简介：Glioblastoma(GBM)isoneofthemostlethalhumancancers.GenomicanalysesdefinethemoleculararchitectureofGBMandhighlightacentralfunctionformechanistictargetofrapamycin(mTOR)signaling.mTORkinaseexistsintwomultiproteincomplexes,namely,mTORC1andmTORC2.Thesecomplexesdifferintermsoffunction,regulationandrapamycinsensitivity.mTORC1iswellestablishedasacancerdrugtarget,whereasthefunctionsofmTORC2incancer,includingGBM,remainspoorlyunderstood.ThisstudyreviewstherecentfindingsthatdemonstrateacentralfunctionofmTORC2inregulatingtumorgrowth,metabolicreprogramming,andtargetedtherapyresistanceinGBM,whichmakesmTORC2asacriticalGBMdrugtarget.

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：恶性胶质瘤颅外转移非常罕见，转移通常发生在神经轴，但颅外转移到肝、脾、肺、腹膜、淋巴结也可发生。不同于许多非神经系统恶性肿瘤。恶性胶质瘤的治疗失败原因主要是局部未控。患者最终死于局部病灶进展或大脑重要区域的复发或无法控制的颅高压。绝大多数脑胶质瘤复发发生在距原发灶2cm内的区域。我科从2010年到2011年共收治了2例该类患者，现结合文献对脑胶质瘤颅外转移流行病学、临床表现、转移分布、自然病史及诊断治疗方法作一报道。

简介：目的总结门静脉压力（FPP）≥35cmH2O肝癌病人的外科治疗经验。方法回顾性分析1998年1月至2004年10月外科手术的11例FPP≥35cmH2O肝癌病人的手术资料、术后近期并发症及随访情况。结果全部病例手术均获得成功，无术中死亡。围手术期死亡率18．2％，术后并发症发生率100％，其中因上消化道大出血及肝功能衰竭死亡各2例（36．4％）。术后3mo、6mo及1年、2年、3年生存率分别为63．4％、36．4％、18．2％、18．2％、0％。结论FPP≥35cmH2O肝癌病人的手术切除有较高的并发症和死亡率，因此作者建议应将FPP≥35cmH2O肝癌视为肝部分切除的相对禁忌症。

简介：Theexpressionofp53Protein,c-erbB-2oncoprotein,Proliferatingcennuclearantigen(usA)werestudiedbythestreptavidinperotidaseconjugated(S-P)immunohistochemicalmethodandDNAcontentinsituwastested,inordertoexplorethesignificanceofP53,c-erbB-2,PCNAinPrimallUng...

简介：Objective:TodeterminewhetherInterferon-alpha-2b(IFN-α2b)canmodulatetheautophagicresponseinhepatocellularcarcinomacells.Methods:HepatocellularcarcinomacellsweretreatedwithIFN-α2b.Autophagywasassessedbyacridineorangestaining,GFP-LC3dottedassay,transmissionelectronmicroscopyandimmunoblotting.Results:AcridineorangestainingshowedthatIFN-α2btriggeredtheaccumulationofacidicvesicularandautolysosomesinHepG2cells.TheacridineorangeHepG2cellratioswere(4.3±1.0)%,(6.9±1.4)%,and(13.1±2.3)%,respectively,aftertreatmentwith100,1,000,and10,000IU/mLIFN-α2bfor48h.AmarkedlypunctatepatternwasobservedinHepG2cellstreatedwith10,000IU/mLIFN-α2bfor48h,butonlydiffuseandweaklyfluorescentGFP-LC3punctawasobservedincontrolcells.HepG2cellstreatedwith10,000IU/mLIFN-α2bfor48hdevelopedautophagosome-likecharacteristics,includingsingle-ordouble-membranevacuolescontainingintactanddegradedcellulardebris.TheBeclin1andLC3-IIproteinexpressionwasup-regulatedbyIFN-α2btreatment.Conclusion:Autophagycanbeinducedinadose-dependentmannerbytreatmentwithIFN-α2binHepG2cells,andtheBeclin1signalingpathwaywasstimulatedbyIFN-α2b.

