断价值。方法:选择2014年1月~2016年5月在我院进行诊治的原发性肝癌患者90例为肝癌组,同期住院诊治的肝硬化患者60例为肝硬化组,以及同期在我院体检健康者60例为对照组。比较三组的AFU、AFP、GP73和GPC3水平和阳性检出率,并观察AFU、AFP、GP73和GPC3单独检测和联合检测对原发性肝癌的诊断效率。结果:肝癌组和肝硬化组的AFU、AFP、GP73和GPC3水平均明显高于对照组(P0.05),且肝癌组明显高于肝硬化组(P0.05);肝癌组和肝硬化组的AFU、AFP、GP73和GPC3阳性率均明显高于对照组(P0.05),且肝癌组明显高于肝硬化组(P0.05);AFU、AFP、GP73和GPC3联合检测对原发性肝癌的特异性、敏感性、阳性预测值及阴性预测值均明显高于单独检测和三项指标联合检测(P0.05)。结论:AFU、AFP、GP73和GPC3联合检测可以提高对原发性肝癌的检出率,具有较高的临床应用价值。     

Topoisomerase IIalpha gene (TOP2A) amplification and deletion in cancer--more common than anticipated.

In solid tumours the predominant genetic mechanism for oncogene activation is through amplification of genes. The HER-2 (also known as ErbB2/c-erbB2/HER-2/neu) oncogene is the most frequently amplified oncogene in breast cancer and is also commonly amplified in other forms of cancer. The HER-2 amplicon also contains other biologically relevant genes with altered copy numbers, among these genes is the topoisomerase IIalpha (TOP2A). TOP2A gene is located adjacent to the HER-2 oncogene at the chromosome location 17q12-q21 and is either amplified or deleted, with equal frequency, in almost 90% of HER-2 amplified primary breast tumours. Recent data suggest that amplification and deletion of TOP2A may account for both sensitivity and resistance to topoII-inhibitor-chemotherapy, depending on the specific genetic defect at the TOP2A locus. In this issue of the Cytopathology, Bofin et al. present preliminary evidence for high prevalance of TOP2A amplification and deletion not only in the HER-2 amplified breast tumours, but also in the primary breast tumours without the HER-2 amplification. This finding together with the concept that TOP2A gene amplification and deletion seem to account for both relative chemosensitivity and resistance to topoII-inhibitor therapy further highlights the importance of screening for TOP2A gene copy number aberrations when topoII-inhibitors are considered either alone or in combination of other chemotherapeutic drugs for the treatment of cancer patients.     

Determination of HER-2/Neu status in hepatocellular carcinoma cases

Specific chromosome abnormalities and genetic changes in hepatocellular carcinoma (HCC) have been demonstrated by conventional cytogenetic studies or molecular cytogenetic approaches like comparative genomic hybridization and loss of heterozygosity analyses. HER-2/Neu amplification and expression has been studied as a molecular target for treatment of HCC, and there are conflicting results. We aimed to determine HER-2/Neu status in archive materials of HCC patients by fluorescence in situ hybridization (FISH). Among the 35 patients, 2 had HER-2/Neu amplification and 3 had increased chromosome 17 copy number. All these patients had grade 2 or 3 tumor with a diameter of 3-12 cm. We conclude that although HER-2/Neu amplification is not the primary mechanism in the development of liver tumors, it might play a role in one of the steps of multistage carcinogenesis.     

Trastuzumab (Herceptin) in the adjuvant treatment of HER-2-positive early breast cancer

The prognosis of HER-2-positive breast cancer (characterized by amplification of the HER-2 oncogene and/or overexpression of HER-2 receptor) is unfavourable. Trastuzumab (Herceptin), a monoclonal antibody against HER-2 receptor can improve the outcome of HER-2-positive breast cancer. Up to now this was proven only in advanced disease. Recently five large multicentric phase III adjuvant trials gave level one evidence on the benefit of adjuvant treatment with Herceptin, concerning disease-free survival (DFS) and overall survival (OS). Herceptin has decreased the relative risk of recurrence with about 50% and that of death with nearly 30% in HER-2-positive early breast cancer. Based on these results Herceptin, together with chemotherapy, has been recently approved for the adjuvant treatment of HER-2-positive breast cancer.     

Overexpression of ZEB2 in peritumoral liver tissue correlates with favorable survival after curative resection of hepatocellular carcinoma

Background

ZEB2 has been suggested to mediate EMT and disease aggressiveness in several types of human cancers. However, the expression patterns of ZEB2 in hepatocellular carcinoma (HCC) and its effect on prognosis of HCC patients treated with hepatectomy are unclear.

