Search results for " Pancreatic"

showing 10 items of 149 documents

CRISPR-mediated strand displacement logic circuits with toehold-free DNA

2021

DNA nanotechnology, and DNA computing in particular, has grown extensively over the past decade to end with a variety of functional stable structures and dynamic circuits. However, the use as designer elements of regular DNA pieces, perfectly complementary double strands, has remained elusive. Here, we report the exploitation of CRISPR-Cas systems to engineer logic circuits based on isothermal strand displacement that perform with toehold-free double-stranded DNA. We designed and implemented molecular converters for signal detection and amplification, showing good interoperability between enzymatic and nonenzymatic processes. Overall, these results contribute to enlarge the repertoire of su…

0106 biological sciencesLetterTranscription GeneticComputer scienceStreptococcus pyogenesRibonuclease HBiomedical EngineeringDNA Single-StrandedNanotechnology01 natural sciencesBiochemistry Genetics and Molecular Biology (miscellaneous)Displacement (vector)law.invention03 medical and health sciencesSynthetic biologychemistry.chemical_compoundComputers MolecularDNA computinglaw010608 biotechnologyCRISPR-Associated Protein 9Biological computingDNA nanotechnologyCRISPRNanotechnologyClustered Regularly Interspaced Short Palindromic RepeatsGene Regulatory NetworksDNA nanotechnologySynthetic biology030304 developmental biologyElectronic circuit0303 health sciencesGeneral MedicineRibonuclease PancreaticchemistryLogic gatebiological computingsynthetic biologyCRISPR-Cas SystemsEndopeptidase KGenetic EngineeringDNARNA Guide Kinetoplastida
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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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Fruit and vegetable consumption and health outcomes: an umbrella review of observational studies

2019

The aim of this study was to provide a comprehensive evaluation of current evidence on fruit and vegetable consumption and health outcomes. A systematic search for quantitative syntheses was performed. Several criteria, including study design, dose-response relationship, heterogeneity and agreement of results over time, and identification of potential confounding factors, were used to assess the level of evidence. The strongest (probable) evidence was found for cardiovascular disease protection; possible evidence for decreased risk of colon cancer, depression and pancreatic diseases was found for fruit intake; and colon and rectal cancer, hip fracture, stroke, depression and pancreatic dise…

0301 basic medicineDatabases FactualColorectal cancerHealth BehaviorDiseasemeta-analysiCOLORECTAL-CANCER0302 clinical medicineRisk FactorsVegetablesMedicinevegetableSettore MED/49 - Scienze Tecniche Dietetiche ApplicateDepression (differential diagnoses)Randomized Controlled Trials as TopicMOLECULAR-MECHANISMSDepressionCOLON-CANCERConfoundingcohort study; evidence; Fruit; meta-analysis; umbrella review; vegetable; Food Sciencecohort study; evidence; Fruit; meta-analysis; umbrella review; vegetable; Cardiovascular Diseases; Colonic Neoplasms; Databases Factual; Depression; Diet Healthy; Health Behavior; Humans; Observational Studies as Topic; Pancreatic Diseases; Randomized Controlled Trials as Topic; Risk Factors; Fruit; VegetablesObservational Studies as TopicCardiovascular DiseasesMeta-analysisColonic NeoplasmsDiet HealthyCohort studyCANCER-RISKBLADDER-CANCER030209 endocrinology & metabolismDIETARY POLYPHENOLSDatabases03 medical and health sciencesLUNG-CANCEREnvironmental healthcohort studyHumansCORONARY-HEART-DISEASEFactualHealthy030109 nutrition & dieteticsumbrella reviewbusiness.industryevidencePancreatic DiseasesEvidence-based medicinemedicine.diseaseDietmeta-analysisFruitObservational studyDOSE-RESPONSE METAANALYSISbusinessGASTRIC-CANCERFood Science
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Telomerase and pluripotency factors jointly regulate stemness in pancreatic cancer stem cells

2021

© 2021 by the authors.

0301 basic medicineHomeobox protein NANOGCancer ResearchTelomerasePancreatic neoplasmsMedicinaBiologyStammzelleArticle03 medical and health sciences0302 clinical medicineSOX2Cancer stem cellPancreatic cancermedicineddc:610BauchspeicheldrüsenkrebsStemnessTelomeraseRC254-282Telomere lengthPancreas; CancerCancer stem cellsNeoplastic stem cellsCancer stem cells; Pancreatic cancer; Self-renewal; Stemness; Telomerase; Telomere lengthNeoplasms. Tumors. Oncology. Including cancer and carcinogensPancreatic cancermedicine.disease3. Good healthTelomere030104 developmental biologyOncologyKLF4030220 oncology & carcinogenesisCancer researchSelf-renewalStem cellDDC 610 / Medicine & health
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Pathophysiology of non alcoholic fatty liver disease

2016

The physiopathology of fatty liver and metabolic syndrome are influenced by diet, life style and inflammation, which have a major impact on the severity of the clinicopathologic outcome of non-alcoholic fatty liver disease. A short comprehensive review is provided on current knowledge of the pathophysiological interplay among major circulating effectors/mediators of fatty liver, such as circulating lipids, mediators released by adipose, muscle and liver tissues and pancreatic and gut hormones in relation to diet, exercise and inflammation.

0301 basic medicineLeptinAdipose tissueReviewDiseaseCatalysilcsh:Chemistry0302 clinical medicineNon-alcoholic Fatty Liver DiseaseInsulinAdiponectin; Cholesterol; Fatty liver; Free fatty acids; Ghrelin; Glucagon; Glucagon-like peptide 1; Insulin; Insulin resistance; Irisin; Leptin; Selenoprotein P; Adipose Tissue; Gastrointestinal Hormones; Humans; Lipids; Muscles; Non-alcoholic Fatty Liver Disease; Pancreatic Hormones; Catalysis; Molecular Biology; Computer Science Applications1707 Computer Vision and Pattern Recognition; Spectroscopy; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic Chemistrylcsh:QH301-705.5SpectroscopyGastrointestinal HormoneFree fatty acidMusclesFatty liverComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineLipidLipidsPathophysiologyGhrelinComputer Science ApplicationsCholesterolAdipose TissueMuscleAdiponectinmedicine.symptomHumanmedicine.medical_specialtyIrisinSettore MED/12 - GASTROENTEROLOGIA030209 endocrinology & metabolismInflammationBiologyFree fatty acidsCatalysisPancreatic HormoneGastrointestinal HormonesInorganic Chemistry03 medical and health sciencesInternal medicineFatty liverSelenoprotein PmedicineHumansPhysical and Theoretical ChemistryGlucagon-like peptide 1Molecular BiologyOrganic ChemistryNon alcoholicInsulin resistancemedicine.diseaseGut hormonesGlucagonPancreatic Hormones030104 developmental biologyEndocrinologylcsh:Biology (General)lcsh:QD1-999Metabolic syndrome
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