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简介：AIMTocompareKAI1incancerofpapillaofVaterandpancreastoevaluatewhethertherearedifferencesinbiologicbehaviorwhichmightaccountforprognosis.METHODSWecomparedtheexpressionin24papillayand29pancreaticcancersusingNorthernblotanalysis,immunochemicalassayandinsituhybridization,andinvestigatedwhetherearlydiagnosisormoleculardifferencespredicttheoutcomeinthesetumorentities.RESULTSByNorthernblotanalysisthereisnostatisticaldifferenceofKAI1levelsinnormalandcancerouspapilla.NoassociationbetweenKAI1mRNAexpressionandtumorstageortumordifferentiationwasfoundinthetumors.Byimmunohistochemicalassay,KAI1stainingincytoplasmofpapillarycancercellswassimilartothatofnormalpapillarycells.Byinsituhybridization,theresultsofKAI1mRNAexpressioninnormalandcancerouspapillaweresimilartothosewithimmunohistochemicalassay.Thenormalandcancerouspancreastissueswerealsoanalyzedbythemethodsusedinpapillarysamples.CONCLUSIONAlthoughthebiologicrolesofKAI1havenotbeenclarified,ourresultssuggestthatKAI1mayrestricttheprogressionofmalignantpapillarycancer,butitsexpressionmightnothaveanyeffectonthecharacteristicsofpapillarytumor,whereasbytheanalysisofKAl1gene,itsreducedexpressioniscloselyrelatedtotheprogressionandmetastasesofpancreaticcancer.

简介：Wehavereviewedthegenetherapyingastrointestinaldiseases^[1].GastriccanceriscommoninChina^(2-20),anditsearlydiagnosisandtreatmentarestilldifficultuptonow^(13-36).Theex-pressionofanexogenousgeneintroducedbygenetherapyintopa-tientswithgliomascanbemonitorednon-invasivelybypositron-emissiontornography^[4].

简介：OurpreviousstudyshowedthattwoMKN45variants,namelyMKN45Lm-andMKN45Lm+selectedbylamininadhesioninvitro,haddifferentabilitiesofinvasionandmetastasisinvivo(inoculatedinnudemice)andinvitro(inBoydenchamber),alsohaddifferentexpressionofcysteineproteinase.Inthepresentstudy,weinvestigatedthecellapoptosisofthisMKN45variantsbyTUNELandFACSmethods.Theresultswereshownsignificantdifferentofcellapoptosisinthiscellsublines.TheMKN45Lm-cellshadasmallsubdiploidypeak(3.5%)inDNAcontentanalyzedbyflowcytometry,

简介：AIM:Tounderstandthecorrelationofserumcholinesterase(CHE)activitywithgastriccancerandtoassesstheirclinicalsignificance.METHODS:ThevelocitymethodwasadoptedtodetecttheactivityofserumCHEinpatientswithgastriccancerandinpatientswithnon-malignanttumorascontrols.RESULTS:TheserumCHEactivityinthetreatmentgroupwassignificantlylowerthanthatinthecontrolgroupwithaverysignificantdifferencebetweenthetwogroups(83.3:113.1,P=0.0003).Agewassignificantlyassociatedwiththeincidenceofgastriccaner.CONCLUSION:SerumCHEactivityhasacloserelationwiththeincidenceofgastriccancer.

简介：InthedevelopedWesternpartoftheworld,theincidenceofGCAhasmarkedlydecreasedoverthepastdecades.ThisdecreaseoftheGCAincidenceseemstobeageneralandglobalevent,suggestingthatoneorsomegloballyandgenerallycommonfactorsplayacriticalroleinthepathogenesisofGCA,andthatthisfactororfactorshavedecreasedininfluenceworldwidelyduringthepastdecades.Theseetiopathogeneticfactorshardlyareexoticdifferencesinlocalhabitsofeatingordrinkingonly.SuchexoticandlocalfactorscannotexplainthestrikingconsistencythatisapparentintheglobalepidemiologyofGCA.RegardingtheH.pyloriinfectionasthekeyfactorinthepathogenesisofgastriccancer,theserequirementsofglobalityarefulfilled.