Methodology/Principal Findings

In this study, the methods of tissue microarray and immunohistochemistry (IHC) were utilized to investigate ZEB2 expression in HCC and peritumoral liver tissue (PLT). Receiver operating characteristic (ROC), spearman''s rank correlation, Kaplan-Meier plots and Cox proportional hazards regression model were used to analyze the data. Up-regulated expression of cytoplasmic/nuclear ZEB2 protein was observed in the majority of PLTs, when compared to HCCs. Further analysis showed that overexpression of cytoplasmic ZEB2 in HCCs was inversely correlated with AFP level, tumor size and differentiation (P<0.05). Also, overexpression of cytoplasmic ZEB2 in PLTs correlated with lower AFP level (P<0.05). In univariate survival analysis, a significant association between overexpression of cytoplasmic ZEB2 by HCCs/PLTs and longer patients'' survival was found (P<0.05). Importantly, cytoplasmic ZEB2 expression in PLTs was evaluated as an independent prognostic factor in multivariate analysis (P<0.05). Consequently, a new clinicopathologic prognostic model with cytoplasmic ZEB2 expression (including HCCs and PLTs) was constructed. The model could significantly stratify risk (low, intermediate and high) for overall survival (P = 0.002).

Conclusions/Significance

Our findings provide a basis for the concept that cytoplasmic ZEB2 expressed by PLTs can predict the postoperative survival of patients with HCC. The combined cytoplasmic ZEB2 prognostic model may become a useful tool for identifying patients with different clinical outcomes.     

Allele loss and down-regulation of heparanase gene are associated with the progression and poor prognosis of hepatocellular carcinoma

Objectives

The role of heparanase (HPSE) gene in cancers including hepatocellular carcinoma (HCC) is currently controversial. This study was aimed at investigating the impact of genetic alteration and expression change of HPSE on the progression and prognosis of HCC.

Methods

The HPSE gene was studied in three different aspects: (1) loss of heterozygosity (LOH) by a custom SNP microarray and DNA copy number by real-time PCR; (2) mRNA level by qRT-PCR; and (3) protein expression by immunohistochemistry. The clinical significances of allele loss and expression change of HPSE were analyzed.

Results

Microarray analysis showed that the average LOH frequency for 10 SNPs located within HPSE gene was 31.6%, three of which were significantly correlated with tumor grade, serum HBV-DNA level, and AFP concentration. In agreement with SNP LOH data, DNA copy number loss of HPSE was observed in 38.74% (43/111) of HCC cases. HPSE mRNA level was notably reduced in 74.1% (83/112) of tumor tissues compared with non-tumor liver tissues, which was significantly associated with DNA copy number loss, increased tumor size, and post-operative metastasis. HPSE protein level was also remarkably reduced in 66.3% (53/80) of tumor tissues, which was correlated with tumor grade. Patients with lower expression level of HPSE mRNA or protein had a significantly lower survival rate than those with higher expression. Cox regression analysis suggested that HPSE protein was an independent predictor of overall survival in HCC patients.

Conclusions

The results in this study demonstrate that genetic alteration and reduction of HPSE expression are associated with tumor progression and poor prognosis of HCCs, suggesting that HPSE behaves like a tumor suppressor gene and is a potential prognostic marker for HCC patients.     

Recent developments in the first detection of hepatocellular carcinoma

Hepatocellular carcinoma (HCC) ranks fifth in frequency of cancers worldwide. The main aetiological factor is hepatitis B virus (HBV) although the importance of hepatitis C virus (HCV) is growing. The most important tumour marker for HCC is alpha-fetoprotein (AFP). The common method of screening high risk patients by AFP and ultrasonography has been shown to result in earlier detection and consequently more easily treatable tumours and longer survival. Proposed screening interval varies from once every 3 months to annually to "as indicated' but, most commonly, is once every 6 months. AFP is a fairly specific but insensitive marker for HCC. Sensitivity of HCC detection by blood markers is improved by combining various other markers with AFP. Of the other markers, the newer high sensitivity des-gamma-carboxy-prothrombin (DCP) has been found to be useful. In addition the AFP fractions L3, P4/5 and the +II band are highly specific for HCC. Among routinely assayed tumour markers in the laboratory, CA 125 is more sensitive for HCC than AFP but far less specific. Various other enzymes, isoenzymes, growth factors, adhesion molecules, other proteins such as interleukin-2 receptor (IL-2R), human cervical cancer oncogene protein (HCCR) and glypican-3 (GPC3), p15 and p16 hypermethylation and nitrite/nitrate ratio have been tested; some of these show promise but none is presently in routine use. The value of other newer markers such as the HBx protein that is produced by HBV, and what are thought to be specific proteins and signatures identified by proteomics remain to be determined.     

