2021
ARID1A Mutation May Define an Immunologically Active Subgroup in Patients with Microsatellite Stable Colorectal Cancer
Sarshekeh A, Alshenaifi J, Roszik J, Manyam G, Advani S, Katkhuda R, Verma A, Lam M, Willis J, Shen J, Morris J, Davis J, Loree J, Lee H, Ajani J, Maru D, Overman M, Kopetz S. ARID1A Mutation May Define an Immunologically Active Subgroup in Patients with Microsatellite Stable Colorectal Cancer. Clinical Cancer Research 2021, 27: 1663-1670. PMID: 33414133, PMCID: PMC7956157, DOI: 10.1158/1078-0432.ccr-20-2404.Peer-Reviewed Original ResearchConceptsMicrosatellite stable colorectal cancerColorectal cancerStable colorectal cancerMutant casesCancer Center databaseT-cell markersTumor mutational burdenAT-rich interactive domain 1AUnique molecular subgroupSignificant higher expressionCancer Genome AtlasImmunologic featuresIFNγ expressionImmune activationImmune subtypesTreatment strategiesPreclinical modelsT cellsImmune responseMutational burdenSeparate cohortPatientsTherapy trialsActive subgroupMolecular subgroups
2018
Regional differences in gallbladder cancer pathogenesis: Insights from a multi‐institutional comparison of tumor mutations
Narayan R, Creasy J, Goldman D, Gönen M, Kandoth C, Kundra R, Solit D, Askan G, Klimstra D, Basturk O, Allen P, Balachandran V, D’Angelica M, DeMatteo R, Drebin J, Kingham T, Simpson A, Abou‐Alfa G, Harding J, O’Reilly E, Butte J, Matsuyama R, Endo I, Jarnagin W. Regional differences in gallbladder cancer pathogenesis: Insights from a multi‐institutional comparison of tumor mutations. Cancer 2018, 125: 575-585. PMID: 30427539, PMCID: PMC6636637, DOI: 10.1002/cncr.31850.Peer-Reviewed Original ResearchConceptsGallbladder cancer pathogenesisErb-b2 receptor tyrosine kinase 3Gallbladder cancerJapanese patientsSMAD family member 4Overall survivalTumor mutationsAT-rich interactive domain 2Associated with worse survivalPhosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alphaAT-rich interactive domain 1AMedian mutational burdenCause of cancer deathKaplan-Meier methodKruskal-Wallis tests assessed differencesTime of surgeryTyrosine kinase 3Cancer-associated genesCatalytic subunit alphaMulti-institutional comparisonsTests assessed differencesPrimary tumorClinicopathological variablesWorse survivalMutational burden
2015
Evasion of anti-growth signaling: A key step in tumorigenesis and potential target for treatment and prophylaxis by natural compounds
Amin ARMR, Karpowicz PA, Carey TE, Arbiser J, Nahta R, Chen ZG, Dong JT, Kucuk O, Khan GN, Huang GS, Mi S, Lee HY, Reichrath J, Honoki K, Georgakilas AG, Amedei A, Amin A, Helferich B, Boosani CS, Ciriolo MR, Chen S, Mohammed SI, Azmi AS, Keith WN, Bhakta D, Halicka D, Niccolai E, Fujii H, Aquilano K, Ashraf SS, Nowsheen S, Yang X, Bilsland A, Shin DM. Evasion of anti-growth signaling: A key step in tumorigenesis and potential target for treatment and prophylaxis by natural compounds. Seminars In Cancer Biology 2015, 35: s55-s77. PMID: 25749195, PMCID: PMC4561219, DOI: 10.1016/j.semcancer.2015.02.005.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsMeSH KeywordsCarcinogenesisCell ProliferationDNA-Binding ProteinsGrowth Differentiation Factor 15Hippo Signaling PathwayHumansKruppel-Like Transcription FactorsMolecular Targeted TherapyNeoplasmsNuclear ProteinsProtein Serine-Threonine KinasesPTEN PhosphohydrolaseRetinoblastoma ProteinSignal TransductionSomatomedinsTranscription FactorsTumor Suppressor Protein p53ConceptsInsulin-like growth factorGrowth signalingCancer cellsGrowth differentiation factor 15Cell growthSuppression of genesActivation of genesDifferentiation factor 15AT-rich interactive domain 1ASignaling processesRetinoblastoma proteinFactor 15Tensin homologRb pathwayClinical settingSignalingGrowth factorAdverse effectsDomain 1AMolecular targetsPotential targetPathwayHippoGenesImportant pathway
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