简介：二维的polyacrylamide胶化电气泳动(2D页)并且帮助矩阵的激光解吸附作用/电离双人脚踏车time-of-flight团spectrometry(MALDI-TOF/TOF-MS)，与联机数据库寻找合并了，被执行调查乳癌和邻近的正常的微分蛋白质胸纸巾。考虑到那浆液白朊富有地在正常被介绍，控制样品，从12在11检测的15个微分点(91.7%)乳癌样品被联机SIENA-2DPAGE数据库寻找和MALDI-TOF/TOF-MS分析识别。结果显示乳癌的病理学的变化涉及物质新陈代谢的扩大，解朊的活动的提升，酶的一些禁止者的活动的衰落等等。与改变的表示涉及乳癌的病理学的进程的一些重要蛋白质可以是有用简历标记，例如alpha-1-antitrypsin，EF-1-beta，组织蛋白酶D，TCTP，SMT3A，RPS12，和PSMA1，SMT3A，RPS12，和PSMA1首先在这研究为乳癌在之中被报导。

简介：Objective:Tofindaneffective,sensitive,specificandnoninvasivediagnosticmethodofbreastcancer.Methods:109massesof102patientswithbreastlesionssmallerthan2cmindiameterweredividedintothreegroupstoundergo99mTc-MIBIimagingandcomparedwiththeresultsofpathologyexamination.20caseswithoutbreastlesionswereselectedascontrol.Abnormalcondensationof99mTc-MIBIinthebreastreaching10%higherthanthatinthecounterpartofthehealthybreastwasregardedaspositive.Results:Of32breastcancers,positiveimagingappearedin25.Negativeimagingwerefoundin31of38benignbreastlesions.Of39occultbreastlesions,positiveimagingappearedin6and3ofthemwerebreastcancer,2of3patientswithslightlyincreased99mTc-MIBIimagingthresholdwerebreastcanceralso.Nopositiveimagingwasfoundinthecontrolgroup.Thediagnosticaccuracy,sensitivity,specificity,positivepredictivevalue,negativepredictivevalueof99mTc-MIBIwas88.4%,89.2%,88.0%,75.0%and95.3%,respectively.Conclusion:99mTc-MIBIimaginghadhighersensitivityandaccuracyinthediagnosisofbreastcanceranddifferentiationbetweenbenignandmalignantbreastlesions.Itcouldprovideusefulinformationforthediagnosisofclinicallysuspectedbreastcancer.

简介：Objective:Toinvestigatetheeffectofbreast-conservationtherapyinearlystagebreastcancer.Methods:Atotalof234earlystagebreastcarcinomapatientsreceivedbreastconservingtreatmentinourhospital.Aftertheoperation,theyunderwentadjuvantchemotherapyandradiotherapy.Allofthesepatientsdesiredtopreservetheirbreasts.Results:Aftermedianfollow-upof29.46months(rangefrom3to100months),3caseshadlocalrelapseand8caseshaddistantmetastasis.Theoverallsurvivalrateof5yearwas96.7%,andthediseasefreesurvivalrateof5yearwas87.85%.Conclusion:Forearlystagebreastcarcinomapatients,classicquadrantectomy,axillarydissectionandpost-operativeadjuvantchemotherapyandradiotherapyleadtoexcellentlocalcontrolandgoodsurvival.

简介：客观：学习在胸方法的ductalcarcinomainsitu的作为一个预示的因素的组织学的分级的意义：根据凡·奈鈥檚分类，胸的ductalcarcinomainsitu(DCIS)的32个盒子被划分成三个组。结果：低等级(很好区分的、低等级DCIS)12个病人(37.5%)；中间的等级，9个病人(28.1%)；高等级(糟糕区分的DCIS)11个病人(34.4%)。在高等级DCIS之中，histologic子类型是粉刺(9个病人)，micropapillary(1个病人)和固体(1个病人)。在高等级DCIS的积极表示ofc-erbB-2，p53和MIB-1在中间、低的等级DCIS比那高。高等级和低等级DCIS之间的差别是重要的(P<0.05)。表示嗯在高等级，DCIS在中间、低的等级DCIS是比那低的。结论：胸ductalcarcinomainsitu的组织学的分级可以是一个好预示的因素。

简介：ＩＮＳＩＴＵＬＡＢＥＬＩＮＧＡＰＯＰＴＯＳＩＳＩＮＢＲＥＡＳＴＣＡＮＣＥＲＡＳＲＥＬＡＴＥＤＴＯＰＲＯＧＮＯＳＩＳＷｕＪｉｏｎｇ吴炅ＳｈａｏＺｈｉｍｉｎ邵志敏ＪｉａｎｇＭｉｎｇ江明ＨａｎＱｉｘｉａ韩企夏ＺｈａｎｇＴｉｎｇｑｉｕ张廷ＳｈｅｎＺｈｅｎｚ...

