简介：目的：探讨原发性胃弥漫大B细胞淋巴瘤（primarygastricdiffuselargeB-celllymphoma，PG-DLBCL）的预后影响因素。方法回顾性分析56例PG-DLBCL患者的临床资料及随访数据，采用Kaplan-Meier法估算患者的生存时间，采用Cox比例风险模型进行预后影响因素分析。结果56例PG-DLBCL患者的1年、2年、3年无事件生存率分别为73.2%，71.3%，68.8%，平均无事件生存时间（event-freesurvival，EFS）为69个月；1年、2年、3年总生存率分别为81.8%，73.3%，70.5%，平均总生存时间（overallsurvival，OS）为72个月。化疗联合放疗组的平均EFS比单纯化疗组长，差异有统计学意义（P﹦0.039）；不同的Musshoff分期、LDH水平、淋巴瘤国际预后指数（internationalprognosticindex，IPI）评分、β2微球蛋白值、美国东部肿瘤协作组（EasternCooperativeOn-cologyGroup，ECOG）体能状态（performancestatus，PS）评分、有无巨块对EFS及OS均有明确的影响（P＜0.05）。影响EFS及OS的独立预后因素为LDH水平及ECOG评分。结论对PG-DLBCL患者推荐采取以化疗为主的非手术治疗，LDH升高及PS评分高是预后不良的重要指标。

简介：目的报告56例Poland综合征,并对其严重程度进行回顾性分析,以提供一种全面的、客观的畸形严重程度评级系统。方法通过查体和影像学检查,对手部、臂部和胸部3个部位影响肢体外形和功能的各种畸形分组进行赋值和评分,每个部位的分值分别为0-10分;然后将其分值累加,得到手-臂-胸（Hand-Arm-Chest,HAC）总分,即Poland综合征畸形严重程度指数,最高为30分;再根据总分的高低,将该56例分为轻（4-8分）、中（9-16分）、重（17-30分）3个等级。结果本研究对所有患者进行详细的评估,轻度畸形有8例（12.3%）,中度畸形有22例（39.3%）,重度畸形有26例（46.4%）。结论该评级系统可以客观、有效、全面地评估Poland综合征中肢体畸形的严重程度,并有助于指导临床治疗,评估治疗效果及预后。

简介：目的：总结结直肠癌合并肠梗阻的诊断和治疗经验，探讨其漏诊原因及手术方法的选择。方法：回顾分析我院2001年2月-2007年5月56例梗阻性结直肠癌病人的临床特点及根据患者不同情况分别行一期手术和分期手术。结果．56例患者均经手术治疗，出现并发症4例，死亡1例，病死率为3．6％，其余均痊愈出院。结论：结直肠癌合并肠梗阻临床特点是：左侧结肠梗阻多见；晚期病例多见；老年患者多见。外科治疗的原则是解除梗阻，尽量切除肿瘤。应根据患者的具体情况选择合适的手术方式。

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：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：目的：观察肝病患者PBMC中CD3+、CD4+、CD8+、CDl6+56+细胞亚群变化研究其在肝脏损伤中的意义。方法：流式细胞仪检测肝病患者PBMC中CD3+、CD4+、CD8+、CDl6+56广卜细胞亚群变化。结果：肝病患者除重型肝炎CD3+下降外，其他急慢性肝病组CD3+稍有上升。重型肝炎、慢乙肝活动期和急性肝炎CD4+下降而慢乙肝静止期、失代偿期肝硬化、恶性肿瘤CD4+下降不明显，而代偿期肝硬化CD4+反而上升。除肝硬化CD8+下降外，其他肝病组则上升。肝病CD4+／CD8+变化与CD4+相类似。除重型肝炎和慢乙肝CDl6+56+变化不明显，失代偿期肝硬化、急性肝炎、代偿期肝硬化和恶性肿瘤CDl6广卜56+下降。相关分析发现，肝病患者CDl6+56+与CD3+和CD4+／CD8+负相关，仅CD8+与急、慢性肝损伤指标有关。结论：PBMC中CD3+、CD4+、CD8+、CDl6+56+细胞亚群的检测在肝病的诊治应用意义有限，不宜仅单凭CD4+、CDl6+56+和CD4+／CD8+上升与否和CD8+下降与否来评判疾病和治疗效果，进一步结合其他亚群标志物可能更有利于疾病机制研制了解和疾病的诊断及治疗效果的评定。

简介：根据世界癌症研究基金会（WCRF）资助的一项最新研究显示，人体血液中维生素B含量较高将有可能降低发生肺癌的风险，这个结果对吸烟、非吸烟以及曾经吸烟的人群是相同的。这项发现将有助于科学家了解肺癌发病的机理，并将对预防其发生提供线索。

