2025
Racial/Ethnic Differences and Effects of Clinical/Socioeconomic Factors on Time from Diagnosis to Treatment in Pancreatic Cancer
Sridharan A, Dotan E, Dorta M, Vemula N, Handorf E, Deng M, Renning A, Sorice K, Laderman L, Whittington K, Cukierman E, Astsaturov I, Vijayvergia N, Meyer J, Reddy S, Lynch S. Racial/Ethnic Differences and Effects of Clinical/Socioeconomic Factors on Time from Diagnosis to Treatment in Pancreatic Cancer. Journal Of Gastrointestinal Cancer 2025, 56: 67. PMID: 39954184, PMCID: PMC11829832, DOI: 10.1007/s12029-025-01188-x.Peer-Reviewed Original ResearchConceptsSocioeconomic statusHazard ratioConfidence intervalsSocioeconomic status populationsCancer CenterComprehensive cancer centerDiagnosis to first treatmentPatient-level variablesAcademic cancer centerCox proportional hazards regressionReceipt of chemotherapyMultivariable Cox proportional hazards regressionProportional hazards regressionT2TCancer disparitiesNeighborhood deprivationRace/ethnic disparitiesDisparity indicatorsRacial/ethnic differencesHospital settingEffects of racePatient raceDiagnosis to treatmentUS CensusMetastatic PDACGPR55 in the tumor microenvironment of pancreatic cancer controls tumorigenesis
Ristić D, Bärnthaler T, Gruden E, Kienzl M, Danner L, Herceg K, Sarsembayeva A, Kargl J, Schicho R. GPR55 in the tumor microenvironment of pancreatic cancer controls tumorigenesis. Frontiers In Immunology 2025, 15: 1513547. PMID: 39885986, PMCID: PMC11779727, DOI: 10.3389/fimmu.2024.1513547.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaModel of pancreatic ductal adenocarcinomaImmune tumor microenvironmentTumor microenvironmentT cellsKO miceEndocannabinoid systemWT miceTumor growthCD8<sup>+</sup> T cellsG protein-coupled receptor 55Suppress T cell functionCancer cellsMurine pancreatic ductal adenocarcinomaCD3<sup>+</sup> T cellsExpression of PDL1T cell influxImmune cell compositionT cell functionTumor microenvironment cellsMigration of T cellsReduced tumor weightImmune cell populationsT cell activationCell linesPractices and perspectives of genetic counselors about high‐risk pancreatic cancer screening: A cross‐sectional survey study
Wiegand A, Chhoda A, Namboodiri A, Grimshaw A, Dalela D, Farrell J. Practices and perspectives of genetic counselors about high‐risk pancreatic cancer screening: A cross‐sectional survey study. Journal Of Genetic Counseling 2025, 34: e2016. PMID: 39814542, DOI: 10.1002/jgc4.2016.Peer-Reviewed Original ResearchConceptsCancer screening programHigher risk of pancreatic cancerPancreatic cancer screeningPancreatic cancer screening programsHigh-risk individualsGenetic counselorsCancer screeningScreening programReferral of high-risk individualsPerspectives of genetic counselorsCancer genetic counselorsCross-sectional survey studyIncrease provider comfortGenetic counseling programsIdentification of high-risk individualsPancreatic cancerConsensus guidelinesProvider comfortPancreas ScreeningExpert consensus guidelinesIdeal providersIdentification of individualsSurveillance of individualsCounseling individualsReferral
2024
Epidemiology, treatment and outcomes of gastroenteropancreatic neuroendocrine neoplasms
Uhlig J, Nie J, Gibson J, Cecchini M, Stein S, Lacy J, Kunz P, Kim H. Epidemiology, treatment and outcomes of gastroenteropancreatic neuroendocrine neoplasms. Scientific Reports 2024, 14: 30536. PMID: 39690170, PMCID: PMC11652651, DOI: 10.1038/s41598-024-81518-4.Peer-Reviewed Original ResearchConceptsGEP-NEN patientsGastroenteropancreatic neuroendocrine neoplasmsOverall survivalGEP-NENsTreatment patternsSystemic therapyNeuroendocrine neoplasmsAssociated with improved survivalLow-grade diseaseNational Cancer DatabaseLonger overall survivalSite-specific incidenceDisease specific factorsG3 NENSurgical resectionCancer DatabaseImproved survivalLow-stageCox regressionImprove outcomesPatientsIncidence increasesInternational guidelinesInvestigate incidenceSurvivalDuctal hamartoma of the pancreas: A clinicopathologic study
