简介:目的观察消积饮、华蟾素联合长春瑞滨对老年ⅢB/Ⅳ期非小细胞肺癌的疗效和毒副作用。方法给予46例老年ⅢB/Ⅳ期非小细胞肺癌患者消积饮30ml/m^2,po,bid×21d;华蟾素20ml/m^2,静滴(iv),qd×10d;长春瑞滨30ml/m^2,iv,d1,8,21天为1个周期,连续治疗4个周期。观察治疗前后瘤体变化、PS评分变化、中位生存时间、1年生存率、疾病无进展时间以及毒副作用。结果符合纳入标准的46名患者平均给予治疗3.2个周期。该研究总有效率(CR+PR)为19.6%,稳定率(CR+PR+NC)为89.1%,中位生存期(MST)为7.5个月,1年生存率为28.3%,疾病无进展时间(TTP)为5.2个月。该方案的主要毒副作用为骨髓抑制,12例出现白细胞下降,2例Ⅲ度疲劳,4例出现肝功能损害,4例出现Ⅰ度神经毒性。结论消积饮、华蟾素联合长春瑞滨的中西医结合治疗方案可提高患者总体生存质量,且毒副作用微弱,更适合作为老年晚期非小细胞肺癌患者的中西医结合治疗方案。
简介:目的观察美罗华联合CHOP方案治疗弥漫性大B细胞淋巴瘤的疗效及不良反应。方法48例CD20阳性的弥漫性大B细胞淋巴瘤患者,随机分为观察组和对照组,每组24例。观察组采用美罗华联合CHOP方案化疗,对照组单用CHOP方案化疗。全部患者完成6个周期化疗后评价疗效。结果观察组和对照组的总有效率分别为91.7%(22/24)和66.7%(16/24),1年总生存率(OS)分别为95.8%和74.7%,3年OS分别为83.3%和50.O%,1年无进展生存率(PFS)分别为82.6%和57.3%,3年PFS分别为62.8%和37.2%,以上两组比较差异均有统计学意义(P〈0.05)。两组患者的不良反应主要为胃肠道反应、骨髓抑制和输液相关不良反应。除畏寒、发热外,其余不良反应的发生率差异均无统计学意义(P〉0.05)。结论美罗华联合CHOP方案治疗弥漫性大B细胞淋巴瘤疗效较好,未增加化疗毒性,安全性好,值得临床推广应用。
简介:Objective:Chroniclymphocyticleukemia(CLL)andmantlecelllymphoma(MCL)cellsover-expressaguanineexchangefactor(GEF),Rasgrf-1.ThisGEFincreasesactiveRasasitcatalyzestheremovalofGDPfromRassothatGTPcanbindandactivateRas.ThisstudyaimstostudythemechanismofactionofRasgrf-1inB-cellmalignancies.Methods:N-terminustruncatedRasgrf-1variantshaveahigherGEFactivityascomparedtothefull-lengthtranscriptthereforeaMCLcelllinewithstableover-expressionoftruncatedRasgrf-1wasestablished.TheB-cellreceptor(BCR)andchemokinesignalingpathwayswerecomparedintheRasgrf-1over-expressingandacontroltransfectedcellline.Results:Cellsover-expressingtruncatedformofRasgrf-1haveahigherproliferativerateascomparedtocontroltransfectedcells.BCRwasactivatedbylowerconcentrationsofanti-IgMantibodyinRasgrf-1over-expressingcellsascomparedtocontrolcellsindicatingthatthesecellsaremoresensitivetoBCRsignaling.BCRsignalingalsophosphorylatesRasgrf-1thatfurtherincreasesitsGEFfunctionandamplifiesBCRsignaling.ThisactivationofRasgrf-1inover-expressingcellsresultedinahigherexpressionofphospho-ERK,AKT,BTKandPKC-alphaascomparedtocontrolcells.BesidesBCR,Rasgrf-1over-expressingcellswerealsomoresensitivetomicroenvironmentstimuliasdeterminedbyresistancetoapoptosis,chemotaxisandERKpathwayactivation.Conclusions:ThisGEFproteinsensitizesB-cellstoBCRandchemokinemediatedsignalingandalsoupregulatesanumberofothersignalingpathwayswhichpromotesgrowthandsurvivalofthesecells.
