简介：AccordingtoGLOBOCAN2012,livercanceristhesixthmostcommoncancerintheworld.Therewere782,000newcasesdiagnosedin2012,with50%inChinaalone.Livercanceristhesecondmostcommoncauseofcancerdeathworldwideanditsprognosisisverypoor.TheWorldHealthOrganization(WHO)declared745,517deathscausedbylivercancerin2012,withmorethanhalffromChina~1.

简介：Primaryandmetastaticlivertumorsareanincreasingglobalhealthproblem,withhepatocellularcarcinoma(HCC)nowbeingthethirdleadingcauseofcancer-relatedmortalityworldwide.SystemictreatmentoptionsforHCCremainlimited,withSorafenibastheonlyprospectivelyvalidatedagentshowntoincreaseoverallsurvival.Surgicalresectionand/ortransplantation,locallyablativetherapiesandregionalorlocoregionaltherapieshavefilledthegapinlivertumortreatments,providingimprovedsurvivaloutcomesforbothprimaryandmetastatictumors.Minimallyinvasivelocaltherapieshaveanincreasingroleinthetreatmentofbothprimaryandmetastaticlivertumors.Forpatientswithlowvolumedisease,thesetherapieshavenowbeenestablishedintoconsensuspracticeguidelines.Thisreviewhighlightstechnicalaspectsandoutcomesofcommonlyutilized,minimallyinvasivelocaltherapiesincludinglaparoscopicliverresection(LLR),radiofrequencyablation(RFA),microwaveablation(MWA),high-intensityfocusedultrasound(HIFU),irreversibleelectroporation(IRE),andstereotacticbodyradiationtherapy(SBRT).Inaddition,theroleofcombinationtreatmentstrategiesutilizingtheseminimallyinvasivetechniquesisreviewed.

简介：ＲＥＳＵＬＴＳＯＦ　ＨＥＰＡＴＥＣＴＯＭＹＦＯＲ６００ＣＡＳＥＳＷＩＴＨＰＲＩＭＡＲＹＬＩＶＥＲＣＡＮＣＥＲＬｉＧｕｏｈｕｉ李国辉；ＬｉＪｉｎｑｉｎｇ李锦清；Ｚｈａｎｇｙａｑｉ张亚奇；Ｙｕａｎｙｕｎｆｅｉ元云飞；ＣｈｅｎＭｉｎｓｈａｎ陈敏山；ＧｕｏＲ...

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简介：Qidong(Jiangsu,China)hasbeenofinteresttocancerepidemiologistsandbiologistsbecause,untilrecently,itwasanendemicareaforlivercancer,havingamongstthehighestincidenceratesintheworld.TheestablishmentoftheQidongCancerRegistrytogetherwiththeQidongLiverCancerInstitutein1972haschartedthepatternsoflivercancerincidenceandmortalityinastablepopulationthroughoutaperiodofenormouseconomic,social,andenvironmentalchangesaswellasofimprovementsinhealthcaredelivery.UpdatedincidencetrendsinQidongaredescribed.Notably,theChinaage-standardizedincidencerateforlivercancerhasdroppedbyover50%inthepastseveraldecades.MolecularepidemiologicandgenomicdeepsequencingstudieshaveaffirmedthatinfectionwithhepatitisBvirusaswellasdietaryexposuretoaflatoxinsthroughcontaminationofdietarystaplessuchascorn,andtomicrocystins–blue-greenalgaltoxinsfoundinditchandpondwater–werelikelyimportantetiologicfactorsthataccountforthehighincidenceoflivercancerinthisregion.PublichealthinitiativestofacilitateuniversalvaccinationofnewbornsagainstHBVandtoimprovedrinkingwatersourcesinthisruralarea,aswellaseconomicandsocialmandatesserendipitouslyfacilitatingdietarydiversity,haveledtoprecipitousdeclinesinexposurestotheseetiologicfactors,concomitantlydrivingsubstantivedeclinesinthelivercancerincidenceseennowinQidong.Inthisregard,Qidongservesasatemplatefortheglobalimpactthatapackageofinterventionstrategiesmayexertoncancerburden.