简介：ＤＩＥＬＥＣＴＲＩＣＰＲＯＰＥＲＴＩＥＳＯＦＨＵＭＡＮＢＲＥＡＳＴＣＡＲＣＩＮＯＭＡＡＮＤＳＵＲＲＯＵＮＤＩＮＧＴＩＳＳＵＥＳＤＩＥＬＥＣＴＲＩＣＰＲＯＰＥＲＴＩＥＳＯＦＨＵＭＡＮＢＲＥＡＳＴＣＡＲＣＩＮＯＭＡＡＮＤＳＵＲＲＯＵＮＤＩＮＧＴＩＳＳＵＥ...

简介：客观：在乳癌学习P-glycoprotein(P-gp)的临床的意义。方法：在乳癌的60种情况中的P-gp的表示被immunohistochemistry检验。到化疗的P-gp表示和反应比较地与变形乳癌在19个病人被调查。结果：P-gp在乳癌的60个案例中的48.3%个中是积极的。P-gp表示不与病人的年龄，月经地位，包含的腋的淋巴节点的数字，临床的阶段，组织学的类型，和神经质的受体地位有关(P>0.05)。转移(62.1%)和死亡(51.7%)的频率比在否定情况中在P-gp积极案例中是更高的(16.1%对12.9%，P<0.005)。P-gp积极案例(48.3%)的5年的幸存率比否定案例(87.1%)的显著地低(P<0.05)。在收到了辅助化疗的病人，远转移比在P-gp否定案例(57.1%)(P=0.0468)中更经常发生在P-gp积极案例(94.7%)中。更多的P-gp否定病人(7/9)对化疗(P=0.0055)比积极病人(1/10)应答。结论：P-gp表示的Immunohistochemical检查在在乳癌病人预言反应到化疗和预后是有用的。P-gp确实与差的预后被联系。

简介：

简介：Objective:Toevaluatethesafetyandefficacyofexternalhigh-intensityfocusedultrasound(HIFU)castrationforbreastcancerouspatientsaftermastectomyiftheyareatahighriskofrecurrence.Methods:Werecruited52consecutivepatientswithprimaryoperablebreastcancerwhoweretreatedwithmastectomywithexcisionofregionallymphnodes.PatientswerepositiveforERandPRimmuno-cytochemicalstaining,node-positive,un-menopause,over40yearsoldandweredividedintotwogroupsrandomly.Forcastration,26patientsreceivedoneortwotimesofHIFUtreatmentwithinfivedays,andtheotherpatientsreceivedradiotherapywithDT18Gy/9f/11days.Duringandafterthetreatment,localchangesandsystemicresponseofthepatientswereobserved.Results:After1monthtreatment,levelsofserumE1andE2weresignificantlydecreasedcomparedtobeforetreatmentinHIFUgroups(P<0.01andP<0.001).Thesamechangeswereoccurredinradiotherapy(RT)groups(P<0.05andP<0.01).ThelevelsofserumE1orE2inRTgroupswerehigherthaninHIFUgroups(P<0.05).Thesymptomdistributionof'climactericsyndrome'ofHIFUgroupsweresignificantlydifferentfromRTgroups(P<0.01).Thefollow-uptimewas4months.Theincidenceofamenorrheawas100%inallpatients.Noseriouscomplicationswereseen.Thetemperature,pulse,bloodpressure,andrespiratoryrateofthepatientswerealmostnormal.Conclusion:WehaveshownthattheuseofHIFUinthecastratingofpatientswithbreastcancerisfeasible,safeandeffective.ThistechnologymayprovidearapidnoninvasivealterativetoconventionalbilateraloophorectomyorRTcastration.

简介：Inthispaper,thecalculatingchartsandformulaeaboutwavepressureonthebreastwallarederivedwithsevenparametersonthebasisofphysicalmodelstudy.Theverificationshowsthatthechartsagreewiththeexample,andareadoptedintheSpecificationsofFisheryHarboursBreakwaterbytheMinistryofAgricultures.