简介：Objective:TheexpressionofB-celllymphoma2(Bcl-2)seemstobeinfluencedbytheendocrineenvironment.NumerousreportsdemonstratethediverseexpressionofBcl-2familymembersundersexsteroidregulation.Withtheexceptionofestrogen-relatedtumors,androgen-relatedtumorshaveshowntheircharacteristicsinBcl-2expression.Inthisstudy,thestatusofBcl-2expressioninmalehepatocellularcarcinoma(HCC)patientswasexaminedtoverifythehighincidenceofHCCinmales.Methods:TumortissuemicroarraywasusedtoexamineBcl-2expressionlevelsin374HCCcasesincluding306malesand68females.Kaplan-Meiermethod,log-ranktest,andCoxproportionalhazardsmodelwereappliedtoinvestigatethepredictivevalueofBcl-2inHCCpatients.Results:ImmunohistochemistryanalysisshowedthatmalepatientswithhigherBcl-2levelshadsignificantlylongermediansurvivaltimeandrecurrencetimethanthosewithlowerlevels.However,nosignificantdifferencesinoutcomeswerefoundbetweendifferentBcl-2levelsinfemalepatients.Whenthemalepatientswerestratifiedintoseveralagepoints,thelevelofBcl-2expressionshowedpoorerpredictiveefficiencyinthe45–49and55–60agegroupsinandropause-agepatientscomparedwithotheragegroups.Bcl-2wasanindependentprognosticfactorforbothoverallsurvival(P<0.0001)andrecurrencetime(P=0.0001)inmalepatients.Afterexcludingmalepatientsinthe45–60agegroup,thepredictiveefficiencywasenhanced(n=147,OS,P=0.0002,TTR,P<0.0001).Conclusions:Bcl-2expressionisanindependentpredictorofsurvivalandrecurrenceinmaleHCC.Bcl-2levelsmayalsoberegulatedbyandrogensorandrogenreceptorsinmaleHCCpatients.Bcl-2levelschangeandexhibitpoorpredictiveefficiencywhenandrogenlevelsvarydramatically(andropauseage).

简介：目的：体外观察黄芪对人喉癌细胞系Hep-2的抑制增殖和转移能力的作用并探讨其作用机制。方法：用20、100、200μg/ml的黄芪作用于Hep-2细胞24h,MTT法检测细胞增殖,流式细胞仪检测细胞周期分布和细胞凋亡率,侵袭实验观察药物对Hep-2细胞侵袭转移能力影响,AO/EB染色观察细胞凋亡,Westernblot检测Bcl-2和Bax蛋白的表达。结果：MTT结果显示黄芪对Hep-2细胞的增殖抑制作用具有明显的剂量依赖性;流式细胞仪检测发现随着黄芪浓度增高,细胞凋亡率逐渐升高,统计学分析,各实验组之间及其与对照组之间的差异均有统计学意义（P〈0.05）;AO/EB染色后可见典型细胞凋亡的形态变化;Hep-2细胞体外侵袭能力明显受抑制,存在剂量依赖性;Westernblot检测显示黄芪可剂量依赖性地抑制Bcl-2蛋白表达。结论：黄芪可通过抑制Bcl-2蛋白表达,上调Bax表达,引起喉癌细胞增殖抑制和凋亡,发挥抗癌作用。

简介：目的：研究microRNA203（miR-203）对胃癌EIF5A2表达的影响,为进一步阐明miR-203与胃癌的关系提供理论基础。方法：分别应用免疫荧光化学和免疫组织化学检测胃癌细胞和组织中EIF5A2的表达;脂质体miR-203转染干预胃癌细胞后,RealtimePCR和Westernblot检测细胞中EIF5A2mRNA和蛋白的表达情况。结果：胃癌细胞株SGC7901胞浆中大量表达EIF5A2蛋白,而细胞核中表达较少;胃癌组织中EIF5A2的表达量明显升高;EIF5A2的表达在脂质体miR-203转染干预胃癌细胞后明显受到抑制。结论：胃癌细胞和组织中存在EIF5A2的表达,且miR-203显著抑制了EIF5A2的表达。

简介：目的探讨Gab2基因在胃癌中的表达及对胃癌细胞增殖、凋亡、迁移及对AKT、P-AKT、Bax、Bcl-2表达的影响。方法采用RT-PCR及WesternBlot检测胃癌组织和癌旁组织中Gab2的表达。培养人胃癌细胞株SGC-7901，分别用Gab2小干扰RNA（Gab2-siRNA）和阴性对照（siRNA-NC）转染细胞，以空脂质体转染的细胞作为对照组，各组细胞培养48h。应用WestemBlot检测细胞中Gab2、AKT、p-AKT、Bax、Bcl-2蛋白表达的变化，CCK．8检测细胞增殖情况，流式细胞仪检测细胞凋亡，Transwell小室检测细胞迁移能力。结果胃癌组织中Gab2的mRNA及蛋白表达水平均明显高于癌旁组织（P〈0．01）；Gab2．siRNA组Gab2蛋白表达水平明显低于对照组（P〈0．01）；siRNA．NC组细胞的存活率、凋亡率、迁移数及AKT、P．AKT、Bax、Bcl．2蛋白表达与对照组比较，差异均无统计学意义（P〉O．05）；Gab2．siRNA组细胞的AKT蛋白表达与对照组比较，差异无统计学意义（P〉O．05），细胞的存活率、迁移数及P．AKT、Bcl．2蛋白表达明显低于对照组（P〈0．01），细胞凋亡率及Bax蛋白表达明显高于对照组（P〈0．01）。结论Gab2在胃癌组织高表达，沉默Gab2的表达能显著抑制人胃癌细胞株SGC-7901的增殖和迁移，并通过调节Bax、Bcl-2蛋白表达促进细胞凋亡，其可能的机制与AKT信号通路的调控有关。

