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简介：9200482人原发性肺癌癌基因表达研究/赵建升…//生物化学与生物物理进展.-1991.18(6).-472～474以myc家族基因(c-myc、L-myc及N-myc)、Ki-ras基因及C-fos基因为探针,用RNA斑点杂交法观察了24例人原发性肺癌癌基因的转录表达特点.结果:癌基因表达增强的有C-myc.占病例的75%(18/24);C-fos占65%(11/17);Ki-ras占58%(15/24);

简介：目的激素难治性前列腺癌（hormonerefractoryprostatecancer,HRPC）的治疗，在2004年取得了突破性进展，TAX327研究证实多西他赛联合泼尼松3wk方案可以延长病人的生存期，从而确立了其一线标准化疗方案的地位。但是，多西他赛联合泼尼松方案失败后的治疗选择仍然是一难题，为此，我们观察多西他赛联合雌二醇氮芥及泼尼松三联方案在一线标准方案失败后治疗HRPC的疗效和安全性。方法2005年11月至2007年3月，6例HRPC在多西他赛联合泼尼松3wk方案治疗过程中病情恶化（血PSA升高）时，用多西他赛联合雌二醇氮芥及泼尼松治疗。治疗方案：多西他赛75mg／m^2，d1，强的松5mgbid，d1起连续应用，雌二醇氮芥280mg，2次，d，d1起连用5d。21d为1疗程。病人平均年龄75．8a，血睾酮维持去势水平，WHO体力状态评分≤2，骨髓、心、肝、肾等重要脏器功能正常。估计生存时间〉3mo。疗效及不良反应判断标准：①血PSA下降〉50％，且维持〉3wk判断为有效。②可测量病灶按RECIST实体瘤评价标准评价。③骨痛者按主诉疼痛程度分级法（VRS）评价，评分下降1级为有效。④不良反应按WHO不良反应标准评定。结果6例共完成27个疗程。PSA有效5例，有效率为83.3％。有效病人PSA从治疗前的10．9～606．2（223．6±218．0）mg／mL下降到治疗后最低1．1～127．6（61．5±50．4）ng／mL。1例肺转移者，转移灶为稳定。1例骨痛者VRS疼痛评分从Ⅱ下降到Ⅰ。到分析日止，已死亡1例。此例从诊断激素非依赖前列腺癌到死亡共53mo。5例存活者从诊断激素非依赖前列腺癌起已存活14～36mo。主要不良反应为骨髓抑制（100％），脱发（100％），乏力（67％）等。结论多西他赛联合雌二醇氮芥及泼尼松三联方案对多西他赛联合泼尼松3wk方案治疗失败后的病人疗效肯定，毒副反应可以耐受，值得进一步观察�

简介：目的：探索苦参碱对人乳腺癌耐药株MCF-7/ADR多药耐药性逆转的作用机制及对PI3K/AKT信号通路下游因子的影响。方法：采用MTT法检测不同浓度苦参碱和MK2206作用MCF-7/ADR细胞24h后的生长抑制率,以抑制率为10%左右为检测标准;用荧光定量RT-PCR、Westernblot检测不同浓度苦参碱作用MCF-7/ADR细胞24h后Bcl-2、Bax、Caspase-3、PARP、GSK-3β、p65六种基因mRNA和蛋白的相对表达量。结果：荧光定量RT-PCR结果显示0.6、1.2g/L的苦参碱处理组与空白对照组相比,随着苦参碱浓度的提高,PI3K/AKT信号通路下游作用因子Bcl-2基因和p65基因的相对表达量逐渐降低,Caspase-3基因的相对表达量变化不显著,而Bax基因、GSK-3β基因及PARP基因的相对表达量逐渐增高;相同抑制率的苦参碱组（0.6g/L）和MK2206组（0.05μmol/L）相比,两组降低基因表达量的差异不明显,苦参碱组更能增加Bax、PARP和GSK-3β基因的相对表达量并且能够明显减低p65基因的相对表达量。Westernblot结果显示0.3、0.6、1.2g/L三组不同浓度苦参碱干预组与空白对照组相比,随着苦参碱浓度的提高Bcl-2和p65蛋白表达量逐渐降低,Bax、PARP和GSK-3β蛋白表达量逐渐增高,Caspase-3蛋白表达量变化不明显;相同抑制率的苦参碱组（0.6g/L）和MK2206组（0.05μmol/L）相比,苦参碱组更明显。结论：苦参碱可能是通过作用AKT靶基因启动PI3K/AKT信号转导通路中下游相关凋亡因子而发挥逆转乳腺癌多药耐药的作用。

