简介:质子放射疗法在hepatocellular癌(HCC)的治疗看见了一个增加的角色。历史上,外部横梁放射疗法由于毒性的高发生在HCC起了一个很有限的作用到包围正常结构。把放射的高剂量送到肿瘤的能力是在在HCC改进结果的一个关键因素。在光子放射疗法的进展改进了剂量一致并且允许剂量逐步上升到肿瘤。然而,尽管有这些进展,仍然有一个大量正常的肝,在处理期间收到可观的放射剂量。一旦他们进入身体,质子横梁没沿着横梁路径有出口剂量。质子放射疗法的固有的物理属性提供一个方法当避免过多的放射到留下的肝时,经由剂量逐步上升最大化肿瘤控制,因此增加的生物有效性。在这评论,我们在HCC为质子放射疗法讨论物理属性和基本原理。我们也关于为HCC的处理使用质子放射疗法的临床的结果考察最近的文学。
简介:AbstractMetabolic (dysfunction) associated fatty liver disease (MAFLD), previously known as non-alcoholic fatty liver disease, is the most common cause of chronic liver disease worldwide. Many risk factors contribute to the pathogenesis of MAFLD with metabolic dysregulation being the final arbiter of its development and progression. MAFLD poses a substantial economic burden to societies, which based on current trends is expected to increase over time. Numerous studies have addressed various aspects of MAFLD from its risk associations to its economic and social burden and clinical diagnosis and management, as well as the molecular mechanisms linking MAFLD to end-stage liver disease and hepatocellular carcinoma. This review summarizes current understanding of the pathogenesis of MAFLD and related diseases, particularly liver cancer. Potential therapeutic agents for MAFLD and diagnostic biomarkers are discussed.
简介:CLINICOPATHOLOGICFEATURESANDDIAGNOSISOFCOMBINEDHEPATOCELLULARANDCHOLANGIOCARCINOMALuJianping路建平;CaiWeimin蔡为民;HayashiKeiki1林肇辉...
简介:尽管有在动物模型获得的出色的结果,船边交货ligand(FasL)的临床的使用被严重毒性作为anticancer药限制。死亡ligands的全身的毒性可以被使用编码膜界限死亡ligands的基因阻止,由指向的transgene,通过也的表示指向了transduction或指向了抄写。肿瘤房间死亡的选择正式就职是有希望的anticancer策略。熔化蛋白质被熔化船边交货ligand(FasL)的细胞外的领域到有选择地在肿瘤endothelial房间上指向av3-integrins的肽arginine-glycine-aspartic酸(RGD)创造。这研究的目的是在鼠科的hepatocellular癌(HCC)在肿瘤生长和幸存上评估RGD-FasL的效果肿瘤模型。有与FasL作为与那相比在HCC肿瘤模型上显示明显的镇压效果的RGD-FasL的处理(p<0.05)并且在这个模型在肿瘤生长延期上导致了更多的添加剂效果。RGD-FasL处理显著地提高了老鼠幸存并且没引起有毒的效果,例如重量损失,机关失败,或另外的处理相关的毒性。Apoptosis被流动cytometric分析和TUNEL试金检测;那些结果也证明RGD-FasL比FasL是为H22和H9101房间线的房间apoptosis的更多的有势力inducer(p<0.05)。在结论,RGD-FasL看起来是肿瘤房间死亡的低毒性的选择inducer,它在现出症状之前的潜、临床的研究应得进一步的调查。而且,这条途径与治疗学的recombinant蛋白质为complexing目标ligands提供一种万用的技术。为了在vivo,肿瘤和肝区分FasL的反肿瘤效果,纸巾被收获由染色的Hematoxylin和曙红(H&E)为坏死的房间,肿瘤房间,或apoptotic房间的证据检验。
简介:Hepatocellularcarcinoma(HCC),thepredominantformofadultlivermalignancies,isaglobalhealthconcern.Itsdismalprognosishaspromptedrecentsignificantadvancesintheunderstandingofitsetiologyandpathogenesis.Thederegulationofepigeneticmechanisms,whichmaintainheritablegeneexpressionchangesandchromatinorganization,isimplicatedinthedevelopmentofmultiplecancers,includingHCC.ThisreviewsummarizesthecurrentknowledgeofepigeneticmechanismsinthepathogenesisofHCC,withanemphasisonHCCmediatedbychronichepatitisBvirusinfection.Thisreviewalsodiscussestheencouragingoutcomesandlessonslearntfromepigenetictherapiesforhematologicalandothersolidcancers,andhighlightsthefuturepotentialofsimilartherapiesinthetreatmentofHCC.
