简介:一、概述趋化因子是一类小分子分泌型(8-14KDa)蛋白,是目前已知的最大的细胞因子家族,已发现超过50种.多数趋化因子氨基端(N端)有4个特征性的保守的半胱氨酸(Cys),相互形成二硫键.
简介:目的探讨骨髓增生异常综合征(MDS)患者接受地西他滨(DAC)治疗前后程序性死亡因子-1/程序性死亡因子-1配体(PD-1/PD-L1)的变化。方法收集2016年1月至2017年1月初治MDS中符合WHO2008分型WPSS预后分层中危组及高危组并接受DAC(20mg/m^2d1-d5,21-28天为1个周期,治疗2个周期)治疗的18例患者,同时以5例非恶性血液病患者为对照。于DAC治疗前后收集外周血和骨髓细胞。流式细胞术(FCM)检测DAC治疗前后外周血CD3+CD4+T、CD3+CD8+T淋巴细胞的PD-1和骨髓单核细胞PD-L1的变化;QPCR检测DAC治疗前后外周血及骨髓单个核细胞PD-1mRNA、PD-L1mRNA相对表达量的变化;比较化疗缓解组(n=5)和未缓解组(n=13)PD-1/PD-L1的表达水平。结果FCM检测显示,DAC治疗后,中危组CD3+CD4+T、CD3+CD8+T淋巴细胞PD-1和骨髓单个核细胞的PD-L1比例分别为(11.43±1.88)%、(11.46±1.60)%和(16.59±0.72)%,高危组分别为(16.36±3.71)%、(16.59±3.81)%和(18.69±1.60)%,均高于治疗前和对照组(P〈0.05);未缓解组CD3+CD4+T、CD3+CD8+T淋巴细胞PD-1和骨髓单个核细胞上PD-L1的比例分别为(18.51±2.62)%和(19.03±2.18)%和(19.22±1.40)%,高于缓解组(P〈0.05)。QPCR检测显示,DAC治疗后,中危组外周血单个核细胞PD-1mRNA和骨髓单个核细胞PD-L1mRNA的相对表达量为6.32±3.37和2.88±1.72,高危组分别为12.55±6.27和7.47±4.90,均高于治疗前(P〈0.05)。MDS未缓解组外周血PD-1mRNA和骨髓单个核细胞PD-L1mRNA的相对表达为16.28±4.64和9.16±5.40,高于缓解组(P〈0.05)。结论DAC治疗后中、高危MDS患者的外周血、骨髓中PD-1/PD-L1表达明显上升,尤其是未缓解组,PD-1/PD-L1高表达可能是介导DAC耐药的原因之一。
简介:目的探讨T3期胃癌行胃癌根治术淋巴结清扫数目与预后的关系.方法回顾性分析2000年1月~2005年1月在我院接受胃癌根治术的426例T3期胃癌患者的临床资料,比较根治术不同淋巴结清扫数目组别问生存率的差异.结果426例患者中,无淋巴结转移者154例,其中清扫淋巴结数超出25枚的患者1、3、5年生存率分别为95.8%、87.6%和83.5%,清扫淋巴结数20~25枚者1、3、5年生存率分别为96.7%、86.5%和80.1%,清扫淋巴结数15~19枚者1、3、5年生存率分别为96.3%、83.2%和69.3%;有淋巴结转移者272例,其中清扫淋巴结数目超过25枚的患者1、3、5年生存率分别为87.1%、67.1%和54.7%,清扫淋巴结数20~25枚者1、3、5年生存率分别为85.6%、63.5%和50.2%,清扫淋巴结数15~19枚者1、3、5年生存率分别为86.5%、61.2%和38.4%.清扫淋巴结数20~25枚组与25枚以上组相比,无论有无淋巴结转移,生存率差异均无统计学意义(P>0.05),而与清扫淋巴结数15-19枚组比较,无沦有无淋巴结转移,5年生存率差异均有统计学意义(P<0.05).结论T3期胃癌行胃癌根治术淋巴结清扫数目应达20枚以上.
简介:Theacquisitionofsecondarychromosomalaberrationsinchronicmyeloidleukemia(CML)patientswithPhiladelphiachromosome-positive(Ph+)karyotypesignifiesclonalevolutionassociatedwiththeprogressionofthediseasetoitsacceleratedorblasticphase.Therefore,theseaberrationshaveclinicalandbiologicalsignificance.T(3;12)(q26;p13),whichisarecurrentchromosomalaberrationobservedinmyeloidmalignancies,istypicallyassociatedwithdysplasiaofmegakaryocytes,multilineageinvolvement,shortdurationofanyblasticphase,andextremelypoorprognosis.Wehaveidentifiedarecurrentreciprocaltranslocationbetweenchromosomes3and12withdifferentbreakpointatbands3q21inthemalignantcellsfroma28-year-oldman.ThepatientwasinitiallydiagnosedashavingPh+CMLinthechronicphase.Thet(3;12)(q21;p13)translocationoccurred4yearsafterthepatientwasfirstdiagnosedwithCMLwhileundergoingtyrosinekinaseinhibitortherapy.Weconfirmedthet(3;12)(q21;p13)translocationviafluorescenceinsituhybridizationassaybyusingwhole-chromosomepaintprobesforchromosomes3and12.Ourfindingsdemonstratethat,similartootherrecurrenttranslocationsinvolving3q26suchast(3;3)andt(3;21),thet(3;12)(q21;p13)translocationisimplicatednotonlyinmyelodysplasticsyndromeandacutemyeloidleukemiabutalsointheprogressionofCML.Thesefindingsextendthediseasespectrumofthiscytogeneticaberration.
简介:Objective:Stromalinteractionmolecule1(STIM1)overexpressionhasbeenreportedtoplayanimportantroleinprogressionofseveralcancers.However,themechanismofSTIM1overexpressionanditsrelationshipwithhypoxiainpancreaticductaladenocarcinoma(PDAC)remainsunclear.Methods:STIM1andHIF-1αexpressionwastestedusingimmunohistochemistryintissuemicroarray(TMA)includingpancreaticcancerandmatchednormalpancreatictissues,andtheirrelationshipswithclinicopathologicalparameterswerestatisticallyanalyzed.q-PCR,Westernblot,ChIP,andluciferaseassaywereemployedto030analyzetranscriptionalregulationbetweenHIF-1αandSTIM1inpancreaticcancerPANC-1cells.Results:BothSTIM1andHIF-1αshowedhigherpositiveratesandup-regulatedexpressionincancertissuescomparedtothatofnormaltissues(P<0.05).TheKaplan–MeiermethodrevealedthathigherHIF-1αandSTIM1expressionlevelsweresignificantlycorrelatedwithdecreaseddisease-freesurvival(P=0.025andP=0.029,respectively).TheexpressionofHIF-1αshowedasignificantpositivecorrelationwiththatofSTIM1incancertissues(rs=0.3343,P=0.0011)andpancreaticcancercelllines.Furthermore,ChIPandluciferaseassaysconfirmedthatHIF-1αboundtotheSTIM1promoterandregulateditsexpressioninPANC-1cells.Conclusions:Inhypoxiamicroenvironment,up-regulatedexpressionofSTIM1mediatedbyHIF-1αpromotesPDACprogression.HIF-1αandSTIM1arepotentialprognosticmarkersand/ortherapeutictargetsforPDACtreatment.