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简介：Livercancer,primarilyhepatocellularcarcinoma(HCC),isamajorcauseofcancer-relateddeathworldwide.HCCisasuitablemodelofinflammation-inducedcancerbecausemorethan90%ofHCCcasesarecausedbyliverdamageandchronicinflammation.Severalinflammatoryresponsepathways,suchasNF-κBandJAK/STAT3signalingpathways,playrolesinthecrosstalkbetweeninflammationandHCC.MicroRNAs(miRNAs)areevolutionarilyconserved,shortendogenous,non-codingsingle-strandedRNAsthatareinvolvedinvariousbiologicalandpathologicalprocessesbyregulatinggeneexpressionandproteintranslation.EvidenceshowedthatmiRNAsplayapivotalroleinhepatitisvirusinfectionandserveaspromotersorinhibitorsofinflammatoryresponse.AberrantmiRNAwasobservedduringliverinflammationandHCC.ManydysregulatedmiRNAsmodulatetheinitiationandprogressionofinflammation-inducedHCC.ThisreviewsummarizestheroleandfunctionsofmiRNAsininflammation-associatedHCC,aswellasthedesignedtherapeuticstargetingmiRNAstotreatliverinflammationandHCC.

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简介：Objective:LivercancerisoneofthemostcommoncancersandmajorcauseofcancerdeathsinChina,whichaccountsforover50%ofnewcasesanddeathsworldwide.Thesystematiclivercancerstatisticsincludingofprojectionthrough2030couldprovidevaluableinformationforpreventionandcontrolstrategiesinChina,andexperienceforothercountries.Methods:TheburdenoflivercancerinChinain2014wasestimatedusing339cancerregistries’dataselectedfromChineseNationalCancerCenter(NCC).Incidentcasesof22cancerregistrieswereappliedfortemporaltrendsfrom2000to2014.Theburdenoflivercancerthrough2030wasprojectedusingage-period-cohortmodel.Results:About364,800newcasesoflivercancer(268,900malesand95,900females)occurredinChina,andabout318,800livercancerdeaths(233,500malesand85,300females)in2014.WesternregionsofChinahadthehighestincidenceandmortalityrates.Incidenceandmortalityratesdecreasedbyabout2.3%and2.6%peryearduringtheperiodof2000-2014,respectively,andwoulddecreasebymorethan44%between2014and2030inChina.Theyounggeneration,particularlyforthoseagedunder40years,showedafasterdowntrend.Conclusions:Basedontheanalysis,incidenceandmortalityratesoflivercancerareexpectedtodecreasethrough2030,buttheburdenoflivercancerisstillseriousinChina,especiallyinruralandwesternareas.MostcasesoflivercancerinChinacanbepreventedthroughvaccinationandmorepreventioneffortsshouldbefocusedonhighriskgroups.

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简介：客观；在忍受肝癌症的老鼠调查鼠科的IL-12基因和HSV-TK基因治疗的synergistic反肿瘤效果。方法：老鼠肝癌症MM45T李(H-2d)房间是有包含IL-12基因或HSV-TK基因的retroviral向量的transfected插入修改基因的肝癌症房间，MM45TLi/IL-12和MM45TLi/TK，与IL-12和TK的稳定的表示被获得。Balb/c老鼠与2X105MM45T李房间皮下地被接种。当肿瘤到达了0.5鈥?.0厘米的一种尺寸时，MM45T.Li/TK房间的混合物照耀and60Co的MM45TLi/IL-12房间intratumoraly被注射。Ganciclovir(GCV)是注射ip(40mg.kg?1.d?1)为10天。Intratumoral注射照耀of60Co的MM45TLi/IL-12房间分开在一个星期内被重复两次。有远肿瘤的老鼠根据一样的协议被对待。怒气房间的CTL活动是测量by51Cr版本试金和由染色的immunohistochemical渗入淋巴细胞的肿瘤的显型。结果：在与MM45T对待的老鼠，Li/IL-12或MM45TLi/TK+GCV个别地在肿瘤生长，而是两个都不导致了中等减小能根除肿瘤完全，当时在加GCV与MM45TLi/IL-12和MM45TLi/TK细胞的混合物对待的60%老鼠，完全的肿瘤回归被观察，没有为二个月的肿瘤复发。远肿瘤的生长也在同样对待的老鼠显著地被禁止。大多数收到的老鼠加GCV联合了基因治疗有的丰富的CD4+，CD8+T淋巴细胞渗入。他们的CTL活动比在老鼠显著地高收到的单个基因治疗。有加GCV的IL-12基因和HSV-TK基因的结论联合治疗为老鼠肝癌症是有效的。