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简介：AIM:Toinvestigatethedamagingeffectofhigh-intensityfocusedultrasound(HIFU)oncancercellsandtheinhibitoryeffectontumorgrowth.METHODS:MurineH22hepaticcancercellsweretreatedwithHIFUatthesameintensityfordifferentlengthsoftimeandatdifferentintensitiesforthesamelengthoftimeinvitro,thedeadcancercellsweredeterminedbytrypanbluestaining.TwogroupsofcancercellstreatedwithHIFUatthelowestandhighestintensitywereinoculatedintomice.Tumormasseswereremovedandweighedafter2wk,tumorgrowthineachgroupwasconfirmedpathologically.RESULTS:ThedeathrateofcancercellstreatedwithHIFUat1000W/cm2for0.5,1,2,4,8,and12swas3.11±1.21%,13.37±2.56%,38.84±3.68%,47.22±5.76%,87.55±7.32%,and94.33±8.11%,respectively.ApositiverelationshipbetweenthedeathratesofcancerceilsandthelengthofHIFUtreatmenttimewasfound(r=0.96,P＜0.01).ThedeathrateofcancercellstreatedwithHIFUattheintensityof100,200,400,600,800,and1000W/cm2for8swas26.31±3.26%,31.00±3.87%,41.97±5.86%,72.23±8.12%,94.90±8.67%,and99.30±9.18%,respectively.ApositiverelationshipbetweenthedeathratesofcancercellsandtheintensitiesofHIFUtreatmentwasconfirmed(r=0.98,P＜0.01).ThecancercellstreatedwithHIFUat1000W/cm2for8swereinoculatedintomiceexvivo.Thetumorinhibitoryratewas90.35%comparedtothecontrol(P＜0.01).IntheexperimentalgroupinoculatedwiththecancercellstreatedwithHIFUat1000W/cm2for0.5s,thetumorinhibitoryratewas22.9%(P＜0.01).Bypathologicalexamination,tumorgrowthwasconfirmedin8outof14mice(57.14%,8/14)inoculatedwiththecancercellstreatedwithHIFUat1000W/cm2for8s,whichwassignificantlylowerthanthatinthecontrol(100%,15/15,P＜0.05).CONCLUSION:HIFUiseffectiveonkillingordamageofH22hepaticcancercellsinvitroandoninhibitingtumorgrowthinmiceexvivo.

简介：INTRODUCTIONInterventiontherapyhasbecomeoneofthemaintherapiesofhepaticcancer.Theintroductionofhepaticarterialperfusionandembolizationhasprovidedopportunitiesforasecondaryoperationonpatientswithintermediateandadvancedcancer,thusprolonging

简介：AIM:Helicobacterpylori(Hpylori)hasbeenlinkedtochronicgastritis,pepticulcer,gastriccancerandMALT-lymphoma.ThelinkofgenotypesofHpyloritogastriccancerremainscontroversial.TheaimofthisstudywastoinvestigatetheHpylorivacAalleles,cagAandiceAinpatientswithgastriccancerinTaiwan.METHODS:Patientswithgastriccancer,pepticulcerandchronicgastritiswereenrolledinthisstudy.Weobtainedbiopsyspecimensfromthestomachatleast2cmawayfromthetumormargininpatientswithgastriccancer,andfromtheantrumofstomachinpatientswithpepticulcerorchronicgastritis.DNAextractionandpolymerasechainreactionwereusedtodetectthepresenceorabsenceofcagAandtoassessthepolymorphismofvacAandiceA.RESULTS:Atotalof168patients(gastriculcer:77,duodenalulcer:66,andchronicgastritis:25)werefoundtohavepositivePCRresultsofthebiopsyspecimensfrompatientswithpepticulcerandchronicgastritis.WefoundpositivecagA(139/168,83%),m2(84/168,50%)andiceA1(125/168,74%)strainsinthemajorityofpatients.Inpatientswithgastriccancer,thevacAslaandslcsubtypeswerelesscommonlyfoundthanthoseinnon-cancerpatients(35/66vs127/168,P=0.0001forslaand13/66vs93/168,P<0.0001forslc).Inthemiddleregion,themlTstraininpatientswithgastriccancerwasmorethanthatofnon-cancerpatients(23/66vs33/168,P=0.02).CONCLUSION:InTaiwan,HpyloriwithpositivevacAsla,cagAandiceA1strainsarefoundinthemajorityofpatientswithgastriccancerornon-cancerpatients.Inpatientswithgastriccancer,thevacAs1aandslcsubtypesarelessandm1Tismorethaninpatientswithpepticulcerandchronicgastritis.

