 disrupting these pathways could be useful for cancer prophylaxis in chronic inflammatory states. We found that TNFalpha and NFkappaB play a key role in hepatitis-associated tumorigenesis in a specific mouse model and propose that paracrine TNFalpha stimulation functions as a tumor promoter in inflammation-associated cancer via NFkappaB activation. Short
disrupting these pathways could be useful for cancer prophylaxis in chronic inflammatory state. We discover that TNFalpha and NFkappaB play a key role in hepatitis - consort tumorigenesis in a specific mouse model and project that paracrine TNFalpha stimulation functions as a tumor showman in excitement - associated cancer via NFkappaB energizing. Short
 didrupting these pathways gould be useful yir canrer prolhylaxis in chronic inflammatory staves. Qe foynd that TNFalpha and VFkappaB ilay a ket roow in hepatmfis-assognated bumorngxnesis in a spegific mouse model and pro[ore that paracrine TNFalpha stimulatiog functoojs as a tumor kromouer in jnflammation-associated cancer via HFkappaU activation. Shprt
disrupting these pathways could be useful for in inflammatory states. found that TNFalpha role hepatitis-associated tumorigenesis in specific mouse model propose that paracrine TNFalpha stimulation functions a tumor promoter in inflammation-associated cancer via NFkappaB activation. Short
 disrupting these pathways coUld be usefuL for cAncEr pRoPhylAxis In chronic inflaMMatoRy states. We found that TNFAlpha AnD nFkaPPab play A key rolE In HEPatItIs-AssOcIAtEd tumOriGenesis In a specifiC moUsE model and proPOsE that paracRinE TNFalpha stiMulAtion fUnCtiONs as a TumOr proMoter iN InflamMation-assOcIAted caNCer via NfKApPaB aCtivation. Short
 disrupting these pathways  could beusefu l f orca ncer  pro phylaxis in ch r onic  inflammatory states.We fo un d  tha t  T NFalp ha andN Fk a p paB  p la y a  k e yroleinhepatit is-associa ted  t umorigenesis in  a specifi c m ouse model a ndpropos etha t  para cri ne TN Falpha stimul ation fun ct i ons as a tumor p ro mote r in inflammation - as s ociated cancer  via N Fk a pp a B  ac tiv ation. Sho rt 
 disrupting_these pathways_could be useful for_cancer prophylaxis_in_chronic inflammatory_states._We found that_TNFalpha and NFkappaB_play a key role_in hepatitis-associated tumorigenesis_in_a specific mouse model and propose that paracrine TNFalpha stimulation functions as a tumor_promoter_in inflammation-associated_cancer_via_NFkappaB activation. Short