2023
Spatial characterization and quantification of CD40 expression across cancer types
Bates K, Vathiotis I, MacNeil T, Ahmed F, Aung T, Katlinskaya Y, Bhattacharya S, Psyrri A, Yea S, Parkes A, Sadraei N, Roychoudhury S, Rimm D, Gavrielatou N. Spatial characterization and quantification of CD40 expression across cancer types. BMC Cancer 2023, 23: 220. PMID: 36894898, PMCID: PMC9996913, DOI: 10.1186/s12885-023-10650-7.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaCarcinoma, Non-Small-Cell LungCD40 AntigensFemaleHumansLung NeoplasmsOvarian NeoplasmsPancreatic NeoplasmsConceptsCD40 expressionSolid tumorsTumor cellsQuantitative immunofluorescencePatient cohortPancreatic cancerCancer typesExpression of CD40Large patient cohortOvarian cancer populationTissue microarray formatDifferent solid tumorsInnate immune responseTNF receptor family membersAvailable patient cohortNSCLC populationOverall survivalPrognostic impactReceptor family membersCancer populationAdenocarcinoma populationImmune cellsOvarian cancerPancreatic adenocarcinomaPositivity rate
2006
Vascular endothelial growth factor, FLT‐1, and FLK‐1 analysis in a pancreatic cancer tissue microarray
Chung GG, Yoon HH, Zerkowski MP, Ghosh S, Thomas L, Harigopal M, Charette LA, Salem RR, Camp RL, Rimm DL, Burtness BA. Vascular endothelial growth factor, FLT‐1, and FLK‐1 analysis in a pancreatic cancer tissue microarray. Cancer 2006, 106: 1677-1684. PMID: 16532435, DOI: 10.1002/cncr.21783.Peer-Reviewed Original ResearchConceptsPancreatic cancer tissue microarrayCancer tissue microarrayTissue microarrayVEGF receptor 1Flt-1Receptor 1Kaplan-Meier survival curvesVascular endothelial growth factor (VEGF) expressionIndependent prognostic factorVascular endothelial growth factorFlk-1Growth factor expressionEndothelial growth factorPrimary antibodyFlt-1 expressionOverall survivalPrognostic factorsWorse survivalAggressive diseaseDisease stagePoor prognosisTumor expressionPancreatic cancerPancreatic adenocarcinomaPrincipal receptor
2005
Hypercalcemia of Malignancy due to Ectopic Transactivation of the Parathyroid Hormone Gene
VanHouten JN, Yu N, Rimm D, Dotto J, Arnold A, Wysolmerski JJ, Udelsman R. Hypercalcemia of Malignancy due to Ectopic Transactivation of the Parathyroid Hormone Gene. The Journal Of Clinical Endocrinology & Metabolism 2005, 91: 580-583. PMID: 16263810, DOI: 10.1210/jc.2005-2095.Peer-Reviewed Original ResearchMeSH KeywordsAgedDNA MethylationDNA, NeoplasmFatal OutcomeFemaleGene ExpressionHumansHypercalcemiaHyperparathyroidismNeuroendocrine TumorsPancreatic NeoplasmsParathyroid GlandsParathyroid Hormone-Related ProteinPromoter Regions, GeneticReverse Transcriptase Polymerase Chain ReactionTranscriptional Activation
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