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61.
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63.
Enxin Wang Lei Liu Dongdong Xia Wenjun Wang Wei Bai Qiuhe Wang Jie Yuan Xiaomei Li Lei Zhang Jing Niu Zhanxin Yin Jielai Xia Hongwei Cai Daiming Fan Guohong Han 《Journal of vascular and interventional radiology : JVIR》2017,28(7):956-962
Purpose
To investigate treatment outcome, prognostic factors for overall survival, and appropriate candidates for transarterial chemoembolization among patients with hepatocellular carcinoma (HCC) and extrahepatic spread (EHS).Materials and Methods
From January 2010 to June 2014, 111 consecutive patients with HCC and EHS treated by transarterial chemoembolization alone were evaluated. Factors associated with overall survival were evaluated using Cox regression analysis, and a scoring equation was established to subgroup patients with EHS.Results
Median follow-up was 3.8 months, and median overall survival was 3.8 months (95% confidence interval [CI], 2.9–4.7 months). Multivariate analysis demonstrated maximum tumor size ≥ 10 cm (hazard ratio [HR] 1.58; 95% CI, 1.02–2.46; P = .041), multifocal intrahepatic tumors (HR 1.55; 95% CI, 1.03–2.33; P = .037), and portal vein tumor thrombosis (PVTT) (HR 1.81; 95% CI, 1.12–2.91; P = .015) as significant predictors of overall survival. Based on these factors, a scoring equation was developed to predict treatment outcome of transarterial chemoembolization, with an area under the receiver operating characteristic curve of 0.76 in predicting 6-month survival. Using a cutoff score of 5.5, patients with HCC and EHS were divided into 2 groups with significantly different overall survival (8.1 months for EHS1 and 2.4 months for EHS2; P < .001). The described method of subgrouping remained discriminatory regardless of baseline characteristics.Conclusions
Maximum tumor size, intrahepatic tumor distribution, and presence of PVTT were significant determinants of overall survival for patients with HCC and EHS. Transarterial chemoembolization may be appropriate for patients with EHS but lower intrahepatic tumor burden. 相似文献64.
TACE联合PEI治疗原发性肝癌血液循环性肝癌细胞的变化及意义 总被引:2,自引:0,他引:2
目的:探讨联合经肝动脉化疗栓塞术(TACE)及B超引导下肿瘤局部无水酒精注射术(PEI),治疗原发性肝癌周围静脉血液循环性肝癌细胞的变化及其意义.方法:应用巢式RT-PCR检测12例原发性肝癌患者血液循环性肝癌细胞,并经TACE及PEI联合治疗,观察其血液循环性肝癌细胞的变化.结果:血液循环性肝癌细胞表达阳性的5例原发性肝癌患者(41.67%),经TACE及PEI联合治疗后,其血液循环性肝癌细胞均转为阴性(100%,P<0.01).结论:联合TACE及PEI治疗原发性肝癌可有效地杀灭血液中播散的循环性肝癌细胞,可预防肝癌的复发和转移. 相似文献
65.
Hepatocellular carcinoma is the commonest primary liver tumor and its incidence is on an increase.Transplantation and surgical
resection are the gold standard curative treatment options but less than 20%patients are surgical candidates because of advanced
liver disease and/or co-morbidities.Various interventional radiological procedures have been developed and intensively investigated
for treatment of inoperable HCC.This review summarizes the various interventional radiological treatments in HCC including
patient selection, procedural considerations and response evaluation. Transarterial chemoembolization, radioembolization and
radiofrequency ablation are mainly discussed. 相似文献
66.
目的探讨Talin与不同来源人肝癌细胞侵袭及迁移的关系,进而为进一步研究Talin与肝癌的侵袭和迁移的可能机制提供理论基础。方法体外培养人高转移肝癌细胞株(MHCC-97H细胞株)、人低转移肝癌细胞株(MHCC-97L细胞株)、人肝癌SMMC-7721细胞株、人肝癌Be L-7402细胞株、人肝癌He PG-2细胞株及人正常肝脏细胞株(LO2细胞株),RT-PCR技术检测各细胞株中Talin-1的mRNA表达水平,Western-blot技术检测各细胞株中Talin-1的蛋白表达水平,Transwell侵袭和迁移实验及细胞划痕实验检测各细胞株侵袭及迁移能力,软琼脂集落形成实验检测各细胞株增殖和克隆能力。结果五种人肝癌细胞株中Talin-1的mRNA表达水平不同(P0.05),五种人肝癌细胞株中Talin-1蛋白表达水平不同,MHCC-97L细胞株中Talin-1的蛋白表达比LO2细胞株高(P0.05);五种人肝癌细胞株的侵袭能力不同(P0.05),五种人肝癌细胞株的迁移能力不同(P=0.0000),与正常人肝脏细胞相比,五种人肝癌细胞株的增值和克隆能力不同(P=0.00017)结论 Talin-1与肝癌的侵袭和迁移能力相关;高表达Talin-1的原发性肝癌的侵袭和迁移能力低,恶性度低,低表达Talin-1的原发性肝癌的侵袭和迁移强,恶性度高,Talin-1可作为原发性肝癌恶性度的预测指标之一。 相似文献
67.
Takayama T Makuuchi M Kojiro M Lauwers GY Adams RB Wilson SR Jang HJ Charnsangavej C Taouli B 《Annals of surgical oncology》2008,15(4):972-978
Background In 1987, Japanese researchers proposed to define the pathological concept of early hepatocellular carcinoma (HCC). However,
there are some conceptual differences between the East and the West in the diagnosis and treatment of early HCC.
