简介：Objective:Theaimofthepresentstudywastoconstructariskassessmentmodelwhichwastestedbydisease-freesurvival(DFS)ofesophagealcancerafterradicalsurgery.Methods:Atotalof164consecutiveesophagealcancerpatientswhohadundergoneradicalsurgerybetweenJanuary2005andDecember2006wereretrospectivelyanalyzed.Thecutpointofvalueatrisk(VaR)wasinferredbystem-and-leafplot,aswellasbyindependent-samplest-testforrecurrence-freetime,furtherconfirmedbycrosstabchi-squaretest,univariateanalysisandCoxregressionanalysisforDFS.Results:ThecutpointofVaRwas0.3onthebasisofourmodel.Therateofrecurrencewas30.3%(30/99)and52.3%(34/65)inVaR<0.3andVaR≥0.3(chi-squaretest,χ2=7.984,P=0.005),respectively.The1-,3-,and5-yearDFSofesophagealcancerafterradicalsurgerywas70.4%,48.7%,and45.3%,respectivelyinVaR≥0.3,whereas91.5%,75.8%,and67.3%,respectivelyinVaR<0.3(Log-ranktest,χ2=9.59,P=0.0020),andfurtherconfirmedbyCoxregressionanalysis[hazardratio=2.10,95%confidenceinterval(CI):1.2649-3.4751;P=0.0041].Conclusions:Themodelcouldbeappliedforintegratedassessmentofrecurrenceriskafterradicalsurgeryforesophagealcancer.

简介：Objective:DiffuseLargeBCellLymphoma(DLBCL)isaheterogeneousgroupoftumorswithdifferentbiologicalandclinicalcharacteristicsthathavediverseclinicaloutcomesandresponsetotherapy.Stromal-1signatureoftumormicroenvironmentofDLBCLrepresentsextracellularmatrixdepositionandhistiocyticinfiltrate,whereasstromal-2representsangiogenesisthatcouldaffecttumorprogression.Methods:Theaimofthepresentstudyistoassessthesignificanceofstromal-1signatureusingSPARC-1andstromal-2signatureusingCD31expressionandthenfinallytoconstructbiologicprognosticmodel(BPM)in60casesofDLBCLviaimmunohistochemistry.Results:Microvesseldensity(P<0.05)andSPARCpercentageofexpression(P<0.001)werehigherinDLBCL,includinggerminalandnongerminalcases,comparedwithreactivefollicularhyperplasia.Highmicrovesseldensitywassignificantlyassociatedwithsplenicinvolvement(P=0.008),highmitoticcount(P=0.045),andpresenceofcapsularinvasion(P=0.035).PercentageofSPARCexpressionwassignificantlyassociatedwithsplenicinvolvement(P=0.03).ConstructingBPMshowedthat42cases(70%)wereoflowbiologicscore(0–1)and18cases(30%)wereofhighbiologicscore(2–3).LowBPMcasesshowedlessprobabilityforsplenicinvolvement(P=0.04)andahigherrateofcompleteresponsetotherapycomparedwithhighscorecases(P=0.08).Conclusions:TheDLBCLmicroenvironmentcouldmodulatetumorprogressionbehaviorsinceangiogenesisandSPARCpositivestromalcellspromotedisseminationbyassociationwithspleeninvolvementandcapsularinvasion.Biologicprognosticmodels,includingmodifiedBPM,whichconsideredcelloriginofDLBCLandstromalsignaturepathways,coulddetermineDLBCLprogressionandresponsetotherapy.