2000
The utility of Ki-ras mutation analysis in the cytologic diagnosis of pancreatobiliary neoplasma.
Dillon DA, Johnson CC, Topazian MD, Tallini G, Rimm DL, Costa JC. The utility of Ki-ras mutation analysis in the cytologic diagnosis of pancreatobiliary neoplasma. The Cancer Journal 2000, 6: 294-301. PMID: 11079168.Peer-Reviewed Original ResearchConceptsFine needle aspiratesBile duct brushingsCytologic diagnosisPositive predictive valueCommon bile duct brushingsDuct brushingsPancreatobiliary carcinomaPredictive valueMutation patternsBiliary tract carcinomaPrevious retrospective studyAvailable clinical informationConsecutive clinical specimensDefinitive cytologic diagnosisPolymerase chain reaction/single-strand conformation polymorphism analysisRoutine cytologic diagnosisPositive cytologyRetrospective studySuspicious morphologyCytologic evaluationSuspicious cytologyPancreatobiliary tractClinical informationMorphologic diagnosisNeoplastic cells
1999
Beta- and gamma-catenin mutations, but not E-cadherin inactivation, underlie T-cell factor/lymphoid enhancer factor transcriptional deregulation in gastric and pancreatic cancer.
Caca K, Kolligs FT, Ji X, Hayes M, Qian J, Yahanda A, Rimm DL, Costa J, Fearon ER. Beta- and gamma-catenin mutations, but not E-cadherin inactivation, underlie T-cell factor/lymphoid enhancer factor transcriptional deregulation in gastric and pancreatic cancer. Molecular Cancer Research 1999, 10: 369-76. PMID: 10392898.Peer-Reviewed Original ResearchMeSH KeywordsAdenomatous Polyposis Coli ProteinAmino Acid SequenceAnimalsBeta CateninCadherinsCytoskeletal ProteinsDesmoplakinsDNA-Binding ProteinsGamma CateninGene Expression Regulation, NeoplasticHMGB ProteinsHumansLymphoid Enhancer-Binding Factor 1Molecular Sequence DataMutagenesisPancreatic NeoplasmsStomach NeoplasmsTCF Transcription FactorsTrans-ActivatorsTranscription Factor 7-Like 1 ProteinTranscription FactorsTranscription, GeneticTumor Cells, CulturedConceptsPhosphorylation sitesMutant proteinsGlycogen synthase kinase 3beta phosphorylation sitesGlycogen synthase kinase-3betaFactor transcription factorsPotential phosphorylation sitesSynthase kinase-3betaTCF transcriptional activityE-cadherin inactivationNH2-terminal deletionsRole of APCImportant binding partnerSerine 28TCF transcriptionTranscriptional deregulationT-cell factorBinding partnerTranscription factorsAPC proteinKinase-3betaTranscriptional activityNH2 terminusAdenomatous polyposis coli (APC) mutationsCell adhesionPancreatic cancer lines