简介：瞄准：评估诊断精确性，敏感，在检测颜色的本地复发的提高对比的计算tomographiccolonography的特性表面的癌症。方法：从2000年1月到2004年12月，434个病人在以后潜在地药品为侵略颜色的切除术表面的癌症被跟随在上面为从20～55瞬间的经期。为复发显示出充分临床的证据的434个病人中的八十个在最后后续期间渲染表面的癌症在这研究被注册。每个病人在一样的天经历了提高对比的计算tomographiccolonography和结肠镜检查。任何损害，活体检视，在colonoscopic期间鉴别检查，立即的复杂并发症和过程的持续时间被记录。提高对比的计算tomographiccolonography的结果被结肠镜检查，发现的surgical，和临床的后续比作那些评估。结果：提高对比的计算tomographiccolonography在检测本地周期性的颜色有100%，83%的特性和94%的全面精确性的敏感表面的癌症。结论：常规结肠镜检查和提高对比的tomographiccolonography能在检测颜色的本地复发补充对方表面的癌症。

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简介：Ithasbeenfoundthatexpressionof15-lipoxygenasc-1(15-LOX-1)anditsmainproduct,13-C-hydroxyoctadecadienoicacid(13-S-HODE),aredecreasedinhumancolorectalandesophagealcancersandthatnonsteroidalanti-inflammatorydrugs(NSAIDs)cantherspeuticallyinduce15-LOC-1expressiontotriggerapoptosisinthosecancercellsindependentlyCOX-2.WefoundthataspecificCOX-2inhibitorSC-236similarlyinduceapoptosisingastriccancercells,althoughthemechanismsoftheseeffectsremaintobedefined.Inthepresentstudy,wetestedwhetherSC-236inducedapoptosisthroughup-regulationof15-LOX-1ingastriccancercells.Wefoundthat,(a)SC-236inhibitedgrowthofgastriccancercellsmainlybyapoptosisinduced;(b)SC-236induced15-LOX-1expressionandincreasedendogenous13-S-HODEproduct,insteadof15-S-HETEduringapoptosisingastriccancercellswithout15-LOX-1expressionbeforetreatmentbySC-236;(c)sc-236didn'teffectexpressionofCOX-1,COX-2,5-LOXand12-LOX;and(d)15-LOX-1inhibitionsuppressedSC-236inducedapoptosis.ThesefindingsdemonstratedthatSC-236inducedapoptosisingastriccancercellsviaup-regulationof25-LOX-1.Theyalsosupporttheconceptthatthelossoftheproapopoticroleof15-LOX-1inepithelialcancersisnotlimitedtohumancolorectalandesophagealcancers.

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：AIM:TOexplorethefeasibilityofenhancingapoptosis-inducingeffectsofchemotherapeuticdrugsonhumangastriccancercellsbystabletransfectionofextrinsicSmacgene.METHODS:AfterSmacgenewastransferredintogastriccancercelllineMKN-45,subclonecellswereobtainedbypersistentG418selection.CellularSmacgeneexpressionwasdeterminedbyRT-PCRandWesternblotting.Aftertreatmentwithmitomycin(MMC)asanapoptoticinducer,invitrocellgrowthactivitieswereinvestigatedbytrypanblue-stainingmethodandMI-Icolorimetry.Cellapoptosisanditsratesweredeterminedbyelectronicmicroscopy,annexinV-FITCandpropidiumiodidestainingflowcytometry.Cellularcaspase-3proteinexpressionanditsactivitieswereassayedbyWesternblottingandcolorimetry.RESULTS:WhencomparedwithMKN-45cells,theselectedsubclonecelllineMKN-45/SmachadsignificantlyhigherSmacmRNA(3.12±0.21vs0.82:1:0.14,t=7.52,P<0.01)andproteinlevels(4.02±0.24vs0.98:1:0.11,t=8.32,P<0.01).Aftertreatmentwith10μg/mLMMCfor6-24h,growthinhibitionrateofMKN-45/Smac(15.8±1.2-54.8±2.9%)wassignificantlyhigherthanthatofMKN-45(5.8±0.4-24.0±1.5%,t=6.42,P<0.01).PartialMKN-45/Smaccancercellspresentedcharacteristicmorphologicalchangesofapoptosisundertheelectronicmicroscopewithanapoptosisrateof36.4=1=2.1%,whichwassignificantlyhigherthanthatofMKN-45(15.2±0.8%,t=9.25,P<0,01).ComparedwithMKN-45,caspase-3expressionlevelsinMKN-45/Smacwereimprovedsignificantly(3.39±0.42vs0.96:1:0.14,t=8.63,P<0.01),whileitsactivitieswere3.25timesasmanyasthoseofMKN-45(0.364±0.010vs0.112:1:0.007,t=6.34,P<0.01).CONCLUSION:StabletransfectionofextrinsicSmacgeneanditsover-expressioningasbiccancercelllinecansignificantlyenhancecellularcaspase-3expressionandactivities,ameliorateapoptosis-inducingeffectsofmitomycinConcancercells,whichisanovelstrategytoimprovechemotherapeuticeffectsongastriccancer.