简介:WithDNA-mRNAhybridizationinsitutechnique,theexpressionoffiveoncogenes,c-N-ras,c-Ki-ras.c-Ha-ras,c-mycandc-fos,wasobservedintwocasesofhumanhepatocellularcarcinoma.Theexpressionofc-N-ras&c-foswasgreatlyenhancedintumortissuesofthetwocases,andabout25%-50%ofthetumorcellsshowedpositiveexpression.Theotherthreeoncogenesnamelyc-Ki-ras,c-Ha-ras&c-myc,werenotdetectedinthesetwocarcinomasorinthenon-cancerouslivertissuesadjacenttothecarcinomas.Itissurmisedthatc-N-rasandc-fosmayplaycoordinativeroleinmaintainingthemalignantphenotypeofhumanprimaryhepatocellularcarcinoma.
简介:流行病学的研究为长期的肝炎B的一个原因的角色提供了压到优势的证据在hepatocellular癌(HCC)的发展的病毒(HBV)感染。然而,HBV感染的致病和联系HBV的HCC的carcinogenesis仍然是逃犯的。这评论将在涉及HBV相关的肝carcinogenesis的机制上总结当前的知识。在肿瘤形成的HBV的角色出现到复杂,并且可以包含直接、间接的机制。进主人染色体的HBVDNA的集成发生在同种细胞的肿瘤的早步扩大,和它被显示了提高主人chromosomal不稳定性,导致大转换复制,删除和chromosomaltranslocations。chromosomal改变的率在HBV相关的肿瘤显著地被增加,这被显示出。病毒的规章的HBVx蛋白质的延长表示可以贡献调整表明小径的细胞的抄写,蛋白质降级,增长,和apoptotic,并且它在hepatocellular癌的发展起一个关键作用。
简介:目的将在hepatocellular癌(HCC)调查cortactin表示并且在HCC病人的预后探索它的意义。方法Immunohistochemistry被执行让119HCC纸巾(HCC)和paratumorous肝纸巾(PTLT)的石蜡样品计算cortactin表达式。在HCC和PTLT的cortactin表示差别被McNemars测试分析。在HCC和clinicopathologic因素的cortactin表情的关系与Mann-WhitneyU测试被分析。Kaplan-Meier方法和木头等级测试被采用比较在Cortactin否定表示组,弱表示组和强壮的表示组之间的全面幸存。cortactin的表示进一步与西方的弄污在19个新鲜HCC和PTLT标本被决定。结果Cortactin表示率在HCC是显著地更高的(53/119,44.5%)比那在PTLT(2/119,1.7%)(P<0.001)。在HCC的upregulatedcortactin表示显著地被相关到形成(P=0.012),脉管的侵略(P=0.037)和高Edmondson啤酒杯杯分级的囊的缺席(P=0.020),并且预言了更短的全面幸存。西方的弄污证明那cortactin表情与相应PTLT相比从19HCC(47.4%)是在9的upregulated。结论Cortactin表示是在HCC的upregulated并且与病人的更短的全面幸存有关,建议cortactin可能起在HCC的转移的作用并且预言HCC病人的差的预后。
简介:Theeffectofportalveintumorthrombus(PVTT)ontheprognosisofpatientswithhepatocellularcarcinomahasbecomeclearoverthepastseveraldecades.However,identifyingthemechanismsandperformingthediagnosisandtreatmentofPVTTremainchallenging.Therefore,thisstudyaimedtosummarizetheprogressintheseareas.AcomputerizedliteraturesearchinMedlineandEMBASEwasperformedwiththefollowingcombinationsofsearchterms:'hepatocellularcarcinoma'AND'portalveintumorthrombus.'AlthoughseveralsignaltransductionormolecularpathwaysrelatedtoPVTThavebeenidentified,theexactmechanismsofPVTTarestilllargelyunknown.Manybiomarkershavebeenreportedtodetectmicrovascularinvasion,butnonehaveprovedtobeclinicallyusefulbecauseoftheirlowaccuracyrates.SorafenibistheonlyrecommendedtherapeuticstrategyinWesterncountries.However,moretreatmentoptionsarerecommendedinEasterncountries,includingsurgery,radiotherapy(RT),transhepaticarterialchemoembolization(TACE),transarterialradioembolization(TARE),andsorafenib.Therefore,weestablishedastagingsystembasedontheextentofportalveininvasion.Ourstagingsystemeffectivelypredictsthelong-termsurvivalofPVTTpatients.Currently,severalclinicaltrialshadshownthatsurgeryiseffectiveandsafeinsomePVTTpatients.RT,TARE,andTACEcanalsobeperformedsafelyinpatientswithgoodliverfunction.However,onlyafewcomparativeclinicaltrialshadcomparedtheeffectivenessofthesetreatments.Therefore,morerandomizedcontrolledtrialsexaminingtheextentofPVTTshouldbeconductedinthefuture.
简介:AIM:Toevaluatetheshort-andlong-termoutcomesofliverresectionforcaudatelobehepatocellularcarcinoma(HCC).METHODS:Weretrospectivelyanalyzed114consecutivepatientswithHCC,originatingfromthecaudatelobe,whounderwentresectionbetweenJanuary2001andJanuary2007.Univariateandmultivariateanalyseswereperformedonseveralclinicopathologicvariablestodeterminethefactorsaffectinglong-termoutcomeandintrahepaticrecurrence.RESULTS:Overallmortalityandmorbiditywere0%and18%,respectively.Afteramedianfollow-upof31mo(interquartilerange,11-66mo),tumorrecurrencehadoccurredin76patients(66.7%).The1-,3-,and5-yeardisease-freesurvivalrateswere65.7%,38.1%,and18.4%,respectively.The1-,3-,and5-yearoverallsurvivalrateswere76.1%,54.7%,and31.8%,respectively.Univariateanalysisshowedthatsubsegmentallocationofthetumor(45.7%vs16.2%,P=0.01),livercirrhosis(12.3%vs47.9%,P=0.03),surgicalmargin(18.5%vs54.6%,P=0.04),vascularinvasion(37.9%vs23.2%,P=0.04)andextendedcaudateresection(42.1%vs15.4%,P=0.04)wererelatedtopoorerlong-termsurvival.Multivariateanalysisshowedthatonlysubsegmentallocationofthetumor,livercirrhosisandsurgicalmarginweresignificantindependentprognosticfactors.CONCLUSION:HepatectomywasaneffectivetreatmentforHCCinthecaudatelobe.Thesubsegmentallocationofthetumor,livercirrhosisandsurgicalmarginaffectedlong-termsurvival.
