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: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.
简介:Chronicalcoholconsumptionisamajorriskfactorworldwideaffectingsignificantlybothmortalityandyearsoflifelost(YLL)(1).Ca.5%ofthewesternworldshowriskyalcoholconsumptionandinsomecountriessuchasChinaaregionalyearlyincreaseofalcoholconsumptionofover400%hasbeenobservedrecently(2,3).Theliveris
简介:Objective:Toobservetheeffectofinhibitionoftelomeraseactivitybyseleniumdioxide(SeO2)onlungcarcinomacelllineGLC-82.Methods:TRAP-PCR-ELISAwasusedtostudythechangesoftelomeraseactivityinhumanpulmonaryadenocarcinomacelllineGLC-82treatedbySeO2atthedifferentconcentrations(3,10,30μmol/L)andfordifferenttimes(24,48,and72h).Results:SeO2inhibitedthetelomeraseactivityofGLC-82atthedifferentconcentrationsaftertreatmentof24,48and72h.Conclusion:SeO2inhibitsfromtelomeraseactivityofhumanlungcarcinomalineGLC-82.Theeffectofinhibitionisdose-dependantandtime-dependant.
简介:背景与目的:不典型的鞍区病变易于误诊,特别是鞍内动脉瘤,误诊后的处理往往十分被动。本文结合我们误诊的两例鞍内动脉瘤,探讨鞍内动脉瘤的临床表现、影像学特点及误诊后的处理措施。方法:分析我们误诊的两例鞍内动脉瘤的临床资料,并复习文献。结果:1例患者术前误诊为鞍区骨源性病变,1例误诊为垂体瘤,均存经蝶手术过程中发生汹涌出血,术后脑血管造影提示为颈内动脉海绵窦段动脉瘤。视力下降、视野缺损、垂体功能低下及高泌乳素血症是其主要临床表现。磁共振上的异常流空信号为其特征性的影像改变。结论:非典型的鞍内动脉瘤诊断困难;当磁共振为非典型的鞍区病变表现,且有垂体功能低下和(或)视力下降时,或磁共振显示有异常的流空信号,应常规行脑血管造影检查。
简介:目的探讨组织中缺氧诱导因子2仪(HIF-2α)的表达在鼻咽癌诊治中的临床价值。方法应用免疫组织化学方法检测51例初诊鼻咽癌组织和20例鼻咽炎性组织中HIF-2α的表达。结果鼻咽癌组织HIF-2α阳性表达率明显高于鼻咽慢性炎性组织(P〈0.01);Ⅰ和Ⅱ期鼻咽癌患者组织中HIF-2α的表达明显低于Ⅲ和Ⅳ期鼻咽癌患者(P=0.039);T1及T2患者鼻咽癌组织的HIF-2α表达阳性率明显低于T3及T4患者鼻咽癌组织的HIF-2α表达阳性率(P=0.026);有颈部淋巴结转移患者鼻咽癌组织的HIF-2α表达阳性率明显高于无颈淋巴结转移患者的HIF-2α表达阳性率(P=0.015)。结论HIF-2α的高表达在鼻咽癌的发生、发展过程中有重要作用,检测HIF-2α的表达对于鼻咽癌的诊断、分期具有一定的临床价值,但仍需积累更多的临床资料进行深入研究。
简介:目的:探讨EZH2对胃癌MKN-28细胞生物学的影响。方法:siRNA干扰EZH2;MTT法检测沉默EZH2后细胞的增殖情况;Transwell小室观察细胞的侵袭情况;Realtime-PCR检测细胞中相关基因的表达情况。结果:siRNA有效干扰了EZH2的表达;沉默EZH2细胞组的细胞增殖明显受到抑制(P〈0.05);细胞的侵袭情况,沉默EZH2明显抑制了细胞的侵袭,与其他两组比较差异显著(P〈0.05);siEZH2细胞组E-cadherinmRNA、β-cateninmRNA的表达水平高于其他两组,Bcl-2mRNA的表达水平低于其他两组(P〈0.05)。结论:沉默EZH2抑制了胃癌MKN-28细胞的增殖,抑制了细胞的侵袭和抗凋亡基因的表达,可能是通过调控E-cadherin的表达水平和Wnt信号途径实现的,为寻找有效的靶点和肿瘤的靶向治疗提供一定的理论依据。
简介:ER、PR和HER-2均为阴性的乳腺癌(三阴乳腺癌)患者是一组特殊的群体,其病理及肿瘤生物学特征有:多为导管癌、组织学分级较高、肿瘤细胞多表达basal细胞角蛋白、EGFR和p53等,并且在表型特征和分子水平上与basal—like乳腺癌和BRCA1相关乳腺癌存在一定的相关性。三阴乳腺癌患者常较早发生局部复发和远处转移,内脏转移率高于骨转移,预后较差,近来研究者开始逐渐重视此亚型群体。由于没有内分泌和靶向HER-2治疗的机会,因此只能将化疗作为主要的治疗手段,目前也有一些关于化疗和靶向治疗等方面的研究报道和临床试验,提示烷化剂、铂类、蒽环类等可能是相对敏感药物,针对EGFR、C—kit和Src等靶点的靶向治疗也有可能发挥较好的治疗效果。但是目前的研究结果还不能明确三阴乳腺癌的生物学特点和最佳治疗策略,本文将有关三阴乳腺癌的最新进展做一综述。