HepPar1, MOC-31, pCEA, mCEA and CD10 for distinguishing hepatocellular carcinoma vs. metastatic adenocarcinoma in liver fine needle aspirates

OBJECTIVE: To investigate immunohistochemical staining of hepatocyte paraffin-1 (HepPar1), alpha-fetoprotein (AFP), polyclonal carcinoembryonic antigen (pCEA), monoclonal CEA (mCEA), MOC-31 and CD10 for differential diagnosis of hepatocellular carcinoma (HCC) from metastatic adenocarcinoma (MA) on fine needle aspiration biopsy (FNAB). STUDY DESIGN: Fifty-one archival, paraffin-embedded FNAB cell blocks, representing 18 HCCs and 33 MAs, were immunostained with antibodies for AFP, CD10, pCEA, mCEA, HepPar1 and MOC-31. RESULTS: HepPar1, AFP, canalicular pCEA and CD10 were positive in 78% (14 of 18), 28% (5 of 18), 72% (13 of 18) and 35% (6 of 17) of cases of HCC, respectively. The 33 MAs were negative for immunostaining of the above antibodies except for one AFP-positive MA. Ninety-seven percent (31 of 32) of the MAs and 6% (1 of 17) of the HCCs were positive for MOC-31. Monoclonal CEA was immunoreactive on 82% (27 of 33) of the MAs and negative on all the HCCs. CONCLUSION: HepPar1 was the most sensitive marker for HCC, followed by canalicular staining for pCEA. For MA, MOC-31 was the most sensitive marker; mCEA was slightly less sensitive but more specific. We suggest using HepPar1, pCEA, CD10, MOC-31 and mCEA as a panel for distinguishing HCC from MA in liver FNAB.     

乙型肝炎病毒驱动甲胎蛋白表达诱导肝细胞恶性转化的分子机制

肝癌细胞的恶性转化与感染乙型肝炎病毒（hepatitis B virus, HBV）和丙型肝炎病毒密切相关．但是HBV没有直接诱导肝癌发生的生物学功能,HBV可通过其x蛋白（HBx）激活生长信号,促进癌基因的表达从而诱导肝细胞恶性转化．在肝细胞恶性转化过程的早期,甲胎蛋白（alpha fetoprotein, AFP）基因被激活,而AFP能激发PI3K/AKT信号传递,由于PI3K/AKT信号途径具有促进细胞恶性转化的作用,所以AFP的表达在HBV诱导肝细胞恶性转化过程发挥关键性作用．本文就HBV通过优先驱动AFP表达促进肝癌细胞增殖和自然重编程从而诱发肝癌的分子机制进行阐述,对认识AFP在HBV相关性肝癌发生过程中的作用以及预警肝癌发生有重要的科学意义．     

Detection and monitoring of HBV-related hepatocellular carcinoma from plasma cfDNA fragmentation profiles

Most hepatocellular carcinomas (HCCs) are associated with hepatitis B virus infection (HBV) in China. Early detection of HCC can significantly improve prognosis but is not yet fully clinically feasible. This study aims to develop methods for detecting HCC and studying the carcinogenesis of HBV using plasma cell-free DNA (cfDNA) whole-genome sequencing (WGS) data. Low coverage WGS was performed for 452 participants, including healthy individuals, hepatitis B patients, cirrhosis patients, and HCC patients. Then the sequencing data were processed using various machine learning models based on cfDNA fragmentation profiles for cancer detection. Our best model achieved a sensitivity of 87.10% and a specificity of 88.37%, and it showed an increased sensitivity with higher BCLC stages of HCC. Overall, this study proves the potential of a non-invasive assay based on cfDNA fragmentation profiles for the detection and prognosis of HCC and provides preliminary data on the carcinogenic mechanism of HBV.     

Preliminary evaluation of HER-2/neu oncogene and epidermal growth factor receptor expression in normal and neoplastic human ovaries.

The HER-2/neu oncogene (a member of the Erb-like oncogene family) is distinct from but closely related to the c-erb B gene which encodes the epidermal growth factor receptor (EGFr). HER-2/neu gene amplification was found in a large number of mammary carcinomas and there was a strong correlation between this phenomenon and poor prognosis. In our study HER-2/neu oncogene expression was determined in 16 malignant ovarian tumors, 2 ovarian lymphomas and 5 normal ovaries. The HER-2/neu gene was found both in normal ovaries and malignant tumors, without any apparent difference among the various histological types. In all the specimens examined, HER-2/neu expression did not seem to be related to EGF binding capacity.