Das D, Gonzalez I, Yeh M, Wu T, Jain D. Ductal hamartoma of the pancreas: A clinicopathologic study. Human Pathology 2024, 153: 105669. PMID: 39362530, DOI: 10.1016/j.humpath.2024.105669.Peer-Reviewed Original ResearchMeSH KeywordsAgedFemaleHamartomaHumansMaleMiddle AgedPancreatectomyPancreatic CystPancreatic DiseasesPancreatic DuctsPancreatic NeoplasmsConceptsPancreatectomy specimensPancreatic mucinous cystic neoplasmsConsecutive pancreatic resectionsVariable cystic changesCyst fluid CEAHigh-grade dysplasiaMucinous cystic neoplasmsClinical suspicionPancreatic resectionAbdominal symptomsPancreatic carcinomaPatient ageClinicopathological featuresCystic changesLow columnar epitheliumSquamous metaplasiaCystic neoplasmsCystic lesionsProliferative lesionsClinicopathological studyDuctal structuresColumnar epitheliumPancreatectomyLesionsLuminal secretionsKeep It Moving: Physical Activity in the Prevention of Obesity-Driven Pancreatic Cancer.
Sogunro A, Muzumdar M. Keep It Moving: Physical Activity in the Prevention of Obesity-Driven Pancreatic Cancer. Cancer Research 2024, 84: 2935-2937. PMID: 39279380, DOI: 10.1158/0008-5472.can-24-1474.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaTumor microenvironmentAntitumor effectPancreatic cancerObese micePhysical activityAdvanced tumor growthSystemic cytokine productionMyeloid cell infiltrationPancreatic ductal adenocarcinoma developmentEffect of obesityHigh-fat diet-induced obesityDiet-induced obesitySyngeneic allograftsAdvanced tumorsProtumorigenic effectsLean miceWhite adipose tissueCell infiltrationDuctal adenocarcinomaObesity-associatedTumor growthCytokine productionImpact of physical activityInflammatory cytokinesCell-specific models reveal conformation-specific RAF inhibitor combinations that synergistically inhibit ERK signaling in pancreatic cancer cells
Sevrin T, Imoto H, Robertson S, Rauch N, Dyn'ko U, Koubova K, Wynne K, Kolch W, Rukhlenko O, Kholodenko B. Cell-specific models reveal conformation-specific RAF inhibitor combinations that synergistically inhibit ERK signaling in pancreatic cancer cells. Cell Reports 2024, 43: 114710. PMID: 39240715, PMCID: PMC11474227, DOI: 10.1016/j.celrep.2024.114710.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaResistance to RAFResistant PDAC cellsPancreatic cancer cellsPancreatic ductal adenocarcinoma cell linesProtein expression profilesTumor-specific variationsIsogenic pairsCell-specific modelsConformational specificityERK signalingInhibitor combinationsERK pathwayKRAS mutationsTargeted therapyExpression profilesMEK inhibitorsDuctal adenocarcinomaCancer cellsKRAS mutantPhospho-ERKCell linesPDAC cellsCell viabilityDifferential sensitivityDeep-Transfer-Learning–Based Natural Language Processing of Serial Free-Text Computed Tomography Reports for Predicting Survival of Patients With Pancreatic Cancer
