Search results for "pancreatic neoplasms"

showing 10 items of 191 documents

Sunitinib in patients with pre-treated pancreatic neuroendocrine tumors: A real-world study.

2018

Abstract Introduction Besides data reported in a Phase-III trial, data on sunitinib in pancreatic Neuroendocrine Tumors (panNETs) are scanty. Aim To evaluate sunitinib efficacy and tolerability in panNETs patients treated in a real-world setting. Patients and methods Retrospective analysis of progressive panNETs treated with sunitinib. Efficacy was assessed by evaluating progression-free survival, overall survival, and disease control (DC) rate (stable disease (SD) + partial response + complete response). Data are reported as median (25th–75th IQR). Results Eighty patients were included. Overall, 71.1% had NET G2, 26.3% had NET G1, and 2.6% had NET G3 neoplasms. A total of 53 patients (66.3…

0301 basic medicineIndolesEndocrinology Diabetes and MetabolismNeuroendocrine tumorsPyrroleGastroenterologyTarget therapyEfficacyAntineoplastic Agent0302 clinical medicineEndocrinologyRetrospective StudieSunitinibPancreadiabetes and metabolismSunitinibGastroenterologyPancreatic NeoplasmMiddle AgedDiabetes and MetabolismNeuroendocrine TumorsTreatment OutcomeTolerabilityNeuroendocrine tumors; Pancreas; Progressive disease; Sunitinib; Target therapy; Endocrinology Diabetes and Metabolism; Hepatology; EndocrinologyItaly030220 oncology & carcinogenesisNeuroendocrine tumorsmedicine.drugHumanAdultmedicine.medical_specialtyAntineoplastic AgentsNeutropenia03 medical and health sciencesNeuroendocrine tumorInternal medicinemedicineHumansPyrrolesProgression-free survivalPancreasCancer stagingAgedRetrospective StudiesHepatologybusiness.industryProgressive diseasemedicine.diseasePancreatic Neoplasms030104 developmental biologyNeuroendocrine tumors; pancreas; progressive disease; Sunitinib; target therapy; endocrinology; diabetes and metabolism; hepatology; endocrinologyIndolebusinessProgressive diseasePancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
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Stromal hyaluronan accumulation is associated with low immune response and poor prognosis in pancreatic cancer

2021

AbstractHyaluronan (HA) accumulation has been associated with poor survival in various cancers, but the mechanisms for this phenomenon are still unclear. The aim of this study was to investigate the prognostic significance of stromal HA accumulation and its association with host immune response in pancreatic ductal adenocarcinoma (PDAC). The study material consisted of 101 radically treated patients for PDAC from a single geographical area. HA staining was evaluated using a HA-specific probe, and the patterns of CD3, CD8, CD73 and PD-L1 expression were evaluated using immunohistochemistry. HA staining intensity of tumour stromal areas was assessed digitally using QuPath. CD3- and CD8-based …

0301 basic medicineMalehyaluronaanibiomarkkeritB7-H1 Antigen0302 clinical medicineProspective StudiesHyaluronic Acid5'-NucleotidasehaimasyöpäCancerAged 80 and overMultidisciplinaryQGastroenterologyRMiddle AgedPrognosisSurvival RateOncology030220 oncology & carcinogenesisimmuunivasteImmunohistochemistryMedicineFemalesyöpätauditCarcinoma Pancreatic DuctalStromal cellScienceImmunologyGPI-Linked Proteins3121 Internal medicineArticle03 medical and health sciencesImmune systemPancreatic cancerCarcinomamedicineHumansSurvival rateAgedbusiness.industryImmunityCancerennusteetmedicine.disease3126 Surgery anesthesiology intensive care radiologyPancreatic Neoplasms030104 developmental biologyCancer researchStromal CellsbusinessCD8Follow-Up Studies
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Bactibilia in women affected with diseases of the biliary tract and pancreas. A STROBE guidelines-adherent cross-sectional study in Southern Italy.

