Search results for " Pancreatic Ductal"

showing 10 items of 44 documents

Effects of the MDM-2 inhibitor Nutlin-3a on PDAC cells containing and lacking WT-TP53 on sensitivity to chemotherapy, signal transduction inhibitors …

2019

Abstract Mutations at the TP53 gene are readily detected (approximately 50–75%) in pancreatic ductal adenocarcinoma (PDAC) patients. TP53 was previously thought to be a difficult target as it is often mutated, deleted or inactivated on both chromosomes in certain cancers. In the following study, the effects of restoration of wild-type (WT) TP53 activity on the sensitivities of MIA-PaCa-2 pancreatic cancer cells to the MDM2 inhibitor nutlin-3a in combination with chemotherapy, targeted therapy, as well as, nutraceuticals were examined. Upon introduction of the WT-TP53 gene into MIA-PaCa-2 cells, which contain a TP53 gain of function (GOF) mutation, the sensitivity to the MDM2 inhibitor incre…

0301 basic medicineCancer ResearchNutlin-3aSettore MED/09 - Medicina Internaendocrine system diseasesmedicine.medical_treatmentmedicine.disease_causePiperazinesTargeted therapy0302 clinical medicineTP53MutationbiologyChemistryImidazolesProto-Oncogene Proteins c-mdm2OxaliplatinTargeted TherapeuticsDrug sensitivity; Nutlin-3a; Nutraceuticals; Targeted therapeutics; TP53030220 oncology & carcinogenesisMolecular MedicineMdm2NutraceuticalNutraceuticalsSignal transductionCarcinoma Pancreatic DuctalSignal Transductionmedicine.drugDrug sensitivityAntineoplastic AgentsIrinotecan03 medical and health sciencesCell Line TumorPancreatic cancerGeneticsmedicineHumansMolecular BiologyneoplasmsChemotherapymedicine.diseasedigestive system diseasesOxaliplatinPancreatic Neoplasms030104 developmental biologyCell cultureDietary Supplementsbiology.proteinCancer researchTERAPÊUTICA MÉDICATumor Suppressor Protein p53
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Concepts to Target MYC in Pancreatic Cancer.

2016

Abstract Current data suggest that MYC is an important signaling hub and driver in pancreatic ductal adenocarcinoma (PDAC), a tumor entity with a strikingly poor prognosis. No targeted therapies with a meaningful clinical impact were successfully developed against PDAC so far. This points to the need to establish novel concepts targeting the relevant drivers of PDAC, like KRAS or MYC. Here, we discuss recent developments of direct or indirect MYC inhibitors and their potential mode of action in PDAC. Mol Cancer Ther; 15(8); 1792–8. ©2016 AACR.

0301 basic medicineCancer ResearchPoor prognosisPancreatic ductal adenocarcinomaendocrine system diseasesGene regulatory networkAntineoplastic AgentsBiologymedicine.disease_causeBioinformaticsProto-Oncogene Proteins c-myc03 medical and health sciencesPancreatic cancerCarcinomamedicineAnimalsHumansGene Regulatory NetworksMolecular Targeted TherapyProtein Kinase InhibitorsCancerGenetic Variationmedicine.diseasedigestive system diseasesGene Expression Regulation NeoplasticPancreatic Neoplasms030104 developmental biologyOncologyCarrier proteinCancer researchKRASCarrier ProteinsCarcinoma Pancreatic DuctalProtein BindingSignal TransductionMolecular cancer therapeutics
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HGF/MET Axis Induces Tumor Secretion of Tenascin-C and Promotes Stromal Rewiring in Pancreatic Cancer

2021

Simple Summary It has been previously shown that activation of the MET receptor by its ligand, the hepatocyte growth factor (HGF), modulates the tumor-stroma cross-talk in models of pancreatic cancer. We now wish to cast light on the molecular mechanisms by which this ligand/receptor pair sustains the interaction between cancer cells and the tumor microenviroment. To this end, we compared data obtained by large-scale analysis of gene expression in pancreatic cancer cells grown in the presence of HGF versus cells grown in the presence of HGF and treated with specific inhibitors of HGF/MET signaling. By clustering differentially expressed genes according to functional groups, we identified ca…

0301 basic medicineCancer ResearchStromal cellpancreatic ductal adenocarcinomaArticle03 medical and health sciences0302 clinical medicinePancreatic tumorPancreatic cancerMET oncogenemedicinetumor microenvironmentmetastasisHepatocyte growth factor; MET oncogene; Metastasis; Pancreatic ductal adenocarcinoma; Tenascin C; Tumor microenvironmentRC254-282Tumor microenvironmentbiologyChemistryTenascin Ctenascin CNeoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease030104 developmental biologyhepatocyte growth factorOncology030220 oncology & carcinogenesisCancer cellHepatic stellate cellbiology.proteinCancer researchHepatocyte growth factormedicine.drugCancers
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Pattern of Invasion in Human Pancreatic Cancer Organoids Is Associated with Loss of SMAD4 and Clinical Outcome