Kim S, Kim S, Kim E, Cecchini M, Park M, Choi J, Kim S, Hwang H, Kang C, Choi H, Shin S, Kang J, Lee C. Deep-Transfer-Learning–Based Natural Language Processing of Serial Free-Text Computed Tomography Reports for Predicting Survival of Patients With Pancreatic Cancer. JCO Clinical Cancer Informatics 2024, 8: e2400021. PMID: 39151114, DOI: 10.1200/cci.24.00021.Peer-Reviewed Original ResearchConceptsArea under the receiver operating characteristic curveSurvival of patientsCT reportsPancreatic cancerNatural language processingC-indexPredicting survivalOverall survival of patientsTertiary hospitalPredicting 1-year survivalPredicting survival of patientsImproved C-indexSurvival informationPancreatic cancer survivalReceiver operating characteristic curveInternal test data setNLP modelsComputed tomography reportsLanguage processingKorean tertiary hospitalOverall survivalConsecutive patientsActual survivalConcordance indexPatientsSWI/SNF Complex-Deficient Undifferentiated Carcinoma of the Pancreas: Clinicopathologic and Genomic Analysis
Yavas A, Ozcan K, Adsay N, Balci S, Tarcan Z, Hechtman J, Luchini C, Scarpa A, Lawlor R, Mafficini A, Reid M, Xue Y, Yang Z, Haye K, Bellizzi A, Vanoli A, Benhamida J, Balachandran V, Jarnagin W, Park W, O'Reilly E, Klimstra D, Basturk O. SWI/SNF Complex-Deficient Undifferentiated Carcinoma of the Pancreas: Clinicopathologic and Genomic Analysis. Modern Pathology 2024, 37: 100585. PMID: 39094734, PMCID: PMC11585460, DOI: 10.1016/j.modpat.2024.100585.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaUndifferentiated carcinomaConventional pancreatic ductal adenocarcinomaSMARCB1 protein expressionPancreatic undifferentiated carcinomaProtein expressionPD-L1SMARCB1 deletionRhabdoid morphologyPD-L1 protein expressionCase of undifferentiated carcinomaNext-generation sequencingCombined positive scoreLoss of SMARCB1 protein expressionKRAS wild typeNegative prognostic impactChromatin remodeling complex subunitMultiple tumor typesPrognostic impactTumor characteristicsOverall survivalSWI/SNF deficiencyTumor groupGene alterationsInactivating alterationsCTHRC1+ fibroblasts and SPP1+ macrophages synergistically contribute to pro-tumorigenic tumor microenvironment in pancreatic ductal adenocarcinoma
Li E, Cheung H, Ma S. CTHRC1+ fibroblasts and SPP1+ macrophages synergistically contribute to pro-tumorigenic tumor microenvironment in pancreatic ductal adenocarcinoma. Scientific Reports 2024, 14: 17412. PMID: 39075108, PMCID: PMC11286765, DOI: 10.1038/s41598-024-68109-z.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaTumor-associated macrophagesTumor microenvironmentEpithelial mesenchymal transitionDuctal adenocarcinomaImmune-suppressive tumor microenvironmentPro-tumorigenic tumor microenvironmentPancreatic cancer casesHeterogeneous tumor microenvironmentCombination of single-cellCancer-associated myofibroblastsSurgical resectionMyeloid cellsCurrent therapiesCancer casesLethal cancersSurvival rateExtracellular matrixTreat cancerMesenchymal transitionTherapeutic targetAdenocarcinomaCellular populationsCancerIntercellular interactionsSpatial patterns and environmental functions of dissolved organic matter in grassland soils of China
Zhou P, Tian L, Graham N, Song S, Zhao R, Siddique M, Hu Y, Cao X, Lu Y, Elimelech M, Yu W. Spatial patterns and environmental functions of dissolved organic matter in grassland soils of China. Nature Communications 2024, 15: 6356. PMID: 39069514, PMCID: PMC11284229, DOI: 10.1038/s41467-024-50745-8.Peer-Reviewed Original ResearchConceptsFunction of dissolved organic matterOrganic matterSoil dissolved organic matterSouthern region of ChinaHumic-likeRegions of ChinaSoil DOMAnnual ecosystem exchangeContinental scaleSpatial patternsDOMGrassland soilsSpatial associationDry seasonEnvironmental functionsSouthern regionEcosystem exchangeSoils of ChinaEcosystem productivityChinaAquatic environmentHumified fractionsSoilGrasslandGeochemistryGenome-Wide Analysis to Assess if Heavy Alcohol Consumption Modifies the Association between SNPs and Pancreatic Cancer Risk.