简介:目的探讨原发性肺癌以单纯指骨转移为首发症状的临床特点以及肺癌发生指骨转移的机理。方法对1991年至2007年间,见诸于有关文献报道的以单纯指骨转移为首发症状的原发性肺癌病人的文献资料进行综合性分析。结果在文献报道的以单纯指骨转移为首发症状的17例原发性肺癌的病人中,其转移病灶位于左手指骨者7例,右手指骨者9例,双手指骨者1例,指骨转移病灶的数量在两手之间的分布大致相等,除3例病人其转移病灶位于近节指骨外,其余病人的转移病灶均位于其末节指骨;有6例病人的患病手指既往曾有外伤史。结论传统的机械一解剖学说和种子一土壤学说的观点均不能解释原发性肺癌发生指骨转移的机理,故临床上如遇久治不愈的手指软组织炎症时,应想到是否有肿瘤细胞转移至此的可能性。
简介:PURPOSE:Todeterminethesafetyandefficacyofgefitinib,anepidermalgrowthfactorreceptor(EGFR)tyrosinekinaseinhibitor,incombinationwithradiationfornewlydiagnosedglioblastoma(GBM)patients.METHODSANDMATERIALS:BetweenMarch21,2002,andMay3,2004,RadiationTherapyOncologyGroup(RTOG)0211enrolled31and147GBMpatientsinthephase1and2arms,respectively.Treatmentconsistedofdailyoralgefinitnibstartedatthetimeofconventionalcranialradiationtherapy(RT)andcontinuedpostRTfor18monthsoruntilprogression.Tissuemicroarraysfrom68caseswereanalyzedforEGFRexpression.RESULTS:Themaximumtolerateddose(MTD)ofgefitinibwasdeterminedtobe500mginpatientsonnon-enzyme-inducinganticonvulsantdrugs(non-EIAEDs).Allpatientsinthephase2componentweretreatedatagefitinibdoseof500mg;patientsreceivingEIADSscouldbeescalatedto750mg.Themostcommonsideeffectsofgefitinibincombinationwithradiationweredermatologicandgastrointestinal.Mediansurvivalwas11.5monthsforpatientstreatedperprotocol.Therewasnooverallsurvivalbenefitforpatientstreatedwithgefitinib+RTwhencomparedwithahistoricalcohortofpatientstreatedwithRTalone,matchedbyRTOGrecursivepartitioninganalysis(RPA)classdistribution.Youngeragewassignificantlyassociatedwithbetteroutcome.Perprotocolstratification,EGFRexpressionwasnotfoundtobeofprognosticvalueforgefitinib+RT-treatedpatients.CONCLUSIONS:TheadditionofgefitinibtoRTiswelltolerated.MediansurvivalofRTOG0211patientstreatedwithRTwithconcurrentandadjuvantgefitinibwassimilartothatinahistoricalcontrolcohorttreatedwithradiationalone.
简介:TherearesomeIndicationsthttherpesaimplexvirus(HSV)maybemutagenic.SpecificchromosomalchangeshavealsobeendemonstratedInculturedcellsinfectedwithHSV.TofurtherInvestigatethemutagenicactivityofHSVtype2(HSV-2)weusedmouseskinasamodelsystemforcardnogenetls.Inoculationofthebackskinof4-week-oldSencarmkewithlivevirustwiceperweekforoneweekorwithInactivatedvirustwiceperweekfortwoweekswasusedtoInitiatethemouseakin.AfterInitiationwithHSV-2,12-O-tetradecanoylphorbol-13-acetale(TPA)wasappliedtwiceweeklyfor50weeksasapromoter.Duringaperiodof52weeks,noskincarcinomawasfoundIntheexperimentalgroups,whereas55%ofcontrolmicetreatedwith9,10-dlmethy1-1,2-benzanthracene(DMBA)andthenwithTPA-developedskincarcinoma.TheresultsdemonstratethatHSV-2couldnotsubstituteforDMBAinthisanimalmodeloftwo-stageskincarcinogenesis.