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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:–Rapiddoublingtime–Highgrowthfraction–Earlydevelopmentofwide-spreadmetsSCLC,fact

oids(cont’d)•Consideredhighlyresponsiveto“chemsandbeams”•BUT…usuallyrelapseswithin2yearsdespitetreatment•Overall,only3–8%ofallpatientssurvivemoretha

n5years•MostcommonmalignancyassociatedwithNeurologicparaneoplasticsyndromesSCLC,pathology•Mostrecent(1999)WHOclassificatio

n–Classicalsmallcellcarcinoma–Largecellneuroendocrinecancer–CombinedsmallcellcarcinomawithsomeNSCLC•Cellsareapp

rox.2X’sthesizeofnormallymphocytesSCLC,pathologySCLC,pathologySCLC,clinicalpresentation•Typicallyarisecentrally•Mostcommonpresentationisalargehila

rmasswithbulkymediastinalLAN•Commonsymptomscough,SOB,wtloss•Approx.70%withovertmetsatpresentation•Commonlyspreadtoliver,adren

als,boneandbrain•CanpresentwithparaneoplasticsyndomeSCLC,tumormarkers•3maingroups:Neural,Epithelial,Neuroendo

crine•Epithelial:virtuallyallSCLCsareimmunoreactiveforKeratinandEpithelialMembraneAntigen•1ormoremarkersofNeural/Neuroe

ndocrinedifferentiationfoundinapprox.75%ofSCLCsSCLC,tumormarkers–Leadstoexpressionofdopadecarboxylase,calcitonin,neuron-specificeno

lase,chromograninA,CD-56(aneuralcelladhesionmolecule)gastrinreleasingpeptideandinsulin-likegrowthhormone–Occasionallypati

entsproduceantibodiesthatcross-reactwithboththeSCLCcellsandtheCNS→cerebellardegenerationsyndromes–SCLCcellscanproduceanumberofpolypeptidehormonesi

ncludingACTHandVasopressinNeurologicParaneoplasticSyndromesLungcancer,ParaneoplasticSyndromesSCLC,genetics•Developmento

flungcancersoccurthroughstimulationofproliferationandmutagenesis,occurringoverYEARSandresultingfromexposuretotobaccoandothercarcinog

ensSCLC,genetics•ThemostcommongeneticsofSCLCare:–P53mutationispresentin75-90%–Lossofheterozygosityofc-

somes9pand10qinthemajority–Deletionof3p→inactivationofasmanyas3tumorsuppressorgenes–Lossoftheretinoblastomagenefunctionisnearlyubiquitous–Activationo

ftelomeraseinapprox.90%(allowscellstodivideforever)TheEndQuestions?