简介：

简介：客观：为了学习表达式和apoptosis的临床的价值，在乳癌控制基因bcl-2和bax。方法：在在1996在我们的医院里从操作获得的41乳癌的蛋白质bax和bcl-2与正常的胸纸巾用ABCimmunohistochemical污点试金并且与10个盒子相比被检测。结果：在正常的胸组织的bax的积极的率是90%并且在乳癌是59%，与他们之间的重要统计差别(P<0.05)，但是在bcl-2没有统计差别蛋白质表示。在41乳癌之中，有淋巴节点转移(21个盒子)的组有显然低的bax表示(43%)和高bcl-2表示(76%)，给没有淋巴节点转移的组显示出重要差别(P<0.05)。结论：bcl-2的antiapoptosis功能是比在乳癌的bax强壮的。蛋白质bax和bcl-2试金可能在理解乳癌的生物行为是有用的。

简介：Objective:Tostudytherelationshipbetweencyclooxygenase-2(COX-2)expressionandtumorangiogenesisinhumanbreastcancer.Methods:Archivalprimarybreastcarcinomas(n=62),adjacentductalcarcinomainsitu(DCIS,n=13)andDCISalone(n=5)wereanalyzedforCOX-2andVEGFexpressionbyimmunohistochemistryusingspecificmonoclonalantibodies.Microvesseldensity(MVD)wasalsoexaminedtheusingCD34staining.Results:AsignificantcorrelationwasfoundbetweenCOX-2andVEGFexpression(P<0.01).BothCOX-2andVEGFweresignificantlycorrelatedwithMVD(P<0.05)andP<0.01,respectively).COX-2andVEGFgeneswereoverexpressedintumorspecimensascomparedwithnormalepithelia.Conclusion:COX-2isrelatedtotumorangiogenesisinbreastcancer.ItislikelythatVEGFisoneofthemostimportantmediatorsoftheCOX-2angiogenicpathway.

简介：Objective:ToinvestigatetheantitumoractivityandthemechanismofBRM-SJSonbreastcancercells.Methods:Flowcytometry,DNAagarosegelelectrophoresisandothertechniqueswereusedtostudytheinvitroandinvivoinhibitoryeffectonBcaP-37cellsbyBRM-SJS.Results:BRM-SJSshowedaninhibitoryrateof33.8%oninvivotransplantedtumor(P<0.05,comparedwithcontrol).TheflowcytometryanalysisofBRM-SJStreatedBcaP-37(2.5μmol/L,5μmol/L,10μmol/Lfor48hand72h)revealedtypicalsub-G1peak.ThespecificDNALadderswereexhibitedwithBRM-SJSBcaP-37cellstreated.Conclusion:BRM-SJShasmarkedantitumoractivityonBcaP-37anditsinhibitoryeffectsontumorwererealizedbybothinductionofapoptosisandnecrosisofthetumorcells.

简介：Objective:Todeterminewhetherpyrrolidinedithio-carbamate(PDTC)enhancesTNFα-inducedapoptosisinculturedbreastcancercellsandexploretheroleofNF-κBinTNFα-inducedapoptosis.Methods:HumanbreastcancercelllinesMCF-7andMDA-MB-435sweretreatedwithTNFα,PDTCandcombinationtherapy.CellsurvivalsweredeterminedbyMTTassay.ApoptosiswasdetectedbyTUNELandflowcytometry.NF-κBDNAbindingactivitywasdetectedusingelectrophoresismobilityshiftassay(EMSA).WesternblotswereperformedtodemonstrateIκBα(InhibitorproteinofnuclearfactorκB)phosphorylationanddegradation.Results:CellgrowthwasnotsuppressedbyeitherTNFα(2000U/mlorless)orPDTCalone.BothcelllinestreatedwithTNFα(2000U/ml)combinedwithPDTC(50μmol/L)showedsignificantgrowthinhibition.PDTCinhibitedTNFα-inducedIκBαphosphorylationanddegradationinbothcelllines.EMSAshowedthatPDTCcontinuouslyinhibitedTNFαinducedNF-κBDNAbindingactivity.TNFαinducedapoptosis(TUNEL)wasincreasedsignificantlywhenbothcellswerepretreatedwithPDTC,andthiswasconfirmedbyFlowcytometry.Conclusion:PDTCenhancesTNFα-inducedapoptosisviainhibitingIκBαphosphorylationanddegradationinhumanbreastcancercells.NF-κBprotectsagainstTNFα-inducedapoptosis.

