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: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.