Ni Z, Kundu P, McKean D, Wheeler W, Albanes D, Andreotti G, Antwi S, Arslan A, Bamlet W, Beane-Freeman L, Berndt S, Bracci P, Brennan P, Buring J, Chanock S, Gallinger S, Gaziano J, Giles G, Giovannucci E, Goggins M, Goodman P, Haiman C, Hassan M, Holly E, Hung R, Katzke V, Kooperberg C, Kraft P, LeMarchand L, Li D, McCullough M, Milne R, Moore S, Neale R, Oberg A, Patel A, Peters U, Rabe K, Risch H, Shu X, Smith-Byrne K, Visvanathan K, Wactawski-Wende J, White E, Wolpin B, Yu H, Zeleniuch-Jacquotte A, Zheng W, Zhong J, Amundadottir L, Stolzenberg-Solomon R, Klein A. Genome-Wide Analysis to Assess if Heavy Alcohol Consumption Modifies the Association between SNPs and Pancreatic Cancer Risk. Cancer Epidemiology Biomarkers & Prevention 2024, 33: 1229-1239. PMID: 38869494, PMCID: PMC11928872, DOI: 10.1158/1055-9965.epi-24-0096.Peer-Reviewed Original ResearchConceptsPancreatic cancer riskHeavy alcohol consumptionCancer riskSingle-nucleotide polymorphismsAlcohol consumptionExpression quantitative trait lociQuantitative trait lociAssociated with pancreatic cancer riskGenome-wide interaction analysisGenome-wide significant evidenceEtiology of pancreatic cancerFixed-effect meta-analysesGenomic regionsGenome-wide significant evidence of associationLead single-nucleotide polymorphismsTrait lociGenetic variantsEuropean ancestry populationsEvidence of associationGenome-wide association studiesAnalysis of single-nucleotide polymorphismsCase-control studyPancreatic cancerGenome-wide analysisAncestry populationsKeratin 17 modulates the immune topography of pancreatic cancer
Delgado-Coka L, Horowitz M, Torrente-Goncalves M, Roa-Peña L, Leiton C, Hasan M, Babu S, Fassler D, Oentoro J, Bai J, Petricoin E, Matrisian L, Blais E, Marchenko N, Allard F, Jiang W, Larson B, Hendifar A, Chen C, Abousamra S, Samaras D, Kurc T, Saltz J, Escobar-Hoyos L, Shroyer K. Keratin 17 modulates the immune topography of pancreatic cancer. Journal Of Translational Medicine 2024, 22: 443. PMID: 38730319, PMCID: PMC11087249, DOI: 10.1186/s12967-024-05252-1.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaCD8+ T cellsT cellsK17 expressionCell carcinomaPatient survivalMolecular subtypes of pancreatic ductal adenocarcinomaIntratumoral CD8+ T cellsSpatial distribution of T cellsKeratin 17CD8+ T cell abundanceImmune responseSubtype of pancreatic ductal adenocarcinomaCervical squamous cell carcinomaAssociated with decreased numbersCD16+ macrophagesTumor-intrinsic variablesDistribution of T cellsLymph node statusSquamous cell carcinomaBasal cell carcinomaCD163+ macrophagesT cell abundanceImmune cell responsesImmunotherapeutic opportunitiesThe crosstalk between macrophages and cancer cells potentiates pancreatic cancer cachexia
Liu M, Ren Y, Zhou Z, Yang J, Shi X, Cai Y, Arreola A, Luo W, Fung K, Xu C, Nipp R, Bronze M, Zheng L, Li Y, Houchen C, Zhang Y, Li M. The crosstalk between macrophages and cancer cells potentiates pancreatic cancer cachexia. Cancer Cell 2024, 42: 885-903.e4. PMID: 38608702, PMCID: PMC11162958, DOI: 10.1016/j.ccell.2024.03.009.Peer-Reviewed Original ResearchConceptsPancreatic cancer cachexiaTumor cellsCancer cachexiaTherapeutic targetLimited treatment optionsPancreatic cancer cellsImmune microenvironmentCCL2/CCR2 axisPotential therapeutic targetTreatment optionsMuscle wastingReprogram macrophagesTumorMuscle atrophyCachexiaCancer cellsMacrophagesNon-autonomous activationMuscle remodelingCancerMuscle degradationSecretionCellsMuscleTWEAKCirculating Tumor DNA Dynamics Fail to Predict Efficacy of Poly(ADP-ribose) Polymerase/VEGFR Inhibition in Patients With Heavily Pretreated Advanced Solid Tumors