简介：AIM:Toinvestigatetheassociationbetweenendogenousgeneexpressionandgrowthregulationincludingproliferationandapoptosisinducedbytransforminggrowthfactor-β1(TGF-β1)inhumangastriccancer(GC)cells.METHODS:Reversetranscriptionpolymerasechainreaction(RT-PCR)wasperformedtodetectthemaincomponentsoftheTGF-β1/SmadssignalpathwayinhumanpoorlydifferentiatedGCcelllineBGC-823.LocalizationofSmadproteinswasalsodeterminedusingimmunofluorescence.Then,theBGC-823cellswereculturedinthepresenceorabsenceofTGF-β1(10ng/mL)for24and48h,andtheeffectsofTGF-β1onproliferationandapoptosisweremeasuredbycellgrowthcurveandflowcytometry(FCM)analysis.TheultrastructuralfeaturesofBGC-823cellswithorwithoutTGF-β1treatmentwereobservedundertransmissionelectronmicroscope.Theapoptoticcellswerevisualizedbymeansoftheterminaldeoxynucleotidyltransferase(TdT)-mediateddTUPinsitunickend-labeling(TUNEL)method.Meanwhile,theexpressionlevelsofendogenousp15,p21andSmad7mRNAandthecorrespondingproteinsinthecellsweredetectedat1,2and3haftercultureinthepresenceorabsenceofTGF-β1(10ng/mL)bysemi-quantitativeRT-PCRandWesternblot,respectively.RESULTS:TheTGF-β1/SmadsignalingwasfoundtobeintactandfunctionalinBGC-823cells.ThegrowthcurverevealedthemostevidentinhibitionofcellproliferationbyTGF-β1at48h,andFCMassayshowedG1arrestaccompaniedwithapoptosisinducedbyTGF-β1.ThetypicalmorphologicalchangesofapoptosiswereobservedincellsexposedtoTGF-β1.Theapoptosisindex(AI)inTGF-β1-treatedcellswassignificantlyhigherthanthatintheuntreatedcontrols(10.7±1.3%vs0.32±0.06%,P＜0.01).Thelevelsofp15,p21andSmad7mRNAandcorrespondingproteinsincellsweresignificantlyup-regulatedat1h,butgraduallyreturnedtobasallevelsat3hfollowingTGF-β1(10ng/mL)treatment.CONCLUSION:TGF-β1affectsbothproliferationandapoptosisofGCcellsth

简介：AIM:TotestthehypothesisthatE-cadheringene(CDH1)C-160Apromotervariantgenotypeisassociatedwithanincreasedriskfordevelopinggastriccancer.METHODS:Inthispopulation-basedcase-controlstudyofgastriccancerinJiangsuProvince,China,weperformedpolymerasechainreaction-restrictionfragmentlengthpolymorphism(PCR-RFLP)togenotypetheC-160ApolymorphismofCDH1promoterin206non-cardiagastriccancerpatientsand261age-andsex-matchedbutunrelatedcancer-freecontrols.RESULTS:ThefrequenciesofgenotypesCC,CAandAAwere57.8%,36.4%and5.8%ingasfriccancercases,respectively,and58.2%,34.9%and6.9%incontrolsrespectively.ThedistributionsofCDH1genotypeswerenotsignificantlydifferentbetweengastriccancercasesandcontrols(P=0.87forgenotypefrequencyandP=0.92forallelefrequency).ComparedwiththeCCgenotype,theCAandAAgenotypeswerenotassociatedwithanincreasedriskfornon-cardiagastriccancer(adjustedoddsratios(OR)=1.15,and95%confidenceinterval(95%CI)=0.78-1.72forCAgenotype,andOR=0.90and95%CI=0.42-2.01forAAgenotype).CONCLUSION:E-cadheringeneC-160Apromoterpolymorphismmaynotplayamajorroleintheetiologyofnon-cardiagastriccancerinChinesepopulation.