2018

Abstract Purpose. Bile is a hepatobiliary lipid-rich sterile solution, and its colonization by microorganisms defines the condition of bactibilia. In this study, we aimed to assess the bile microbiological flora and its potential link with comorbidity in women. Methodology. We performed a microbiologic investigation on 53 female patients with biliopancreatic diseases who granted consent, and we analysed the data using a MATLAB platform. Results. We found that the most frequent disease associated with bactibilia was pancreas head carcinoma (PHC) (P=0.0015), while the least frequent disease was gall bladder carcinoma (GBC) (P=0.0002). The most common microorganisms were Pseudomonas spp. (P&lt…

0301 basic medicineMicrobiology (medical)medicine.medical_specialtyPancreatic diseaseMediterranean dietCross-sectional studyMicrobiologyGastroenterologyBiliary disease03 medical and health sciences0302 clinical medicineInternal medicineGram-Negative BacteriamedicineCarcinomaBileHumansBiliary TractAgedAged 80 and overbusiness.industryMortality rateGeneral MedicineMiddle Agedmedicine.diseaseComorbidityBactibiliaPancreatic Neoplasms030104 developmental biologyBiliary Tract NeoplasmsCross-Sectional StudiesItalyBiliary tract030220 oncology & carcinogenesisFemalebusinessJournal of medical microbiology
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Phospho-Akt overexpression is prognostic and can be used to tailor the synergistic interaction of Akt inhibitors with gemcitabine in pancreatic cancer

2017

Background There is increasing evidence of a constitutive activation of Akt in pancreatic ductal adenocarcinoma (PDAC), associated with poor prognosis and chemoresistance. Therefore, we evaluated the expression of phospho-Akt in PDAC tissues and cells, and investigated molecular mechanisms influencing the therapeutic potential of Akt inhibition in combination with gemcitabine. Methods Phospho-Akt expression was evaluated by immunohistochemistry in tissue microarrays (TMAs) with specimens tissue from radically-resected patients (n = 100). Data were analyzed by Fisher and log-rank test. In vitro studies were performed in 14 PDAC cells, including seven primary cultures, characterized for their…

0301 basic medicineOncologyMaleCancer ResearchBiopsyAKT1ApoptosisAkt; Gemcitabine; Pancreatic ductal adenocarcinoma; Synergism; Hematology; Molecular Biology; Oncology; Cancer ResearchDeoxycytidinePancreatic ductal adenocarcinoma0302 clinical medicineCell MovementTumor Cells CulturedGlucose Transporter Type 1medicine.diagnostic_testChemistryCell CyclePancreatic NeoplasmDrug Synergismlcsh:Diseases of the blood and blood-forming organsHematologyCell cycleMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisOncologyAkt; Gemcitabine; Pancreatic ductal adenocarcinoma; Synergism; Aged; Apoptosis; Biopsy; Carcinoma Pancreatic Ductal; Cell Cycle; Cell Movement; Deoxycytidine; Drug Synergism; Female; Glucose Transporter Type 1; Humans; Male; Middle Aged; Pancreatic Neoplasms; Phosphoproteins; Prognosis; Proto-Oncogene Proteins c-akt; RNA Messenger; Spheroids Cellular; Tumor Cells Cultured; Hematology; Molecular Biology; Oncology; Cancer Research030220 oncology & carcinogenesisPhosphoproteinFemalemedicine.drugHumanCarcinoma Pancreatic Ductalmedicine.medical_specialtyPrognosilcsh:RC254-282Flow cytometry03 medical and health sciencesInternal medicinePancreatic cancerSpheroids CellularmedicineHumansRNA MessengerProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayAgedlcsh:RC633-647.5ResearchAktSynergismApoptosimedicine.diseasePhosphoproteinsGemcitabineGemcitabinePancreatic Neoplasms030104 developmental biologyCancer cellCancer researchProto-Oncogene Proteins c-akt
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Systematic review and meta-analysis on targeted therapy in advanced pancreatic cancer

2015

Abstract Aim A systematic review and meta-analysis from literature has been performed to assess the impact of targeted therapy in advanced pancreatic cancer. Methods By searching different literature databases and major cancer meetings proceedings, data from all randomized clinical trials designed to investigate molecular targeted agents in the treatment of advanced pancreatic cancer were collected. The time-frame between January 2007 and March 2015 was selected. Data on predefined end-points, including overall survival, progression-free survival in terms of Hazard Ratio and response-rate were extracted and analyzed by a random effects model. Pooled data analysis was performed according to …

0301 basic medicineOncologymedicine.medical_specialtyFunnel plotEndocrinology Diabetes and Metabolismmedicine.medical_treatmentAntineoplastic AgentsBioinformaticslaw.inventionTargeted therapy03 medical and health sciences0302 clinical medicineRandomized controlled triallawInternal medicineAntineoplastic Combined Chemotherapy ProtocolsHumansMedicineGenetic Predisposition to DiseaseMeta-analysiAdvanced pancreatic cancerHepatologybusiness.industryHazard ratioGastroenterologyCancerPancreatic cancerPublication biasmedicine.diseasePancreatic NeoplasmsClinical trial030104 developmental biology030220 oncology & carcinogenesisMeta-analysisRandomized clinical trialbusinessSignal TransductionPathwayPancreatology
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CXCL10 and CCL21 Promote Migration of Pancreatic Cancer Cells Toward Sensory Neurons and Neural Remodeling in Tumors in Mice, Associated With Pain in…