简介:目的探讨宫腔镜对子宫内膜癌筛查的临床意义。方法选择2012年1月至2015年1月在安徽省第二人民医院就诊的超声检查提示子宫内膜增厚的患者共120例。按患者意愿,60例行宫腔镜检查及活检,60例行诊刮术,对比分析两组子宫内膜病变的诊断的符合率、灵敏度、特异度。结果宫腔镜和病理检查诊断总符合率为90.0%(54/60),诊断性刮宫和病理检查诊断总符合率为78.3%(47/60),两组诊断符合率相比差异有统计学意义(χ2=2.365,P=0.034)。宫腔镜检查的特异度高于诊断性刮宫(P〈0.05)。结论宫腔镜对子宫内膜增厚患者筛查子宫内膜癌及癌前病变有较高的临床价值。
简介:背景和目的目前研究已表明索拉非尼、肝动脉栓塞化疗术(TACE)与射频消融(RFA)联用对不可切除的肝癌患者有效。由此,本项多中心回顾性队列研究旨在比较联用索拉非尼和RFA及单用RFA对BCLC0-B1期肝癌的疗效,为临床联用索拉非尼及RFA提供证据。方法研究最终纳入了来自中国多个地区12个中心的128名肝癌患者,其中64名患者接受索拉非尼+RFA治疗,与之配对的余下64名患者仅接受RFA治疗。入选标准包括:18~75岁、病理确诊或至少两项影像学研究同时证实诊断、肿瘤数目≤3个、最大肿瘤直径≤7cm、肿瘤为BCLC0-B1期、不愿行肝切除或肝移植术、肝功能储备良好、ECOG状态评分≤2分。剔除标准为:主要血管癌栓形成和/或肝外转移、既往或现在有难以控制的腹水、肝性脑病或食管胃底静脉曲张出血、有其他恶性肿瘤史、心、肾或其他器官严重功能不全、除外病毒性肝炎的感染活动期。索拉非尼的剂量为400mgBid,并在RFA治疗前后60天内开始应用。在毒副反应较大的患者中,减少索拉非尼剂量至200mgBid,如还无缓解则停药。研究人员定期对患者进行随访,主要包括临床评估、肝功能、AFP、超声检查、动态CT扫描等。随访至2013年10月31日。结果两组的主要治疗并发症均包括消化道出血、胸腔积液、发热等。索拉非尼+RFA组总并发症发生率为9.38%,RFA组为4.69%,无统计学差异。RFA组中位肿瘤复发时间为41.1周,1年、2年、3年的累积复发率分别为62.8%、85.4%和92.7%。索拉非尼+RFA组患者中位肿瘤复发时间为65.1周,1年、2年、3年的累积复发率分别为40.5%、62.9%和74.5%。RFA组中位生存时间为118.6周,1年、2年、3年、4年的累积生存率分别为80.7%、47.2%、30.9%和30.9%。索拉非尼+RFA组中位生存时间为161.8周,1年、2年、3年、4年的累积生存率分别为85.6%、64.0%、58.7%和50.3%。统计学分析�
简介:目的探讨利妥昔单抗联合CHOP方案对弥漫型大B细胞淋巴瘤(diffuselargeB-celllymphoma,DLBCL)的疗效,观察影响化疗疗效的相关因素。方法本组选择我院2006年1月至2011年1月收入的DLBCL患者17例,患者给予利妥昔单抗联合CHOP方案治疗。观察化疗后疗效及淋巴结亚群改变情况,收集患者的性别、年龄、PS评分、AnnArbor分期、结外浸润情况、LDH水平、体力状态(PS)评分、B症状、血红蛋白及T细胞浸润等相关情况,观察其对化疗的相关影响。结果本组所有17例患者完成治疗,治疗后疗效评估显示CR7例,PR6例,SD3例,PD1例,治疗有效率为76.4%(13/17)。影响化疗疗效相关因素分析中显示,血清LDH水平、PS评分、AnnArbor分期为影响患者化疗疗效的相关因素,P〈0.05。结论利妥昔单抗联合CHOP对弥漫型大B细胞淋巴瘤疗效显著,其中Ps评分低、AnnArbor分期低、血清LDH水平正常的患者化疗疗效相对较好。
简介:ThechronicinfectionofhepatitisBvirus(HBV)iscloselyrelatedtotheoccurrenceanddevelopmentofhepatocellularcarcinoma(HCC).AccumulatedevidencehasshownthatHBVXprotein(HBxprotein)isamultifunctionalregulatorwithacrucialroleinhepatocarcinogenesis.However,informationonthemechanismbywhichHBVinducesHCCislacking.ThisreviewfocusesonthepathologicalfunctionsofHBxinHBV-inducedhepatocarcinogenesis.Asatransactivator,HBxcanmodulatenuclearfactorkappa-light-chain-enhancerofactivatedBcells(NF-κB)andtranscriptionfactorAP-2.Moreover,HBxcanaffectregulatorynon-codingRNAs(ncRNAs)includingmicroRNAsandlongncRNAs(lncRNAs),suchasmiRNA-205andhighlyupregulatedinlivercancer(HULC),respectively.HBxisalsoinvolvedinepigeneticmodification,includingmethylationandacetylation.HBxinteractswithvarioussignal-transductionpathways,suchasproteinkinaseB/Akt,Wnt/β-catenin,signaltransducerandactivatoroftranscription,andNF-κBpathways.Moreover,HBxaffectscellularfatebyshiftingthebalancetowardcellsurvival.HBxmayleadtothelossofapoptoticfunctionsordirectlycontributestooncogenesisbyachievingtransformingfunctions,whichinducehepatocarcinogenesis.Additionally,HBxcanmodulateapoptosisandimmuneresponsebydirectorindirectinteractionwithhostfactors.WeconcludethatHBxhastensthedevelopmentofhepatoma.