简介：

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：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：研究miR-940对胃癌细胞增殖的影响,探讨miR-940和Cbl-b信号转导通路在此过程中的作用。方法：采用Real-timePCR法检测胃癌细胞中miR-940的表达,MTT法检测胃癌细胞的增殖能力,双荧光素酶报告基因检测系统检测miR-940与Cbl-b的结合,Westernblotting实验观察蛋白的表达。结果：MTT法显示miR-940可促进胃癌细胞MGC803的增殖,BLAST对比分析结果显示Cbl-b与miR-940存在结合位点。双荧光素酶报告基因检测系统证实Cbl-b是miR-940的靶基因。Westernblotting结果显示过表达miR-940后,Cbl-b的表达明显下调。Cbl-b抑制胃癌细胞MGC803的增殖。miR-940通过负向调节Cbl-b的表达促进胃癌细胞的增殖。结论：miR-940通过抑制Cbl-b的表达,促进胃癌细胞MGC803的增殖。

简介：目的：研究B7-H4在乳腺癌中的表达情况及其与各临床病理变量之间的相关性。方法：应用免疫组织化学染色分析51例乳腺癌手术患者切除的肿瘤标本的B7-H4的表达情况，分析其与年龄、肿瘤类型、大小、淋巴结转移、肿瘤分期、激素受体表达情况、Her-2／neu状态的相关性。结果：B7-H4可表达于乳腺癌细胞的胞膜上、胞浆内或同时表达于两者之内。88．2％（45／51）的标本B7-H4阳性，并且与肿瘤中Her-2／neu状态（P=0．04）、组织学类型（P=0．002）明显相关，Her-2／neu阳性患者中B7-H4的表达要明显高于阴性的患者，浸润性导管癌细胞中B7-H4的表达显著高于原位癌，而与其他临床病理参数无关。结论：B7-H4可能与肿瘤的预后和肿瘤的进展相关。

简介：目的观察由吉西他滨（GEM）联合顺铂（DDP）、地塞米松（DXM）组成的GDP方案治疗难治性弥漫大B细胞淋巴瘤（DLBCL）的疗效和毒副反应。方法2006年3月至2008年9月收治的25例难治性DLBCL患者，给予吉西他滨1000mg／m^2，第1、8天，静脉滴注；顺铂25mg／m^2，第1—3天，静脉滴注；地塞米松40mg／d，第1—4天，口服。21天为1周期。2个周期后评价疗效，并随访疾病进展情况。结果25例患者中，18例获缓解（72％），其中完全缓解8例（32％），部分缓解10例（40％）。25例患者中位肿瘤进展时间（TTP）为7．5个月（95％CI：7．17～7．82个月）。主要不良反应为骨髓抑制和轻中度的消化道反应。骨髓抑制主要表现为3—4级白细胞减少7例，3级血小板减少5例。结论吉西他滨联合顺铂、地塞米松的GDP方案治疗难治性DLBCL的近期疗效较好，安全性较高。

简介：Objective:TostudythesynergiceffectsofIL-12andB7-1transfectantonantitumorimmunityinvivo.Methods:TheretrovirusvectorencodingmIL-12andmB7-1genewastranfectedintoEL-4thymiclymphomacellsrespectively.Thecellswereusedastumorvaccineandthetherapeuticeffectwasobserved.Results:IncontrasttothemiceimmunizedwithEL-4/WtorEL-4/Neogroups,thetumorigenicityofEL-4/IL-12transfectantwasdecreased(P<0.001).TheEL-4/IL-12andEL-4/B7-1cellsirradiatedwith60CoshowedsignificantsystematicprotectiveeffectsagainsttherechallengeofEL-4/Wt.60CoirradiatedEL-4/IL-12cellsdelayedtheoccurrenceoftumorandprolongedthesurvivalperiodoftumorbearingmice.CombinationofthevaccinesofEL-4/IL-12andEL-4/B7-1resultedintheenhancedtherapeuticeffectcomparedwitheachsingletransfectantgroup(P<0.001).Conclusion:TheresultsshowedthatIL-12transducedcellscouldenhancetheantitumorimmunityofhostascancervaccine.CombinationoftheEL-4/IL-12andEL-4/B7-1transfectantcouldimproveimmunityofhostandisaprospectcancervaccine.

简介：1病案摘要患者,男,39岁.因左鼻塞1年伴双颈肿块1月入院.该患者于1年前无诱因下出现左侧鼻塞,未经处理.1月前双颈出现无痛性肿块而来我院就诊.