2018

Background & Aims Pancreatic ductal adenocarcinoma (PDAC) is frequently accompanied by excruciating pain, which has been associated with attraction of cancer cells and their invasion of intrapancreatic sensory nerves. Neutralization of the chemokine CCL2 reduced cancer-associated pain in a clinical trial, but there have been no systematic analyses of the highly diverse chemokine families and their receptors in PDAC. Methods We performed an open, unbiased RNA-interference screen of mammalian chemokines in co-cultures of mouse PDAC cells (K8484) and mouse peripheral sensory neurons, and confirmed findings in studies of DT8082 PDAC cells. We studied the effects of chemokines on migration of PD…

0301 basic medicineReceptors CCR7ChemokineReceptors CXCR3Sensory Receptor Cellsendocrine system diseasesC-C chemokine receptor type 7CXCR303 medical and health sciencesChemokine receptor0302 clinical medicineCell MovementCell Line TumorGanglia SpinalPancreatic cancermedicineAnimalsHumansCXCL10AnalgesicsChemokine CCL21Hepatologybiologybusiness.industryGastroenterologyCancer Painmedicine.diseaseAntibodies NeutralizingCoculture Techniquesdigestive system diseasesChemokine CXCL10Mice Inbred C57BLPancreatic Neoplasms030104 developmental biologyCancer cellCancer researchbiology.protein030211 gastroenterology & hepatologybusinessCarcinoma Pancreatic DuctalSignal TransductionCCL21Gastroenterology
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Molecular profiling of pancreatic neuroendocrine tumors (pNETS) and the clinical potential

2018

Abstract: Introduction: Pancreatic neuroendocrine tumors (pNETs) represent a small part of pancreatic neoplasms, and the knowledge about their indolent clinical course remains a subject of investigation. They occur sporadically or as part of familial cancer syndromes and are classified by WHO in 3 categories. There is ongoing research to understand their molecular profiling and leading mutations.Areas covered: The aim of this review is to clarify the overall aspects of tumorigenesis, to expose the latest developments in understanding the course of the disease and the possible therapeutic implications of these. The review also discusses functional and non-functional pNETs and associated inhe…

0301 basic medicineSettore MED/06 - Oncologia Medicamedicine.medical_treatmentClinical Decision-MakingAntineoplastic AgentsDiseaseNeuroendocrine tumorsBioinformaticsTargeted therapy03 medical and health sciences0302 clinical medicinePredictive Value of TestsFunctional tumorBiomarkers TumormedicineHumansProfiling (information science)Molecular Targeted Therapyneurondocrine tumorPrecision MedicineTherapeutic strategymolecular pathwayHepatologybusiness.industryGene Expression ProfilingGastroenterologyClinical coursehereditary syndrometargeted therapymedicine.diseaseGene Expression Regulation NeoplasticPancreatic NeoplasmsNeuroendocrine Tumors030104 developmental biology030220 oncology & carcinogenesispancreatic tumorFamilial CancerHuman medicinebusinessSignal TransductionExpert review of gastroenterology & hepatology
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MET/HGF Co-Targeting in Pancreatic Cancer: A Tool to Provide Insight into the Tumor/Stroma Crosstalk

2018

The ‘onco-receptor’ MET (Hepatocyte Growth Factor Receptor) is involved in the activation of the invasive growth program that is essential during embryonic development and critical for wound healing and organ regeneration during adult life. When aberrantly activated, MET and its stroma-secreted ligand HGF (Hepatocyte Growth Factor) concur to tumor onset, progression, and metastasis in solid tumors, thus representing a relevant target for cancer precision medicine. In the vast majority of tumors, wild-type MET behaves as a ‘stress-response’ gene, and relies on ligand stimulation to sustain cancer cell ‘scattering’, invasion, and protection form apoptosis. …