简介：Objective:Toinvestigatetheeffectoftwoantisenseoligonucleotidesoncellsurviving,bcl-2expressionandapoptosisofleukemiacells.Methods:Theexperimentalassayswereperformedwithcellculture,immunochemistryandflowcytometry.Results:Thetwoantisenseoligodeoxynucleotides,combinedwithVp16orAra-corDNR,wereabletodeclinethesurvivalrateofmyeleukemiccells,downregulatebcl-2geneexpressionandinduceapoptosisofleukemiccellssignificantly,ascomparedwithVp16orAra-corDNRalone.Conclusion:Itispossibleforthetwonewbcl-2antisensestobedevelopedintoclinicaltrialsforleukemiaandtumorwithbcl-2geneoverexpression.

简介：Objective:TostudythedifferencesandsimilaritiesoftheantisensedrugswithdifferentstructuresonthebiologicalfunctionsofK562cells.Methods:Cytotoxiceffectsweremeasuredbyuseofacellviabilityassay.FlowcytometricanalysisandagarosegelelectrophoresisofDNAfragmentationwerealsoperformed.Theexpressionlevelofproteinwasassayedbyimmunofluorescenceusingfluoresceisothiocyanatelabel.Results:PNAtargetingthecodingregionoftheBcl-2messengerRNAcouldeffectivelyinhibitK562cellviability,down-regulatethesynthesisoftheBcl-2proteinandincreasecellapoptosis.By72haftertheBcl-2antisensePNAtreatment,K562cellsshowedmorereductioninthelevelofBcl-2proteincomparedwithcellstreatedwiththeantisenseODN.Aftertreatmentwith10μmol/LofBcl-2antisensePNAorantisenseODNfor72h,apoptoticratesofK562cellswere13.15±1.13and11.72±1.12,respectively.Furthermore,therewassignificantdifferenceinthepercentageofapoptoticcellsbetweenantisensePNAgroupandantisenseODNgroup.Conclusion:TheresultssuggestthatantisensePNAtargetingthecodingregionofBcl-2mRNAhasbetterantisenseeffectsthantheantisenseoligonucleotidesoninducingapoptosisofK562cells.

简介：目的比较线粒体融合蛋白-2（Mfn2）在乳腺癌、甲状腺癌和大肠癌组织及相应正常组织中的表达差异,探讨Mfn2与肿瘤发生的关系.方法选取经病理检查确诊的乳腺癌、甲状腺癌和大肠癌标本各20例,另取相应癌旁正常组织作为对照,采用免疫组织化学染色SABC法对Mfn2在不同组织中的表达水平进行测定和对比分析.结果免疫组化染色显示,在乳腺癌、甲状腺癌、大肠癌组织中表达水平均明显低于相应正常组织（P〈0.01）.结论Mfn2在乳腺癌、甲状腺癌和大肠癌组织中表达低于正常组织,Mfn2与这3种恶性肿瘤的发生、发展密切相关,可作为预测三种恶性肿瘤转移及其预后的参考指标.

简介：Minimalresidualdisease(MRD)playsacausativeroleintumorrecurrenceandestablishmentofeffectiveandsensitiveassessmentofMRDcouldbeveryusefulforstagingandevaluationoftreatmentofdisease.Inthisstudy,weassessedtheusefulnessofhcf-2/JHPCRanalysisonoccultlymphoma...