简介:客观:在人的hepatocellular癌(HCC)在HLA医生表示上调查干扰素(IFN)的管理效果。方法:房间衬里的在4种HCC的HLA医生的表示,HHCC,SMMC-7721,BEL-7402,HCC-9204和一个正常的肝房间衬里QZG在被IFN-或IFN-的不同剂量刺激前后与immunohistochemicalABC和ELISA方法被检测。结果:仅仅SMMC-7721房间的小部分表示了另外的房间线的HLA医生,和所有是在有IFN-或IFN-的刺激前否定的HLA医生。HLA医生表示在刺激以后5根房间线在所有被提高,并且它与IFN的剂量被相关。QZG房间不比HCC房间明显。IFN-的效果比IFN-的更明显。结论:IFN能在HCC房间提高HLA医生表示。
简介:瞄准:在人的肝细胞癌(HCC)检验E-cadherin的免疫反应和catenin家庭的四种子类型并且调查在HCC病人的E-cadherin/catenin复杂、临床病理的参数的表示之间的关联。方法:免疫为E-cadherin和catenins的组织化学的学习在HCC的97个修理福尔马林的、嵌入石蜡的标本上被执行。结果:E-cadherin的减少的表示,alpha-,贝它--,gamma-catenin和p120分别地在69%,76%,63%,71%和73%被观察。E-cadherin和catenin部件的两表示显著地与肿瘤等级被相关(P=0.000)。它显示出在catenin成员和肿瘤舞台的表示之间的有效差量(P=0.003,P=0.017,P=0.007并且P=0.000,分别地)。在HCC的E-cadherin的减少的表示显著地与肝内转移(IM)和胶囊的侵略被相关(P=0.008,P=0.03,分别地)。靠近的关联也在catenins和肿瘤尺寸的表示之间被观察(P=0.002,P=0.034,P=0.016并且P=0.000,分别地)。另外,每catenin的表示被发现与IM相关(P=0.012,P=0.049,P=0.026并且P=0.014,分别地)。不,统计上,有效差量在E-cadherin/catenin建筑群和淋巴节点允许的表达式水平之间被观察,脉管的侵略和卫星小瘤。有趣地,仅仅p120的表示与法新社价值显示出关联(P=0.035)。E-cadherin的表示与alpha-一致,贝它--,gamma-catenin和p120表示(P=0.000)。最后,E-cadherin/catenin建筑群的反常表示显著地与病人的幸存被联系(P=0.0253,P=0.0052,P=0.003,P=0.0105并且P=0.0016,分别地)。不过,E-cadherin/catenin建筑群的部件都不是HCC病人的独立预示的因素。结论:E-cadherin,catenins和p120的下面调整的表达式在HCC经常发生并且贡献肿瘤的前进和开发。检测复杂的E-cadherin/catenin的合作表示可以比在预言肿瘤侵略,转移和病人是幸存探索他们之一是准确、珍贵的更多。
简介:Objective:IL-22-producingCD4+Thelpercells(Th22cells)havebeenidentifiedasmajorinducersoftissueinflammationandimmuneresponses.Currently,nopreviousstudyexploredtheroleofTh22cellsinthepathogenesisofhepatocellularcarcinoma(HCC).ThestudyaimedtodeterminethebiologicalfunctionofTh22cellsanditseffectorIL-22inHCCpatients.Methods:Forty-fiveHCCpatientsand19healthycontrolswererecruitedandtheirperipheralbloodwascollected.ThefreshHCCtissues,adjacentHCCtissuesandtennormallivertissueswerealsocollected.FlowcytometryanalysiswasusedtodeterminethefrequenciesofcirculatingTh22cellsandTh17cells.SerumIL-22levelsweretestedbyenzyme-linkedimmunosorbentassay(ELISA).Immunohistochemicalstainingandreal-timepolymerasechainreaction(PCR)wereusedtodetectIL-22proteinandmRNAintissuesspecimens,respectively.Results:CirculatingTh22cells,Th17cellsandserumIL-22levelsweresignificantlyelevatedinHCCpatientscomparedwiththoseofhealthycontrols(P<0.001).Th22cellswereshowedtobepositivelycorrelatedwithIL-22inHCCpatients(P<0.05),butnotinhealthycontrols.NosignificantdifferenceswerefoundinHCCpatientswithHBeAgpositivityornegativityintermofTh22cellsandserumIL-22levels.TheexpressionofIL-22proteinandmRNAwashighestinHCCtissues,followedbyadjacentHCCtissuesandnormallivertissues.Furthermore,Th22cells,serumIL-22levelsandIL-22mRNAwereelevatedatstageIII-IVcomparedwithstageI-IIofHCC(P<0.05).Conclusions:ElevationofcirculatingTh22cellsandIL-22maybeimplicatedinthepathogenesisofHCC,andpotentiallybecellulartargetsfortherapeuticintervention.