简介：Chronicalcoholconsumptionisamajorriskfactorworldwideaffectingsignificantlybothmortalityandyearsoflifelost(YLL)(1).Ca.5%ofthewesternworldshowriskyalcoholconsumptionandinsomecountriessuchasChinaaregionalyearlyincreaseofalcoholconsumptionofover400%hasbeenobservedrecently(2,3).Theliveris

简介：瞄准：学习三氧化二砷的anti-hepatoma效率(作为(2)O(3))在试验性的老鼠肝细胞的治疗，癌(HCC)由2-acetamidofluorene(2-FAA)导致了并且阐明可能的机制。方法：SD老鼠(2瞬间旧)用2-FAA被喂了让8wk导致HCC，然后他们被对待与作为(2)O(3)或妈三倍。在d上29，老鼠被打死，肝被称，肝肿瘤被数。肝织物的组织学的变化在显微镜下面被观察，并且细胞的动态参数被流动血细胞计数学习。Immunohistochemistry(二拍子的圆舞方法)被用来在连续的节上观察脉管的内皮生长因素(VEGF)和微容器的密度(MVD)的表示。病理学的参数也被分析，浆液aspartateaminotransferase(著名计算机生产厂商)的层次，丙氨酸aminotransferase(中高音)，全部的胆红素(TBi)，和直接胆红素(DBi)。结果：肝肿瘤的数字在对待与的组显著地减少了作为(2)O(3)，在特别中等剂量(1mg/kg)组织(t=2.80，P<0.01)。当(2)O(3)经由apoptosis引起了HCC细胞死亡；坏死被看见，当剂量是1mg/kg时，apoptosis是普通的。增长索引严厉地减少了在中等剂量(1mg/kg)组织(7.87+/-4.11对24.46+/-6.49，t=2087，P<0.01)，然而并非在0.2mg/kg组。然而，S阶段部分在两个组戏剧性地减少了，仅仅当剂量与控制相比是1mg/kg时，它到达了底部水平(0.40+/-0.13对3.01+/-0.51，t=2.97，P<0.01)，并且它显然在G(0)/G(1)(G(0)/G(1)限制)伴有房间的累积。VEGF和MVD在的表情中等剂量(1mg/kg)组比生理盐水组显著地低(0.63+/-0.74对2.44+/-0.88，P<0.05；15.75+/-3.99对47.44+/-13.41，t=2.80，P<0.01)。与生理盐水组相比，是的中等剂量、低剂量的组(2)O(3)和妈三倍在浆液降低了中高音的层次(61.46+/-9.46，63.75+/-20.40，61.18+/-13.00对108.98+/-29.86，t=2.14，P<0.05)，但是没有浆液著名计算机生产厂商诚实

简介：Objective:Toassesstheimpactofpastlivermetastasesonthesurvivaldurationofpatientswhoareundergoingsurgeryforlungmetastases.Methods:Weconductedareviewofliteraturepublishedfrom2007to2014.ThestudieswereidentifiedbysearchingPubMed,MEDLINE,andEmbaseandweresupplementedbyamanualsearchofthereferenceslistedbytheretrievedstudies.Thefollowingsearchtermswereused:lungmetastasectomy,pulmonarymetastasectomy,lungmetastases,andlungmetastasis.Weselectedretrospectiveandprospectivestudiespublishedfrom2007to2014onpatientswithlungmetastasesfromcolorectalcancerandwereundergoingsurgerywithcurativeintent.Weexcludedreviews,studiesthatfocusedonsurgicaltechniques,patientswhoweretreatednon-surgically,analysesofspecificsubgroupsofpatients,andthosethatdidnotreportfollow-upofthepatientsundergoingsurgery.Results:Weidentified28papersthatassessedsurvivalafterlungmetastases,21ofwhichweremostlyretrospectivestudiesthatidentifiedpreviouslivermetastasestoexploretheirimpactonpatientsurvival.Inmorethanhalfofthepapersanalyzed(63.2%),patientswithahistoryofresectedlivermetastaseshadalowersurvivalratethanthosewhodidnothavesuchahistory,andthedifferencewasstatisticallysignificantineightofthesestudies.However,datawerepresenteddifferently,andauthorsreportedmeansurvivaltime,survivalrates,orhazardratios.Conclusions:Ahistoryoflivermetastasesseemstobeanegativeprognosticfactor,buttheindividualdataneedtoundergoameta-analysis.