Hu Y, Narayan A, Xu Y, Wolfe J, Vu D, Trinh T, Kantak C, Ivy S, Eder J, Deng Y, LoRusso P, Kim J, Patel A. Circulating Tumor DNA Dynamics Fail to Predict Efficacy of Poly(ADP-ribose) Polymerase/VEGFR Inhibition in Patients With Heavily Pretreated Advanced Solid Tumors. JCO Precision Oncology 2024, 8: e2300289. PMID: 38412387, PMCID: PMC10914240, DOI: 10.1200/po.23.00289.Peer-Reviewed Original ResearchConceptsCell-free circulating tumor DNANon-small-cell lung cancerSmall-cell lung cancerTriple-negative breast cancerPancreatic ductal adenocarcinomaAdvanced solid tumorsVariant allele fractionRadiographic responseOverall survivalCombination therapySolid tumorsCtDNA levelsLung cancerPretreated advanced solid tumorsDays of combination therapyMetastatic pancreatic ductal adenocarcinomaResponse to anticancer therapyAssociated with disease progressionProgression-free survivalPlasma samplesLead-inPoly(ADP-riboseInferior OSTumor DNASurvival outcomesPlasticity-induced repression of Irf6 underlies acquired resistance to cancer immunotherapy in pancreatic ductal adenocarcinoma
Kim I, Diamond M, Yuan S, Kemp S, Kahn B, Li Q, Lin J, Li J, Norgard R, Thomas S, Merolle M, Katsuda T, Tobias J, Baslan T, Politi K, Vonderheide R, Stanger B. Plasticity-induced repression of Irf6 underlies acquired resistance to cancer immunotherapy in pancreatic ductal adenocarcinoma. Nature Communications 2024, 15: 1532. PMID: 38378697, PMCID: PMC10879147, DOI: 10.1038/s41467-024-46048-7.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaEpithelial-to-mesenchymal transitionResistance to immunotherapyT cell killingDuctal adenocarcinomaAcquired resistance to immunotherapyResistance to cancer immunotherapyMouse model of pancreatic ductal adenocarcinomaModel of pancreatic ductal adenocarcinomaExpression of immune checkpointsInterferon regulatory factor 6Effect of TNF-aEMT transcription factor ZEB1Antigen presentation machineryTumor immune microenvironmentCell-intrinsic defectsPro-apoptotic effectsPresentation machineryCancer immunotherapyImmune checkpointsTumor relapseImmune microenvironmentPrimary resistanceT cellsAcquired resistanceDNA Methylation Profiling Enables Accurate Classification of Nonductal Primary Pancreatic Neoplasms
Verschuur A, Hackeng W, Westerbeke F, Benhamida J, Basturk O, Selenica P, Raicu G, Molenaar I, van Santvoort H, Daamen L, Klimstra D, Yachida S, Luchini C, Singhi A, Geisenberger C, Brosens L. DNA Methylation Profiling Enables Accurate Classification of Nonductal Primary Pancreatic Neoplasms. Clinical Gastroenterology And Hepatology 2024, 22: 1245-1254.e10. PMID: 38382726, DOI: 10.1016/j.cgh.2024.02.007.Peer-Reviewed Original ResearchConceptsPancreatic neoplasmsMachine learning modelsAnalysis of biopsy specimensNonpancreatic neoplasmsNon-pancreatic originDiagnosis of pancreatic neoplasmsPrimary pancreatic neoplasmDiagnostic work-upArea under the curvePre-operative settingLearning modelsMethylation profilesPrimary tumorBiopsy specimensHistopathological diagnosisResected samplesDetecting neoplasmsDNA methylation signaturesTumor typesCancer entitiesLogistic regression modelsNeoplasmsClassifier performanceNeural networkConcordant classification