简介:DuckhepatitisBvims(DHBV)DNAwasdetectedindifferenttumorousnodulesofduckswithhepaticmulticentriccancerorintrahepaticmetastasisbySouthernblottechnique.Among7duckswithhepatocellularcarcinomaofmultipletumornodules,thehybridizationpatternofIntegratedDHBVDNAIndifferenttumorousnoduleswasidenticalin3casesanddifferentin2cases.OnecaseshowedasimilarhybridizationpatternintwotumorousnodulesandotheronewasnegativetorDHBVDNA.IntegratedDHBVDNAwasalsoidentifiedinametastaticlungcancerofduckswithhepatocellularcarcinoma.Thehybridizationpatternofmetastasisoflungswasasthesomeasthatinprimaryhepatocellularcarcinoma.ThesamediscretehybridizationbandsInthedifferenttumorousnodulesindicatethatthesenodulesmightarisefromonetransformedcell.ThedifferenthybridizationpatternsInvarioustumorousnodulesshowthatthesetumorousnodulesmightarisefromvarioustransformedcells.Theresultssuggestthatthehyb
简介:Objective:ToassesstheeffectofantiviraltherapyforhepatitisBvirus(HBV)-relatedhepatocellularcarcinoma(HCC)afterradicalhepatectomy.Methods:Atotalof478HBV-relatedHCCpatientstreatedbyradicalhepatectomywereretrospectivelycollected.Patientsinthetreatmentgroup(n=141)receivedpostoperativelamivudinetreatment(100mg/d),whereaspatientsinthecontrolgroup(n=337)didnot.Recurrence-freesurvival(RFS)rates,overallsurvival(OS)rates,treatmentsforrecurrentHCCandcauseofdeathwerecomparedbetweenthetwogroups.Propensityscorematching(PSM)analysiswasalsoconductedtoreduceconfoundingbiasbetweenthetwogroups.Results:The1-,3-,and5-yearRFSratesdidn’tsignificantlydifferbetweenthetwogroups(P=0.778);however,the1-,3-,and5-yearOSratesinthetreatmentgroupweresignificantlyhigherthanthoseinthecontrolgroup(P=0.002).Similarresultswereobservedinthematcheddata.SubgroupanalysisshowedthatantiviraltreatmentconferredasignificantsurvivalbenefitforBarcelonaClinicalLiverCancerstageA/Bpatients.FollowingHCCrecurrence,morepeopleinthetreatmentgroupwereabletochoosecurativetreatmentsthanthoseinthecontrolgroup(P=0.031).Forcauseofdeath,fewerpeopleinthetreatmentgroupdiedofliverfailurethanthoseinthecontrolgroup(P=0.041).Conclusion:PostoperativeantiviraltherapyincreaseschancesofreceivingcurativetreatmentsforrecurrentHCCandpreventsdeathbecauseofliverfailure,therebysignificantlyprolongingOS,especiallyinearly-orintermedian-stagetumors.