Methods To provide up-to-date data for making a worldwide consensus, this article has collected six papers focused on the management
of early HCC, which were presented in the Fifth International Meeting of “Hepatocellular Carcinoma: Eastern and Western Experiences”
in Houston in January 2007.
Results In the pathological perspective, the common criteria to discriminate early HCC from dysplastic nodule included hepatocytic
invasion of portal triads and septa (stromal invasion). The current imaging modalities such as contrast-enhanced ultrasound
(CEUS), computed tomography (CT), and magnetic resonance imaging (MRI) with the use of intravenous contrast material with
multiphasic imaging could enhance their ability to accurately characterize early HCC. From the treatment perspective, a single
early HCC had a high chance for cure by resection, ablation, or transplantation, which proved to be the earliest clinical
entity (Stage 0 HCC).
Conclusions Early HCC is characterized by its incipient malignant nature and by an extremely favorable clinical outcome, thereby justifying
its definition.
Proceedings of the Fifth International Meeting Hepatocellular Carcinoma: Eastern and Western Experiences held in Houston,
TX, January 11–13, 2007. 相似文献
68.
Ron C. Gaba Nasya Mendoza-Elias Daniel P. Regan Kelly D. Garcia R. Peter Lokken Regina M. Schwind Michael Eichner Faith M. Thomas Lauretta A. Rund Lawrence B. Schook Kyle M. Schachtschneider 《Journal of vascular and interventional radiology : JVIR》2018,29(8):1194-1202.e1
Purpose
This study used the Oncopig Cancer Model (OCM) to develop alcohol-induced fibrosis in a porcine model capable of developing hepatocellular carcinoma.Materials and Methods
Liver injury was induced in 8-week-old Oncopigs (n = 10) via hepatic transarterial infusion of 0.75 mL/kg ethanol-ethiodized oil (1:3 v/v). Feasibility was assessed in an initial Oncopig cohort (n = 5) by histologic analysis at 8 weeks after induction, and METAVIR results were compared to age- and sex-matched healthy controls (n = 5). Liver injury was then induced in a second OCM cohort (n = 5) for a time-course study, with post-induction disease surveillance via biweekly physical exam, lab analysis, and liver biopsies until 20 weeks after induction.Results
In Cohort 1, 8-week post-induction liver histologic analysis revealed median METAVIR F3 (range, F3–F4) fibrosis, A2 (range, A2–A3) inflammation, and 15.3% (range, 5.0%–22.9%) fibrosis. METAVIR and inflammation scores were generally elevated compared to healthy controls (F0–F1, P = 0.0013; A0–A1, P = .0013; median percent fibrosis 8.7%, range, 5.8%–12.1%, P = .064). In Cohort 2, histologic analysis revealed peak fibrosis severity of median METAVIR F3 (range, F2–F3). However, lack of persistent alcohol exposure resulted in liver recovery, with median METAVIR F2 (range, F1–F2) fibrosis at 20 weeks after induction. No behavioral or biochemical abnormalities were observed to indicate liver decompensation.Conclusions
This study successfully validated a protocol to develop METAVIR F3–F4 fibrosis within 8 weeks in the OCM, supporting its potential to serve as a model for hepatocellular carcinoma in a fibrotic liver background. Further investigation is required to determine if repeated alcohol liver injury is required to develop an irreversible METAVIR grade F4 porcine cirrhosis model. 相似文献69.
70.
目的:探究驱动蛋白-13家族2C(KIF2C)对肝细胞癌(HCC)细胞增殖、侵袭和迁移以及人脐静脉内皮细胞(HUVEC)血管生成的影响,为HCC治疗提供潜在靶点。方法:用数据库数据分析KIF2C mRNA和蛋白在HCC组织中的表达及其与血管生成相关因子(VEGFR2 和HIF-1α)表达的相关性,常规培养人正常肝细胞QSG-7701、HUVEC 和HCC细胞Huh-7、Hep3B2.1-7,用 Lipofectamine 3000 转染试剂将 sh-NC 和 sh-KIF2C 转染至 Huh-7、Hep3B2.1-7 细胞,qPCR 检测各组 QSG-7701、Huh-7 和Hep3B2.1-7 细胞中KIF2C mRNA 的表达,WB 法检测各组细胞中KIF2C 蛋白的表达,细胞克隆形成实验检测敲低KIF2C 对Hep3B2.1-7 和Huh-7 细胞克隆形成的影响,小管生成实验检测敲低KIF2C 表达的Huh-7 和Hep3B2.1-7 细胞的条件培养液对HUVEC 血管生成能力的影响。结果:数据库分析结果显示,KIF2C mRNA 和蛋白在HCC 组织中均呈高表达(均P<0.01),用qPCR 和WB法检测人HCC中KIF2C mRNA和蛋白的表达水平,结果显示其mRNA和蛋白在各HCC 细胞中也呈高表达(均P<0.01),与数据库数据分析结果相符。数据库数据分析还显示,KIF2C 与HCC组织中VEGFR2、HIF-1α的表达水平呈正相关(P<0.05 或P<0.01)。成功构建了稳定低表达KIF2C 的Huh-7 和Hep3B2.1-7 细胞(均P<0.01),敲低KIF2C 表达均可明显抑制Huh-7和Hep3B2.1-7细胞的增殖能力(均P<0.01)、侵袭和迁移能力(均P<0.01),敲低KIF2C表达的HCC细胞条件培养液均可显著抑制体外HUVEC的血管生成能力(P<0.05 或P<0.01)。结论:KIF2C可促进Huh-7和Hep3B2.1-7细胞增殖、侵袭和迁移以及HUVEC血管生成的能力,提示KIF2C可能是治疗HCC的潜在靶点 相似文献