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SmallCellLungCancer(SCLC):Diagnosis,TreatmentandNaturalHistoryGaryL.WeinsteinM.D.SCLC•Lungcancerepidemiology•SCLC–Pathology–Tumormarkers–G

enetics–Clinicalcourse–Staging–TreatmentSCLC,factoids•15–25%ofalllungcancers•Almostexclusivelyinsmokers•DistinguishedfromNSCLCby:–R

apiddoublingtime–Highgrowthfraction–Earlydevelopmentofwide-spreadmetsSCLC,factoids(cont’d)•Consideredhighlyrespon

siveto“chemsandbeams”•BUT…usuallyrelapseswithin2yearsdespitetreatment•Overall,only3–8%ofallpatientssurvivemorethan5years•Mo

stcommonmalignancyassociatedwithNeurologicparaneoplasticsyndromesSCLC,pathology•Mostrecent(1999)WHOclassification–C

lassicalsmallcellcarcinoma–Largecellneuroendocrinecancer–CombinedsmallcellcarcinomawithsomeNSCLC•Cellsareapprox.2X’sthesizeofnormallymphocytesS

CLC,pathologySCLC,pathologySCLC,clinicalpresentation•Typicallyarisecentrally•Mostcommonpresentationisalargehilarmasswithb

ulkymediastinalLAN•Commonsymptomscough,SOB,wtloss•Approx.70%withovertmetsatpresentation•Commonlyspreadtoliver,adrenals,boneandb

rain•CanpresentwithparaneoplasticsyndomeSCLC,tumormarkers•3maingroups:Neural,Epithelial,Neuroendocrine•Ep

ithelial:virtuallyallSCLCsareimmunoreactiveforKeratinandEpithelialMembraneAntigen•1ormoremarkersofNeural/Ne

uroendocrinedifferentiationfoundinapprox.75%ofSCLCsSCLC,tumormarkers–Leadstoexpressionofdopadecarboxylase,calcitonin,neuron-specif

icenolase,chromograninA,CD-56(aneuralcelladhesionmolecule)gastrinreleasingpeptideandinsulin-likegrowthhormone–Occasionallypatientsp

roduceantibodiesthatcross-reactwithboththeSCLCcellsandtheCNS→cerebellardegenerationsyndromes–SCLCcellscanproduceanumberofpol

ypeptidehormonesincludingACTHandVasopressinNeurologicParaneoplasticSyndromesLungcancer,ParaneoplasticSyndromesSCLC,genetics•Developmentoflungcance

rsoccurthroughstimulationofproliferationandmutagenesis,occurringoverYEARSandresultingfromexposuretotobaccoandothercarcinogensSCLC,genetics•Themos

tcommongeneticsofSCLCare:–P53mutationispresentin75-90%–Lossofheterozygosityofc-somes9pand10qinthemajority–Deletionof3p→inactiva

tionofasmanyas3tumorsuppressorgenes–Lossoftheretinoblastomagenefunctionisnearlyubiquitous–Activationoftelomeraseinapprox.90%(allowsce

llstodivideforever)TheEndQuestions?