2020

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy characterized by extensive local invasion and systemic spread. In this study, we employed a three-dimensional organoid model of human pancreatic cancer to characterize the molecular alterations critical for invasion. Time-lapse microscopy was used to observe invasion in organoids from 25 surgically resected human PDAC samples in collagen I. Subsequent lentiviral modification and small-molecule inhibitors were used to investigate the molecular programs underlying invasion in PDAC organoids. When cultured in collagen I, PDAC organoids exhibited two distinct, morphologically defined invasive phenotypes, mesenchymal an…

0301 basic medicineCancer Researchendocrine system diseasesPancreatic ductal adenocarcinoma (PDAC)RAC1CDC42AdenocarcinomaBiologyArticle03 medical and health sciences0302 clinical medicineHuman Pancreatic CancerCell MovementPancreatic cancerBiomarkers TumorTumor Cells CulturedmedicineOrganoidHumansNeoplasm InvasivenessCell ProliferationSmad4 ProteinRegulation of gene expressionCell growthMesenchymal stem cellPrognosismedicine.diseasePhenotypedigestive system diseasesGene Expression Regulation NeoplasticOrganoidsPancreatic NeoplasmsSurvival Rate030104 developmental biologyOncology030220 oncology & carcinogenesisembryonic structuresCancer researchCarcinoma Pancreatic DuctalSignal TransductionCancer Research
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Abilities of β-Estradiol to interact with chemotherapeutic drugs, signal transduction inhibitors and nutraceuticals and alter the proliferation of pa…

2019

Improving the effects of chemotherapy and reducing the side effects are important goals in cancer research. Various approaches have been examined to enhance the effectiveness of chemotherapy. For example, signal transduction inhibitors or hormonal based approaches have been included with chemo- or radio-therapy. MIA-PaCa-2 and BxPC-3 pancreatic ductal adenocarcinoma (PDAC) cells both express the estrogen receptor (ER). The effects of β-estradiol on the growth of PDAC cells has not been examined yet the ER is expressed in PDAC cells. We have examined the effects of combining β-estradiol with chemotherapeutic drugs, signal transcription inhibitors, natural products and nutraceuticals on PDAC.…

0301 basic medicineCancer Researchendocrine system diseasesβ estradiolmedicine.medical_treatmentβ-EstradiolEstrogen receptorAntineoplastic AgentsNatural product03 medical and health sciencesFood-Drug Interactions0302 clinical medicineNutraceuticalPancreatic cancerCell Line TumorGeneticsmedicineHumansMolecular BiologyChemotherapeutic drugCell ProliferationChemotherapyNatural products?-EstradiolEstradiolbusiness.industryQUIMIOTERÁPICOSChemotherapeutic drugs; Natural products; Nutraceuticals; Pancreatic cancer; β-EstradiolPancreatic cancerMiddle Agedmedicine.diseasedigestive system diseasesPancreatic Neoplasms030104 developmental biology030220 oncology & carcinogenesisDietary SupplementsCancer researchSettore BIO/14 - FarmacologiaMolecular MedicineChemotherapeutic drugsFemaleChemotherapeutic drugsNutraceuticalsNutraceuticalSignal transductionbusinessHormoneCarcinoma Pancreatic DuctalSignal TransductionAdvances in biological regulation
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Interrelationship between miRNA and splicing factors in pancreatic ductal adenocarcinoma

2021

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers because of diagnosis at late stage and inherent/acquired chemoresistance. Recent advances in genomic profiling and biology of this disease have not yet been translated to a relevant improvement in terms of disease management and patient’s survival. However, new possibilities for treatment may emerge from studies on key epigenetic factors. Deregulation of microRNA (miRNA) dependent gene expression and mRNA splicing are epigenetic processes that modulate the protein repertoire at the transcriptional level. These processes affect all aspects of PDAC pathogenesis and have great potential to unravel new therapeutic targets…

0301 basic medicineCancer Researchsplicing deregulationinteractionDiseaseBiologymedicine.disease_causeinteraction; miRNA; PDAC; splicing deregulation; splicing modulation03 medical and health sciencesSplicing factor0302 clinical medicineDownregulation and upregulationCell Line TumormicroRNAGene expressionmedicineHumansEpigeneticsMolecular BiologymiRNAPDACDNA MethylationGene Expression Regulation NeoplasticPancreatic NeoplasmsRepressor ProteinsMicroRNAs030104 developmental biology030220 oncology & carcinogenesisRNA splicingCancer researchKRASRNA Splicing Factorssplicing modulationCarcinoma Pancreatic Ductal
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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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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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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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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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