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简介：AbstractObjective:Liver cancer stem cells (CSCs) are the culprits of hepatocellular carcinoma metastasis and recurrence. Only by eliminating tumor stem cells can malignant tumors be fundamentally cured. This study aimed to identify the role and underlying mechanism of aberrant Collagen Type XIV Alpha 1 Chain (COL14A1) overexpression in liver CSCs, and improve understanding of the molecular basis of hepatocellular carcinoma metastasis and recurrence.Methods:First, quantitative real-time polymerase chain reaction was used to confirm aberrant high-expression of COL14A1 in liver CSCs. Next, interference experiments were performed to determine the key role of COL14A1. To explore the mechanism of COL14A1 overexpression in liver CSCs, putative microRNA (miRNAs) targeting COL14A1 were analyzed using the miRTarBase database. Next, quantitative real-time polymerase chain reaction, western blotting, and luciferase reporter assays were performed to verify the interaction between miR-7108-3p and COL14A1. Lastly, key target proteins of the COL14A1-extracellular-regulated signal kinase (ERK) signaling pathway were identified through western blotting analysis. This study was approved by the Ethics Committee of Shanghai Fourth People’s Hospital, Tongji University School of Medicine, China (approval No. 2019tjdx17) on February 21, 2019.Results:COL14A1 is abnormally highly expressed in liver CSCs, which is necessary for liver CSCs to maintain their self-renewal capability. Mechanistically, COL14A1 is post-transcriptionally regulated by miR-7108-3p in a negative manner. Low expression of miR-7108-3p increased translation of COL14A1, which subsequently activated ERK signaling, ultimately maintaining the self-renewal and stem cell-like properties of liver CSCs.Conclusion:COL14A1, which is negatively regulated by miR-7108-3p, was found to play a crucial role in maintaining the self-renewal and stem cell-like properties of liver CSCs through activation of ERK signaling.

简介：Nonalcoholicfattyliverdisease(NAFLD),definedasabnormalaccumulation(>5%)ofhepatictriglyceridewithoutexcessalcoholintake,isthemostcommonformofchronicliverdiseaseinadultsandchildrenintheUnitedStates.NAFLDencompassesaspectrumofhistologicfindingsincludinguncomplicatedsteatosis,steatosiswithinflammationandsteatohepatitis[nonalcoholicsteatohepatitis(NASH)];thelattercanadvancetocirrhosisandhepatocellularcarcinoma.NASHiscurrentlyacceptedasthehepaticmanifestationofthesetofcardiovascularriskfactorscollectivelyknownasmetabolicsyndrome.In1999asystemforhistologicgradingandstagingforNASHwasproposed;thiswasrevisedbytheNASHClinicalResearchNetworkin2005fortheentirespectrumoflesionsinNAFLD,includingthelesionsandpatternsofpediatricNAFLD,andforapplicationinclinicalresearchtrials.Diagnosisremainsdistinctfromgradeandstage.ArecentEuropeanproposalseparatessteatosisfromactivitytoderiveanumericdiagnosisofNASH.Eventhoughtherehavebeenpromisingadvancementsinnon-invasivetesting,thesetestsarenotyetdetailedenoughtoreplacethefullrangeoffindingsprovidedbyliverbiopsyevaluation.Limitationsofbiopsyareacknowledged,butliverbiopsyremainsthe'goldstandard'fordiagnosisanddeterminationofamountsofnecroinflammatoryactivity,andlocationoffibrosis,aswellasremodelingoftheparenchymainNASH.ThisreviewfocusesonthespecifichistologiclesionsofNAFLDandNASH,gradingandstaging,differentialdiagnosestobeconsidered,andthecontinuingroleoftheliverbiopsyinthisimportantliverdisease.