0301 basic medicineStromal cellpancreatic cancerReviewHGF; MET; Metastasis; Pancreatic cancer; Target therapy; Tumor microenvironment; Animals; Hepatocyte Growth Factor; Humans; Neoplasm Metastasis; Pancreatic Neoplasms; Proto-Oncogene Proteins c-metCatalysisMetastasisInorganic Chemistrylcsh:Chemistry03 medical and health sciences0302 clinical medicinePancreatic cancermedicineAnimalsHumansmetastasistumor microenvironmentHGFPhysical and Theoretical ChemistryNeoplasm MetastasisMolecular Biologylcsh:QH301-705.5SpectroscopyTumor microenvironmentbusiness.industryHepatocyte Growth Factortarget therapyOrganic ChemistryGeneral MedicineProto-Oncogene Proteins c-metmedicine.diseaseComputer Science ApplicationsPancreatic Neoplasms030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Tumor progressionHepatocyte Growth Factor Receptor030220 oncology & carcinogenesisCancer cellCancer researchMETHepatocyte growth factorbusinessmedicine.drugInternational Journal of Molecular Sciences
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Galectin-3 Released by Pancreatic Ductal Adenocarcinoma Suppresses γδ T Cell Proliferation but Not Their Cytotoxicity

2020

Pancreatic ductal adenocarcinoma (PDAC) is characterized by an immunosuppressive tumor microenvironment with a dense desmoplastic stroma. The expression of β-galactoside-binding protein galectin-3 is regarded as an intrinsic tumor escape mechanism for inhibition of tumor-infiltrating T cell function. In this study, we demonstrated that galectin-3 is expressed by PDAC and by γδ or αβ T cells but is only released in small amounts by either cell population. Interestingly, large amounts of galectin-3 were released during the co-culture of allogeneic in vitro expanded or allogeneic or autologous resting T cells with PDAC cells. By focusing on the co-culture of tumor cells and γδ T cells, we obse…

0301 basic medicinelcsh:Immunologic diseases. AllergyAdultAdoptive cell transferT cellproliferationGalectinsPopulationCellImmunologypancreatic cancerT cellsautologous03 medical and health sciences0302 clinical medicineLymphocytes Tumor-InfiltratingPancreatic cancerCell Line Tumorgalectin-3medicineotorhinolaryngologic diseasesImmunology and AllergyCytotoxic T cellHumansCytotoxicityeducationα3β1 integrinIntraepithelial LymphocytesOriginal ResearchCell Proliferationgammadelta T cellsTumor microenvironmenteducation.field_of_studyChemistryBlood Proteinsmedicine.diseasePancreatic Neoplasms030104 developmental biologymedicine.anatomical_structureCancer researchbispecific antibodieslcsh:RC581-607030215 immunologyCarcinoma Pancreatic DuctalFrontiers in Immunology
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The Unfolded Protein Response Plays a Predominant Homeostatic Role in Response to Mitochondrial Stress in Pancreatic Stellate Cells.

2016

Activated pancreatic stellate cells (PaSC) are key participants in the stroma of pancreatic cancer, secreting extracellular matrix proteins and inflammatory mediators. Tumors are poorly vascularized, creating metabolic stress conditions in cancer and stromal cells that necessitate adaptive homeostatic cellular programs. Activation of autophagy and the endoplasmic reticulum unfolded protein response (UPR) have been described in hepatic stellate cells, but the role of these processes in PaSC responses to metabolic stress is unknown. We reported that the PI3K/mTOR pathway, which AMPK can regulate through multiple inputs, modulates PaSC activation and fibrogenic potential. Here, using primary a…

0301 basic medicinelcsh:MedicineApoptosisMitochondrionAMP-Activated Protein KinasesEndoplasmic ReticulumBiochemistrychemistry.chemical_compoundMiceeIF-2 KinasePhosphatidylinositol 3-Kinases0302 clinical medicineFluorescence MicroscopyCell SignalingTumor Microenvironment2.1 Biological and endogenous factorsSmall interfering RNAsAetiologylcsh:ScienceEnergy-Producing OrganellesCancerMice KnockoutMicroscopyMultidisciplinarySecretory PathwayCell DeathTOR Serine-Threonine KinasesLight MicroscopySignaling CascadesCell biologyMitochondriaNeoplasm ProteinsUp-RegulationNucleic acidsCell Processes030220 oncology & carcinogenesisCellular Structures and OrganellesResearch ArticleSignal TransductionProgrammed cell deathCell PhysiologyGeneral Science & TechnologyAutophagic Cell DeathKnockoutBiologyBioenergeticsResearch and Analysis MethodsStress Signaling Cascade03 medical and health sciencesGeneticsAutophagyAnimalsNon-coding RNAPancreasPI3K/AKT/mTOR pathwaylcsh:RAutophagyAMPKBiology and Life SciencesCell BiologyCell MetabolismGene regulationPancreatic NeoplasmsEnzyme Activation030104 developmental biologychemistryHepatic stellate cellUnfolded protein responseUnfolded Protein ResponseRNAlcsh:QGene expressionInterleukin-4Digestive DiseasesRottlerinTranscription Factor CHOP
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