简介：Objective:Avarietyofionchannelshavebeenimplicatedinbreastcancerproliferationandmetastasis.VoltagegatedK+(Kv)channelsnotonlycauserepolarizationinexcitablecells,butarealsoinvolvedinmultiplecellularfunctionsinnon-excitablecells.InthisstudyweinvestigatedtheroleofKvchannelsinmigrationofBT474breastcancercells.Methods:Transwelltechniquewasusedtoseparatemigratorycellsfromnon-migratoryonesandthesetwogroupsofcellsweresubjecttoelectrophysiologicalexaminationsandmicrofluorimetricmeasurementsforcytosolicCa2+.CellmigrationwasexaminedintheabsenceorpresenceofKvchannelblockers.Results:Whencomparedwithnon-migratorycells,migratorycellshadmuchhigherKvcurrentdensities,butratherunexpectedly,moredepolarizedmembranepotentialandreducedCa2+influx.Reversetranscriptasepolymerasechainreaction(RT-PCR)analysisrevealedthepresenceofKv1.1,Kv1.3,Kv1.5,Kv2.1,Kv3.3,Kv3.4andKv4.3channels.Cellmigrationwasmarkedlyinhibitedbytetraethylammonium(TEA),adelayedrectifierKvchannelblocker,butnotby4-aminopyridine,anA-typeKvchannelblocker.Conclusions:Takentogether,ourresultsshowthatincreasedKvchannelexpressionplayedaroleinBT474cellmigration,andKvchannelscouldbeconsideredasbiomarkersorpotentialtherapeutictargetsforbreastcancermetastasis.Themechanism(s)bywhichKvchannelsenhancedmigrationappearedunrelatedtomembranehyperpolarizationandCa2+influx.

简介：Objective:Tounderstandwhetherverapamil(VER)resistancedevelopmentinthemultidrug-resistantcelllineanditsmechanism.Methods:K562/ADM/VERcellsublineresistanttoverapamilwasestablishedthroughagradualincreaseofVERconcentrationinthemedia.MTTmethodwasusedtoassayresistancetoVER,crossresistancetodipyriamole(DPM),cyclosporinA(CsA)inthecells,andHPLCandspectrofluorometertodetectintracellularaccumulationofVERorADMrespectively,aswellasS-Pimmunocytochemicaltechniquefordetectionofgenesexpression.Results:Itwereobservedthat7.9-foldincreaseinVERresistance,significantlyreducedintracellularaccumulationofVERorADMandalsodevelopacrossresistancetoDPMandCsAinK562/ADM/VERcells,comparedwithitsparentcell,K562/ADM.High-levelofp-glycoprotein(pgp),middle-levelofp53,p16,waspresentintwocelllineswithoutexpressionofGSTPI,C-myc,C-myc,C-fosandC-erbB-2.Bc1-2proteinexpressionwasfoundonlyinK562/ADMcells.Conclusion:K562/ADMcellswerecapableofbeinginducedtodevelopresistancetoVER.

简介：目的评价髓核摘除联合K-Rod动态固定治疗腰椎间盘突出症的临床疗效及影像学变化。方法2009年1月至2011年11月，对39例单节段或双节段腰椎间盘突出症患者分别采用髓核摘除联合K-Rod动态固定（A组，19例）和经椎间孔椎体间融合（transforaminallumbarinterbodyfusion，TLIF）（B组，20例）治疗。两组患者一般资料比较差异无统计学意义（P＞0.05），有可比性。手术前后采用疼痛视觉模拟评分（visualanaloguescale，VAS）及Oswestry功能障碍指数（oswestrydisabilityindex，ODI）进行比较评价，并动态观察术后责任椎间隙高度及腰椎活动度变化情况。结果A组随访时间18～32个月，平均22个月；B组随访时间18～37个月，平均23个月。末次随访两组患者腰腿痛症状明显改善。A组末次随访时VAS为1.16±0.50，ODI为（3.72±3.63）%，较术前VAS5.52±1.58及ODI（50.83±20.28）%有明显降低（P＜0.001）；B组末次随访时VAS为2.13±0.69，ODI为（18.61±4.07）%，较术前VAS6.50±1.21及ODI（60.56±9.92）%有明显降低（P＜0.001）。A组术后手术节段ROM减小，但末次随访时已恢复至术前近60%，B组术后手术节段将为0°。两组相邻节段及腰椎总活动度维持在术前水平。A组末次随访时手术节段椎间隙高度较术前降低约10%，但术后维持在一个较稳定的水平。两组相邻椎间隙高度无明显差异。两组均未见内固定松动、物断裂等情况。结论与融合相比，K-Rod系统保留了腰椎生理曲度和固定节段的活动度，对相邻节段退变无明显影响，短期临床疗效满意，长期疗效有待进一步观察。