简介:许多人类疾病的发生和发展可归因于一些基因的异常表达,从而导致疾病的发生。其中一部分基因是在核因子kappaB(nuclearfactor-kappaB,NF—κB)调控下进行的。NF—κ是广泛存在于哺乳动物中的转录因子,是由Sen等于1986年首先在B细胞中发现的一种核蛋白。因它能与B细胞免疫球蛋白上的K轻链基因增强子κB序列(GGGACTITCC)特异结合而得名。实际上它能与多种细胞基因的启动子和增强子序列位点发生特异性结合,并促进转录和表达,参与众多与免疫和炎症反应有关的基因转录的调控。它的异常激活或完全抑制与多种疾病的发生有关。在控制细胞增殖、凋亡、肿瘤的发生、发展和耐药问题上均起着重要的作用。因此深入探讨NF—κB在体内病理状态下的活化机制以及其与细胞、基因之间的调节作用具有重要的意义。现就NF—κB的组成、结构、激活途径以及与肿瘤的关系作一综述。
简介:Objective:Cancercellradioresistanceisastumblingblockinradiationtherapy.TheactivityinthenuclearfactorkappaB(NFκB)pathwaycorrelateswithanti-apoptoticmechanismsandincreasedradioresistance.TheIKKcomplexplaysamajorroleinNFκBactivationuponnumeroussignals.Inthisstudy,weexaminedtheinteractionbetweenionizingradiation(IR)anddifferentmembersoftheIKK-NFκBpathway,aswellasupstreamactivators,RAF1,ERK,andAKT1.Methods:Theeffectof4GyofIRontheexpressionoftheRAF1-ERK-IKK-NFκBpathwaywasexaminedinA549andH1299lungcancercelllinesusingWesternblotanalysisandconfocalmicroscopy.WeexaminedchangesinradiationsensitivityusinggenesilencingorpharmacologicalinhibitorsofERKandIKKβ.Results:IKKα,IKKγ,andIκBαincreaseduponexposuretoIR,therebyaffectingnuclearlevelsofNFκB(phospho-p65).ERKinhibitionorsiRNA-mediateddown-regulationofRAF1suppressedthepost-irradiationsurvivaloftheexaminedlungcancercelllines.AsimilareffectwasdetectedonsurvivaluponsilencingIKKα/IKKγorinhibitingIKKβ.Conclusions:ExposureoflungcancercellstoIRresultsinNFκBactivationviaIKK.ThegeneticorpharmacologicalblockageoftheRAF1-ERK-IKK-NFκBpathwaysensitizescellstotherapeuticdosesofradiation.Therefore,theIKKpathwayisapromisingtargetfortherapeuticinterventionincombinationwithradiotherapy.
简介:目的评价高频彩超检查对腮腺肿块的诊断及鉴别诊断的价值。方法应用高频彩超对58例腮腺肿块的患者进行检查,并结合病理检查结果分析、总结腮腺肿块的超声图像特征。结果高频彩超检查对腮腺肿块的总检出率为100%,对腮腺良、恶性肿块的诊断符合率分别为87.2%、68.4%,其中腮腺囊肿诊断符合率为100%。二维超声检查中腮腺良、恶性肿块在形态、边界、边缘和内部回声方面的差异均有统计学意义(P〈0.05)。彩色多普勒血流显像对腮腺良、恶性肿块血流信号的检出率分别为82.1%、94.7%。以收缩期峰值流速≥23.8cm/s作为诊断腮腺恶性肿块阈值的标准,脉冲多普勒诊断的敏感度和特异度分别为73.7%和71.8%;以阻力指数≥0.68(除混合瘤外)作为诊断腮腺恶性肿块阈值的标准,其诊断敏感度和特异度分别为73.3%和85.0%。结论高频彩超检查对腮腺肿块的检出率及诊断符合率均较高,对腮腺肿块的定性诊断有重要的临床应用价值。
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:Toinvestigatephospho-(-cateninexpressioninnon-smallcelllungcancer(NSCLC)andtostudytherelationshipbetweenphospho-(-cateninexpressionandsomeclinicalpathologicalfactors.Methods:Theexpressionofphospho-(-cateninin67primaryNSCLCcasesdetectedimmunohistochemically.Results:phospho-(-cateninwasnotexpressedinnormalbronchialmucouscellandshowedcytoplasmicandnuclearexpressioninNSCLCcell.Totalpositiveexpressionratereached62.7%,andpositiveexpressionrateofnucleuswas38.8%.Thepositiveexpressionrate(87.5%)andnuclearexpressionrateofadenocarcinoma(62.5%)wereapparentlyhigherthanthoseofsquamouscellcancer(40.0%and17.1%)(P<0.01).Expressionofphospho-(-cateninhadnorelationshiptodifferentiationdegreeandlymphaticmetastasis.Thepostoperativesurvivaltimeisnotrelatedtophospho-(-cateninexpression.(Log-ranktest,P=0.9198;P=0.6274).COXmodelanalysisshowedthattumorstageanddifferentiationareindependentriskfactorstoprognosis(P=0.001;P=0.020).Conclusion:NSCLCcellsshowpositiveexpressionofphospho-(-catenin,phospho-(-cateninnuclearexpressionisrelevanttohistologicaltypes.Thereisnodifferenceinpostoperativesurvivaltimebetweenpatientswithphospho-(-cateninpositiveexpressionandpatientswithnegativeexpression,expressionofphospho-(-cateninisnotindependentriskfactortoprognosis.