简介：Objective:Toexplorethereversaleffectofmifepristoneonmultidrugresistance(MDR)indrug-resistanthumanbreastcancercelllineMCF7/ADRanditsmechanisms.Methods:ExpressionofMDR1andMDR-associatedprotein(MRP)mRNAinMCF7/ADRcellswasdetectedusingreversetranscription-polymerasechainreaction(RT-PCR).WesternblottingwasusedtoassaytheproteinlevelsofP-glycoprotein(P-gp)andMRP.Intracellularrhodamine123retentionand[3H]vincristine(VCR)accumulationweremeasuredbyflowcytometryandliquidscintillationcounter,respectively.MTTreductionassaywasusedtodeterminethesensitivityofcellstotheanticanceragent,adriamycin(ADR).Additionally,aMCF7/ADRcellxenograftmodelwasestablishedtoassessthereversaleffectofmifeprisoneonMDRinMCF7/ADRcellsinvivo.Results:Miferpristonedose-dependentlydown-regulatedtheexpressionofMDR1andMRPmRNAinMCF7/ADRcells,accompaniedbyasignificantdecreaseintheproteinlevelsofP-gpandMRP.Afterexposureto5,10,and20μmol/Lmifepristone,MCF7/ADRcellsshoweda3.87-,5.81-,and7.40-foldincreaseintheaccumulationofintracellularVCR(aknownsubstrateofMRP),anda2.14-,4.39-,and5.53-foldincreaseintheretentionofintracellularrhodamine123(anindicatorofP-gpfunction),respectively.MTTanalysisshowedthatthesensitivityofMCF7/ADRcellstoADRwasenhancedby7.23-,13.62-,and20.96-foldafterincubationwithmifepristoneasabove-mentioneddosesfor96h.Invivo,mifepristoneeffectivelyrestoredthechemosensitivityofMCF7/ADRcellstoADR.After8weeksofadministrationwithADR(2mg·kg-1·d-1)aloneorincombinationwithmifepristone(50mg·kg-1·d-1),thegrowthinhibitoryrateofxenograftedtumorsinnudemicewas8.08%and37.25%,respectively.Conclusion:MifepristoneexertspotentreversaleffectsonMDRinMCF7/ADRcellsinvitroandinvivothroughdown-regulationofMDR1/P-gpandMRPexpressionandinhibitionofP-gp-andMRP-dependentdrugefflux,thusincreasing

简介：ThepresentstudyisaimedatstudyingthegeneforTIMP-3,amammaliantissueinhibitor,byconstructingarecombinanteukaryoticcellvectorforgenetherapyinhumanbreastcancer.WeobtainedtheTIMP-3genefromthehumanplacentbyRT-PCR.TIMP-3genewassubclonedintopcDNA3.1vetorfrompMD18TvectorbymeansofgenecloningtoconstructpcDNA3.1recombinantvector.HumanbreastcancercelllineMDA-MB-453wastransfectedwithpcDNA3.1-TIMP3recombinantvectorusinglipofectaminereagent.ThentheexpressionofTIMP-3andtheeffectonthemetastasisofMDA-MB-453wereexamined.ThecorrectconstructionofpcDNA-TIMP3wasidentifiedbymeansofrestrictionenzymeanalysis,PCRamplicationandnucleotidesequencing.WesternblottingshowedthatthetransfectedcellswereabletoexpressTIMP-3,indicatingthatourconstructionofthepcDNA-TIMP3eukaryoticexpressionvectorwasconstructedsuccessfully.OurexperimentsfurtherindicatedthatthepotentialofmetastasiswassignificantlyreducedforthetransfectedcelllineMDA-MB-453.

简介：

简介：OverexpressionandactivationofHER-2/neu(alsoknownasc-erbB-2),aproto-oncogene,wasfoundinabout30%ofhumanbreastcancers,promotingcancergrowthandmakingcancercellsresistanttochemo-andradio-therapy.Wild-typep53iscrucialinregulatingcellgrowthandapoptosisandisfoundtobemutatedordeletedin60-70%ofhumancancers.Andsomecancerswithawild-typep53donothavenormalp53function,suggestingthatitisimplicatedinacomplexprocessregulatedbymanyfactors.Inthepresentstudy,weshowedthattheoverexpressionofHER-2/neucoulddecreasetheamountofwild-typep53proteinviaactivatingPI3Kpathway,aswellasinducingMDM2nucleartranslocationinMCF7humanbreastcancercells.BlockageofPI3KpathwaywithitsspecificinhibitorLY294002causedG1-Sphasearrest,decreasedcellgrowthrateandincreasedchemo-andradio-therapeuticsensitivityinMCF7cellsexpressingwild-typep53.However,itdidnotincreasethesensitivitytoadriamycininMDA-MB-453breastcancercellscontainingmutantp53.OurstudyindicatesthatblockingPI3KpathwayactivationmediatedbyHER-2/neuoverexpressionmaybeusefulinthetreatmentofbreasttumorswithHER-2/neuoverexpressionandwild-typep53.