2023
High-sensitivity deuterium metabolic MRI differentiates acute pancreatitis from pancreatic cancers in murine models
Montrazi E, Sasson K, Agemy L, Peters D, Brenner O, Scherz A, Frydman L. High-sensitivity deuterium metabolic MRI differentiates acute pancreatitis from pancreatic cancers in murine models. Scientific Reports 2023, 13: 19998. PMID: 37968574, PMCID: PMC10652017, DOI: 10.1038/s41598-023-47301-7.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsDeuteriumDisease Models, AnimalHumansLactic AcidMagnetic Resonance ImagingMicePancreatic NeoplasmsPancreatitisPyruvic AcidHOXC6 drives a therapeutically targetable pancreatic cancer growth and metastasis pathway by regulating MSK1 and PPP2R2B
Malvi P, Chava S, Cai G, Hu K, Zhu L, Edwards Y, Green M, Gupta R, Wajapeyee N. HOXC6 drives a therapeutically targetable pancreatic cancer growth and metastasis pathway by regulating MSK1 and PPP2R2B. Cell Reports Medicine 2023, 4: 101285. PMID: 37951219, PMCID: PMC10694669, DOI: 10.1016/j.xcrm.2023.101285.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaHomeobox C6PDAC growthInsulin-like growth factor 1 receptorGrowth factor 1 receptorKinase MSK1Factor 1 receptorTranscription factorsPancreatic cancer growthMSK1Tumor growthPDAC tumor growthMost pancreatic ductal adenocarcinomasMammalian targetIGF1R inhibitorsTherapeutic vulnerabilitiesRapamycin (mTOR) pathway activationMEK inhibitor trametinibMetastasis pathwaysPDAC mouse modelPDAC cellsMTOR inhibitionPharmacological inhibitionPathway activationInhibition blocksElucidating the role of blood metabolites on pancreatic cancer risk using two‐sample Mendelian randomization analysis
Zhong H, Liu S, Zhu J, Xu T, Yu H, Wu L. Elucidating the role of blood metabolites on pancreatic cancer risk using two‐sample Mendelian randomization analysis. International Journal Of Cancer 2023, 154: 852-862. PMID: 37860916, PMCID: PMC10843029, DOI: 10.1002/ijc.34771.Peer-Reviewed Original ResearchMeSH KeywordsCanadaCarcinoma, Pancreatic DuctalGenome-Wide Association StudyHumansLongitudinal StudiesMendelian Randomization AnalysisPancreatic NeoplasmsConceptsPancreatic ductal adenocarcinomaPDAC riskBlood metabolitesGenetic instrumentsTwo-sample Mendelian randomization studyPancreatic Cancer Case-Control ConsortiumEPIC-Norfolk cohortPancreatic cancer riskEuropean ancestryPancreatic Cancer Cohort ConsortiumPotential side effectsCanadian Longitudinal StudyAssociations of metabolitesMendelian randomization studyTwo-sample Mendelian randomization (MR) analysisGenome-wide association studiesMendelian randomization analysisFatal malignancyDuctal adenocarcinomaCancer riskPDAC casesSide effectsAging CohortMetabolite biomarkersRandomization study
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