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：目的将在对待matrine的K562房间上调查CGI-100-击倒的K562房间的特征和CGI-100RNA干扰(RNAi)的效果。指向CGI-100基因和与一个不同序列包含一样的核苷酸作文的一双否定控制的三oligonucleotides被设计并且化学上综合了的方法。由在K562房间的shRNA-CGI-100的CGI-100表示的抑制效率用semiquantitativeRT-PCR和点污点杂交被决定。K562房间的生长上的CGI-100RNAi的效果用MTT试金被检验，房间区别被不同途径包括流动cytometry，benzidine染色和电子显微镜测量。在CGI-100-konckdownK562细胞为48h与matrine的0.2mg/ml或hemin的30mol/L被孵化以后，GlycophorinA(GPA)(CD235a)和生长因素independence-1BmRNA(Gfi-1BmRNA)的表示层次被RT-PCR和GPA的蛋白质层次测量，CD14和CD15被流动cytometry检测。结果CGI-100RNAi的真核细胞的表示向量成功地被构造。K562/shRNA-CGI-100房间线在由shRNA-CGI-100的CGI-100基因表示的抑制效率在哪个是54%被建立。CGI-100-knockdown禁止了增长并且在K562房间导致了erythroid区别。与控制K562房间相比，K562/shRNA-CGI-100房间证明减少的吸收度价值由MTT试金，减少的enchromation，增加的heterochromation，G0/G1阶段房间的增加的百分比，S阶段房间的减少的人口，减少的PI(房间的增长索引)，和benzidine积极的房间的提高的百分比检测了。而且，到matrine或hemin的K562/shRNA-CGI-100房间的敏感被提高，到matrine的这些房间的敏感对hemin比那高。与控制K562房间相比，在K562/shRNA-CGI-100房间的matrine处理导致了增长，benzidine积极的房间的提高的百分比，GPA和Gfi-1B的显然起来调整的mRNA表达式，和GPA的增加的吝啬的荧光紧张(MFI)的增加的禁止的率。没有CD14表示被检测，没有统计意义被作出对有利的裁决检测CD15。最后，在与hemin对待并�

简介：Prostatecancergene3(PCA3,alsoknownasDD3)isanewbiomarkerthatcouldimprovetheaccuracyofprostatecancerdiagnosis.Itisagreatbiomarkerwithfairlyhighspecificityandsensitivity.Theincidenceofprostatecancerisrisingsteadilyinmostcountries.Thecommonlyusedprostate-specificantigen(PSA)testoncegavepeoplehopeforearlydiagnosisofprostatecancer.However,thelowspecificityofthePSAtesthasresultedinalargenumberofunnecessarybiopsiesandovertreatment.Duringthepastdecade,manynewprostatecancerbiomarkershavebeenfound.Amongthese,PCA3isthemostpromising.Duetoitsgreatperformanceindistinguishingprostatecancerfromotherprostateconditions,PCA3couldlikelybeappliedforearlydiagnosisofprostatecancer,patientfollow-up,prognosisprediction,andtargetedtherapy.Afteryearsofresearch,wehaveobtainedsomeknowledgeaboutthesequenceofPCA3gene.WehavealsodeterminedtherelationshipbetweenPCA3andtheproliferationofprostatecancercellsandlearnedsomeinformationabouthowPCA3affectstumor-relatedgenesandproteins.APCA3scorehasbeencreated,andithasbeenusedinavarietyofstudies.SomeresearchershaveevenappliedPCA3totargetedtherapyandobtainedagoodeffectinvitro.Thisreviewdescribesthecurrentstateofresearch,andexploresthefutureprospectsforPCA3.更多还原

简介：Forelectronicmicroscopicobservation,wefoundSSV-transformedNIH3T3cellsweredifferentfromnon-transformedcells.InSSV-transformedNIH3T3cellsnucleicytoplasmaratiowasincreasedandincytoplasmatheribosomes(polyribosomeswereattachedtotheswollenroughendoplasmicreticulum.Itwaslikelythatribosomeswerelinedtogetherfunctionallyandstructionallytoproducespecificprotein(PDGF-likeprotein).

简介：Objective:ToexploretheeffectsofnuclearM-CSFontheprocessoftumorigenesis.Methods:FunctionalpartofM-CSFcDNAwasinsertedintoaneukaryoticexpressionplasmidpCMV/myc/nuc,whichcanaddthreeNLStotheC-terminaloftheexpressedproteinanddirecttheproteinintothecellnuclei.TheconstructedplasmidwastransferredintoNIH3T3cellsandthecellcloneswereselectedbyG-418selection.CellclonesstableexpressingtargetproteinwereidentifiedbyRT-PCR,ABCimmunohistochemistryassayandWesternblot.Cellgrowthkineticsanalysesthroughgrowthcurves,celldoublingtime,MTTtestandanti-senseoligodeoxynucleotide(ASODN)inhibitingcellgrowthtestwereperformedtoidentifycellsproliferationpotential.Results:Thetransfectedcellsshowedelevatedproliferationpotentialoverthecontrolcells.Conclusion:AbnormalappearanceofM-CSFinnucleuscouldenhancecellproliferation,whichsuggeststhatcytokineisoformswithincellnucleusmightplaytranscriptionfactor-likerole.