简介:无
简介:MicroRNAs(miRNAs)areendogenoussmallnon-codingRNAsthatrepresstheirtargetsatposttranscriptionallevel.ExistingstudieshaveshownthatmiRNAsareimportantregulatorygenesinhepatocellularcarcinoma(HCC),aseithertumorsuppressorsoroncogenes.MiR-122isnormallydownregulatedinHCCandregardedasatumorsuppressor.RecentlymiR-122hasbeenreportedtoberegulatedbyCEBPA,whichistheninvolvedinanovelpathwaytoinfluenceproliferationoftumorcells.HoweveritisunknownwhetherCEBPAisregulatedbymiRNAsinHCC.Inthisstudy,wefindthatmiR-182isupregulatedinHCCmodelrat,andrepressesCEBPAinbothratandhuman.ThisfurtherimprovesthecurrentCEBPA/miR-122pathwaythatcontrolstheproliferationoftumorcells.TheseresultssuggestthatmiR-182isapotentialoncogeneinHCCandcouldbeusedasadiagnosticmarkeranddrugtargetofHCC.
简介:瞄准:估计联合transcatheter的效果动脉的chemoembolization(不作声)并且在有大hepatocellular癌(HCC)的病人的经皮的乙醇脱离(豌豆)。方法:有unresectable的63个病人的一个总数大HCC被对待与不作声由豌豆列在后面。肿瘤的最大的尺寸从5.3厘米到17.8厘米。幸存率,尖锐效果,毒性和预示的因素被分析。结果:在1,3和5年的累积幸存率是59.4%,28.4%和15.8%,分别地(27.7瞬间的中部的幸存)。肿瘤区域被超过50%在30减少(47.6%)盒子。在有增加的-fetoprotein(法新社)的56种情况中珍视,法新社水平被超过75%拒绝。联合治疗很好通常被容忍。仅仅二个病人从variceal流血死了与治疗联系了。比例的危险建模的艇长证明肿瘤,肿瘤边缘和乙醇剂量的数字是独立预示的因素。结论:联合不作声并且豌豆治疗是为unresectable的一条有希望的途径大HCC。
简介:AIM:Tostudythediagnosisofhepatocellularcarcinoma(HCC)presentingasbileducttumorthrombuswithnodetectableintrahepaticmass.METHODS:SixpatientswithpathologicallyprovenbileductHCCthrombibutnointrahepaticmassdemonstratedonthepreoperativeimagingorpalpatedintrahepaticmassduringoperativeexploration,werecollected.Theirclinicalandimagingdatawereretrospectivelyanalyzed.Themajorfindingsorsignsoncomprehensiveimagingwerecorrelatedwiththesurgicalandpathologicfindings.RESULTS:Jaundicewasthemajorclinicalsymptomofthepatients.Theelevatedserumtotalbilirubin,directbilirubinandalanineaminotransferaselevelswereinconcordancewithobstructivejaundiceandtheunderlyingliverdisease.Ofthe6patientsshowingevidenceofviralhepatitis,5werepositiveforserumalphafetoproteinandcarbohydrateantigen19-9,and1waspositiveforserumcarcinoembryonicantigen.Nopatientwascorrectlydiagnosedbyultrasound.Themainfeaturesofpatientsoncomprehensiveimagingwerefillingdefectswithcup-shapedendsofthebileduct,withlargefillingdefectspresentingascastingmouldsintheexpandedbileduct,hypervascularintraluminalnodules,debrisorbloodclotsinthebileduct.Noobviouscircularthickeningofthebileductwallswasobserved.CONCLUSION:Evenwithnodetectableintrahepatictumor,bileductHCCthrombusshouldbeconsideredinpatientspredisposedtoHCC,andsomeimagingsignsareindicativeofitsdiagnosis.