简介：瞄准：学习SSTR1，2，3，4，有在颜色的clinico病理学的因素，房间增长，Bcl-2和p53表示的5表示和他们的关系表面的癌症房间。方法：五种SSTR子类型，Ki-67，Bcl-2和p53染色的Immunohistochemical被标准streptavidin-peroxidase(SP)执行为127颜色的石蜡节的技术表面的癌症。并且在正常的40个标本的五种SSTR子类型的表示渲染表面的mucosae与一样的方法被检测。结果：为五种SSTR子类型的积极染色在颜色被观察表面的癌症房间和正常颜色表面的mucosae。SSTR1是最占优势的子类型在渲染表面的癌症，正常渲染表面的粘膜，并且第二是SSTR5或SSTR2。作为与正常相比渲染表面的粘膜，SSTR4更经常在颜色被表示表面的癌症房间(2.5%对18.9%，P<0.05)；SSTR2的表示，4，5在里面中等到很好区分的颜色，表面的腺癌在糟糕区分的(P<0.05)比那显著地高，在有积极淋巴节点转移的表面的癌症是的颜色的SSTR1表示比那显著地高与否定淋巴节点转移(72.2%和54.5%，P<0.05)。另外，颜色在溃疡的打表面的癌症，SSTR2表示显然被减少(P<0.05)；关联没到达在五SSTR子类型表情和Dukes'stages(P>0.05)之间的统计意义，但是SSTR1表示的频率与Dukes'stage增加，当SSTR3和SSTR5表示与公爵的阶段减少了时。而且，在象年龄那样的五种SSTR子类型和另外的clinicopathological因素的表示之间没有关联，性别，肿瘤地点，肿瘤深度，远转移。在肤色的增生的索引有SSTR2和SSTR3的否定表示的表面的癌症房间与积极表示(P<0.05)比那显著地高。在肤色的Bcl-2表示有SSTR1的积极表示的表面的癌症房间，2，3，5与否定表示(P<0.05)是比那显著地低的。在五种SSTR子类型和p53表示之间没有关联。结论：最占优势的SSTR子类型是SSTR1，并且第二是SSTR2或SSTR5。五�

简介：AIM:Heatshockprotein(HSP)70isover-expressedinhumangastriccancerandplaysanimportantroleintheprogressionofthiscancer.WeinvestigatedtheeffectsofantisenseHSP70oligomeronhumangastriccancercelllineSGC-7901,anditspotentialroleingenetherapyforthiscancer.METHODS:HumangastriccancercelllineSGC-7901wastreatedinvitrowithvariousconcentrationsofantisenseHSP70oligonucleotidesatdifferentintervals.Growthinhibitionwasdeterminedaspercentagebytrypanbluedyeexclusiontest.ExtractedDNAwaselectrophoresedonagarosegel,anddistributionofcellcycleandkineticsofapoptosisinductionwereanalyzedbypropidiumiodideDNAincorporationusingflowcytometry,whichwasalsousedtodetecttheeffectsofantisenseoligomerpretreatmentonthesubsequentapoptosisinducedbyheatshockinSGC-7901cells.ProteinswereextractedforsimultaneousmeasurementofHSP70expressionlevelbySDS-PAGEWesternblotting.RESULTS:Thenumberofviablecellsdecreasedinadoseandtime-dependentmanner,andladder-likepatternsofDNAfragmentswereobservedinSGC-7901cellstreatedwithantisenseHSP70oligomersataconcentrationof10μmol/Lfor48hor8μmol/Lfor72h,whichwereconsistentwithinter-nucleosomalDNAfragmentation.Flowcytometricanalysisshowedadose-andtime-dependentincreaseinapoptoticratebyHSP70antisenseoligomers.ThisresponsewasaccompaniedwithadecreaseinthepercentageofcellsintheG1andSphasesofthecellcycle,suggestinginhibitionofcellproliferation.Inaddition,flowcytometryalsoshowedthatpretreatmentofSGC-7901cellswithHSP70antisenseoligomersenhancedthesubsequentapoptosisinducedbyheatshocktreatment.WesternblottingdemonstratedthatHSP70antisenseoligomersinhibitedHSP70expression,whichprecededapoptosis,andHSP70wasundetectableattheconcentrationof10μmol/Lfor48hor8μmol/Lfor72h.CONCLUSION:AntisenseHSP70oligomerscanabrogateHSP70expressioninSGC-7901cells,wh