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会计学Modelofsequentialgeneticalterationsleadingtometastaticcoloncancer.Eachofthestagesindicatedatthebottomismorphologicallydistinct,allowingresearcherstodeterminethesequenceofgeneticalterations.一、肿瘤特异性抗原二、肿瘤相关性抗原化学和物理致癌因素诱发的肿瘤抗原病毒诱发的肿瘤抗原癌基因和突变型抑癌基因表达的肿瘤抗原正常静止基因表达的肿瘤抗原Micewereinducedtoproducetumorsbytheinjectionofachemicalcarcinogen(methyl-cholanthrene).Tumorcellsfromthesemiceweretheninjectedsubcutaneouslyintogeneticallyidenticalmice.Later,thegrowingtumorwereremovedsurgically.Micechallengedwiththesametumorwereabletorejectit,butthosechallengedwithadifferenttumor(inducedwiththesamecarcinogen)werenot.Theabilitytorejectthetumorcouldbetransferredwithlymphoidcells.Experimentalinductionofimmunityagainsttumorcellsinducedbypolyomavirus(PV)癌基因和突变型抑癌基因表达的肿瘤抗原Activationofagrowthfactorreceptorinvolvesligandbinding,dimerization,andautophosphorylation,Atruncatedoncogenicreceptorthatlackstheligand-bindingregionisconstitutivelyactivebecauseitisnotrepressedbytheN-terminaldomain.Translocationsbetweenchromosome22andchromosome9generatePhiladephiachromosomesthatsynthesizebcl-ablfusiontranscriptsthatareresponsiblefortwotypesofleukemia.AlterationFunctionofproteinTumortypePointmutationERBB2GrowthfactorreceptorBreastcarcinomaFMSCSF-1receptorAML,myelodysplasiaRasGTP-bindingproteinCarcinomasandothersp53TumorsuppressorcellcyclecontrolManyincludingbladder,colon,lungRB1TumorsuppressorcellcyclecontrolRetinoblastoma,osteosarcomaPancreaticcarcinomaChromosomaltranslocationBCR-ABLTyrosinekinaseCML,ALLEZA-PRLTranscriptionfactorPre-BcellALLH4-RETGrowthfactorreceptor/tyrosinekinaseThyroidcarcinomaTPR-METGrowthfactorreceptor/tyrosinekinaseGastriccarcinomaLMYC-RLFTranscriptionfactorSmallcelllungcarcinomaNPM/ALKTyrosinekinaseLymphomaDeletionmutationsERB-BGrowthfactorreceptorGlimasTumourantigensrecognizedbyTlymphocytes:atthecoreofcancerimmunotherapy.NATUREREVIEWS|CANCERVOLUME14|FEBRUARY2014ImmunogenicityofNY-ESO-1,MAGE-A1,MAGE-A3,andSSX-2CTantigenmRNAE
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