简介：目的分析绝经前雌激素受体（ER）阳性、人类表皮生长因子受体2（HER2）阴性乳腺癌患者复发转移特征。方法回顾性分析154例ER阳性HER2阴性绝经前复发转移性乳腺癌患者的临床资料,对患者临床及复发转移特征进行总结分析。结果154例绝经前ER阳性HER2阴性乳腺癌患者,中位发病年龄45岁（26~53岁）,中位无病生存时间（DFS）52.4个月（6.1~329.1个月）,复发转移多发生在术后2~5年（49.4%,76/154）;非内脏转移较内脏转移多发（55.8%vs44.2%）;骨转移最多（52.6%,81/154）,内脏转移以肺多见（26.6%,41/154）;多因素分析显示,淋巴结转移状态是DFS的主要影响因素（P﹤0.05）。结论绝经前ER阳性HER2阴性乳腺癌患者复发转移多发生在术后2~5年,主要为非内脏转移,骨转移最多;淋巴结转移状态是影响DFS的重要因素。

简介：背景与目的：ABCG2是ATP转运蛋白（ATPbindingcassette，ABC）家族中G2成员，具有编码乳腺癌耐药蛋白（breastcancerresistanceprotein，BCRP）功能，在肿瘤研究中又可作为SP细胞标志蛋白来筛选肿瘤干细胞，本研究旨在逆转其耐药作用。方法：尼卡地平（NCDP）、尼莫司汀（AGNU）分别和联合作用于人脑多形性胶质母细胞瘤（GBM）体外细胞系和裸小鼠脑移植瘤。体外实验：用MTr比色法检测药物作用后GBM细胞存活率，流式细胞仪检测细胞凋亡率；体内实验：观察荷瘤裸小鼠的生存期及移植瘤病理。结果：体外实验中，AC-NU＋NCDP组对肿瘤抑制和促进凋亡作用都显著高于ACNU组（P〈0．01）。体内实验中，ACNU＋NCDP组的生存期比ACNU组明显延长（P〈O．01）。结论：随着胶质瘤恶性程度增高而表达率增加的ABCG2耐药基因功能因被NCDP抑制后增强了ACNU对胶质瘤细胞的杀伤、促进凋亡和延长荷瘤鼠生存期的作用。

简介：Objective:Toinvestigatetheimpactofbeta-elemeneinjectiononthegrowthandalpha-tubuleofhumanhepatocarcinomaHepG2cells.Methods:CellproliferationwasassessedbyMTTassay.Cellcycledistributionwasdetectedbyflowcytometry(FCM).ThemRNAexpressionofalpha-tubulinwasmeasuredbyRT-PCR.Westernblotanalysiswasusedtodetermineproteinexpressionofalpha-tubulinandthepolymerizationoftubulin.Results:Beta-elemeneinjectioninhibitedHepG2cellsproliferationinadose-andtime-dependentmanner;FCManalysisindicatedbeta-elemeneinjectioninducedcellcyclearrestedatSphase.RT-PCRandwesternblotanalysisshowedthatbeta-elemeneinjectiondown-regulatedalpha-tublinatbothmRNAandproteinlevels,presentingadose-dependentmanner.Moreover,beta-elemeneinjectionreducedthepolymerizationofmicrotubulesinadose-dependentmanner.Conclusions:Beta-elemeneinjectioncaninhibittheproliferationofhepatomaHepG2cellsandinducecellapoptosis,themechanismmightbepartlyrelatedtothedown-regulationofalpha-tubulinandinhibitionofmicrotubularpolymerization.

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：

简介：Objective:ToinvestigatewhethertheBc1-2antisenseoligonucleotide(ASODN)mayenhanceradiation-inducedapoptosisinRajicellline.Methods:Cellsurvivingfractionwasdeterminedusingthetrypanbluedyeexclusionassay.Theexpressionlevelofbc1-2proteinwasassayedbyimmunofluorescenceusingfluoresceisothiocyanatelabel.ApoptosiswasdetectedbyGiemsastainingandflowcytomertriccellcycleanalysis.Results:ItwasfoundthatBc1-2ASODNcombinedwithradiationhadsignificantlyreducedthenumberofviablecells(P<0.05).TherewasnodifferenceoncellsurvivalbetweenmismatchBc1-2oligodeoxynucleotide/radiationcombinationandradiation-treatedcellsalone.Bc1-2ASODNcombinedwithradiationcouldsignificantlyinhibitexpressionofBc1-2proteininRajicells(P<0.05).CellstreatedwithBc1-2ASODNcombinedwithradiationat72hdisplayedclassicapoptoticchanges.ApoptosisratesofRajicellstreatedwithBc1-2oligodeoxynucleotide/radiationcombinationandradiation-treatedcellsalone,respectively.Conclusion:Bc1-2antisenseoligonucleotidecanenhanceradiation-inducedapoptosisinRajicellline.