简介:Objective:Toassesstheclinicalfeatures,survivalandprognosticfactorsofprimarytesticulardiffuselargeB-celllymphoma(DLBCL).Methods:Aretrospectivestudyof37patientswithprimarytesticularDLBCLwascarriedoutfromNovember2003toMay2012.Theirclinicalfeatures,survivalandprognosticfactorswereanalyzed.Results:Duringamedianfollow-upperiodof39.8months(5.4-93.0months),themedianprogression-freesurvival(PFS)was26.2months(95%CI:0-65months)andthe3-yearoverallsurvival(OS)ratewas78.4%.Withinthewholecohort,thefactorssignificantlyassociatedwithasuperiorPFSwerelimitedstage(stageI/II),lactatedehydrogenase(LDH)≤245U/L,internationalprognosticindex(IPI)≤1,primarytumordiameter<7.5cm,andpatientswhohadcompleteresponse(CR)andreceiveddoxorubicin-containedchemotherapy(P<0.05).Therewasatrendtowardsuperioroutcomeforpatientswhoreceivedcombinedtherapy(surgery/chemotherapy/radiotherapy)(P=0.055).PatientswhohadCR,primarytumordiameter<7.5cmandIPIscore≤1weresignificantlyassociatedwithlongerPFSatmultivariateanalysis.Conclusions:PrimarytesticularDLBCLhadpoorersurvival.CR,primarytumordiameterandIPIwereindependentprognosticfactors.Thecombinedtherapyoforchectomy,doxorubicin-containedchemotherapyandcontralateraltesticularradiotherapy(RT)seemedtoimprovesurvival.
简介:目的:评价前程加速超分割治疗食管癌放疗疗效及放射反应.方法:对96例食管癌随机分为前程加速超分割组(前超组)和常规组,每组48例,全部经病理证实.男性63例,女性33例;年龄41岁~70岁,中位年龄57岁;病变部位胸上段21例,胸中段63例,胸下段12例.病变长度:<5cm29例,5.0cm~7.0cm57例,>10cm10例.全部采用6MVX线外照射,常规组1次/天,2.0Gy/次,5次/周,总剂量64Gy~68Gy,44~45天完成.前超组2次/天,1.5Gy/次,间隔6小时以上,总剂量64~68Gy,35~37天完成.结果:随访率96.9%.1、3、5年生存率前超组为81.15%、44.1%和26.8%,常规组为61.7%、25.1%和16.9%.前超组1、3年生存率高于常规组(u值为2.97及2.64,P<0.01),5年生存率无显著意义(u=1.71,P>0.05).前超组和常规组放射性食管炎发生率分别为27.16和16.7%(χ2=1.52,P=0.20);放射性气管炎发生率前超组为18.8%,常规组为12.5%(χ2=0.71,P=0.40).结论:食管癌前程加速超分割治疗的1年和3年生存率高于常规组,5年生存率无明显差异,患者对前超组放疗副作用与常规组相比无明显增加.
简介:目的评价食管癌全程加速超分割放射治疗疗效及并发症。方法60例食管癌随机分为两组:常规分割(conventionalFractionation,CF)组30例,1次/d,2Gy/次,5次/wk,总剂量66Gy,6.6wk完成;全程加速超分割(wholecourseacceleratedhyperfractionation,WCAHF)30例,2次/d,1.5Gy/次,10次/wk,总剂量66Gy,4.4wk完成。结果比较两组1a、3a、5a局部控制率,WCAHF组明显优于CF组(P〈0.05),分别为73.3%、53.3%、43.3%和56.7%、36.7%、26.7%;比较两组1a、3a、5a生存率,WCAHF组明显优于CF组(P〈0.05),分别为70.0%、36.7%、30.0%和56.7%、26.7%、16.7%。WCAHF组急性反应发生率较CF组高,但差异无显著性(P〉0.05).结论食管癌WCAHF放疗能明显提高局部控制率和生存率,不明显增加放射治疗反应及并发症。