Search results for "OCR"

showing 10 items of 13223 documents

Aerobic Exercise and Pharmacological Treatments Counteract Cachexia by Modulating Autophagy in Colon Cancer

2016

Recent studies have correlated physical activity with a better prognosis in cachectic patients, although the underlying mechanisms are not yet understood. In order to identify the pathways involved in the physical activity-mediated rescue of skeletal muscle mass and function, we investigated the effects of voluntary exercise on cachexia in colon carcinoma (C26)-bearing mice. Voluntary exercise prevented loss of muscle mass and function, ultimately increasing survival of C26-bearing mice. We found that the autophagic flux is overloaded in skeletal muscle of both colon carcinoma murine models and patients, but not in running C26-bearing mice, thus suggesting that exercise may release the auto…

0301 basic medicineCachexiaColorectal cancerMuscle Fibers SkeletalMicevoluntary physical activityChloroquineMice Inbred BALB CMultidisciplinaryMuscle WeaknessMyogenesis3. Good healthmedicine.anatomical_structureColonic NeoplasmsFemalecancer cachexiamedicine.drugmedicine.medical_specialty[SDV.CAN]Life Sciences [q-bio]/Cancerautophagic fluxBiologyArticleCachexia03 medical and health sciencesAtrophyInternal medicineCell Line TumorPhysical Conditioning AnimalmedicineAutophagyAerobic exerciseAnimalsHumansMuscle SkeletalSirolimusrapamycinAutophagyAutophagosomesSkeletal musclemuscle wasting[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyRibonucleotidesmedicine.diseaseAminoimidazole CarboxamideSurvival Analysisexercise mimetics030104 developmental biologyEndocrinology5-amino-1-beta-D-ribofuranosyl-imidazole-4-carboxamide (AICAR)LysosomesNeoplasm Transplantationmuscle wasting; cancer cachexia; voluntary physical activity; exercise mimetics; 5-amino-1-beta-D-ribofuranosyl-imidazole-4-carboxamide (AICAR); rapamycin; autophagic flux
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IL4 Primes the Dynamics of Breast Cancer Progression via DUSP4 Inhibition

2017

Abstract The tumor microenvironment supplies proinflammatory cytokines favoring a permissive milieu for cancer cell growth and invasive behavior. Here we show how breast cancer progression is facilitated by IL4 secreted by adipose tissue and estrogen receptor–positive and triple-negative breast cancer cell types. Blocking autocrine and paracrine IL4 signaling with the IL4Rα antagonist IL4DM compromised breast cancer cell proliferation, invasion, and tumor growth by downregulating MAPK pathway activity. IL4DM reduced numbers of CD44+/CD24− cancer stem-like cells and elevated expression of the dual specificity phosphatase DUSP4 by inhibiting NF-κB. Enforced expression of DUSP4 drove conversio…

0301 basic medicineCancer ResearchBlotting WesternCA 15-3Breast Neoplasms03 medical and health sciencesParacrine signalling0302 clinical medicineBreast cancerCell Line TumorTumor MicroenvironmentmedicineHumansskin and connective tissue diseasesAutocrine signallingDual-Specificity PhosphataseBlotting Western; Breast Neoplasms; Cell Line Tumor; Disease Progression; Dual-Specificity Phosphatases; Female; Flow Cytometry; Heterografts; Humans; Interleukin-4; Mitogen-Activated Protein Kinase Phosphatases; Tumor Microenvironment; Oncology; Cancer ResearchTumor microenvironmentbiologyCD44CancerFlow Cytometrymedicine.disease030104 developmental biologyOncology030220 oncology & carcinogenesisImmunologyCancer cellDisease Progressionbiology.proteinCancer researchDual-Specificity PhosphatasesHeterograftsMitogen-Activated Protein Kinase PhosphatasesFemaleInterleukin-4HeterograftMitogen-Activated Protein Kinase PhosphataseBreast NeoplasmHumanCancer Research
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ER+ Breast Cancers Resistant to Prolonged Neoadjuvant Letrozole Exhibit an E2F4 Transcriptional Program Sensitive to CDK4/6 Inhibitors

2018

AbstractPurpose: This study aimed to identify biomarkers of resistance to endocrine therapy in estrogen receptor–positive (ER+) breast cancers treated with prolonged neoadjuvant letrozole.Experimental Design: We performed targeted DNA and RNA sequencing in 68 ER+ breast cancers from patients treated with preoperative letrozole (median, 7 months).Results: Twenty-four tumors (35%) exhibited a PEPI score ≥4 and/or recurred after a median of 58 months and were considered endocrine resistant. Integration of the 47 most upregulated genes (log FC > 1, FDR < 0.03) in letrozole-resistant tumors with transcription-binding data showed significant overlap with 20 E2F4-regulated genes (P =…

0301 basic medicineCancer ResearchBreast NeoplasmsE2F4 Transcription FactorArticle03 medical and health sciences0302 clinical medicineText miningDownregulation and upregulationCell Line TumorBiomarkers TumormedicineHumansEndocrine systemProtein Kinase InhibitorsE2F4GeneAgedCell ProliferationAged 80 and overAromatase Inhibitorsbusiness.industryGene Expression ProfilingLetrozoleEndocrine therapyComputational BiologyMiddle AgedEMTREE drug terms: aromatase inhibitorcyclin dependent kinase 4cyclin dependent kinase 6cyclin dependent kinase inhibitorfulvestrantletrozolepaclitaxelpalbociclibtranscription factor E2F4estrogen receptorletrozoleprotein kinase inhibitortranscription factor E2F4transcriptometumor marker030104 developmental biologyReceptors EstrogenOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisLetrozoleMutationRetreatmentCancer researchFemaleTranscriptomebusinessmedicine.drug
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Melanoma in the liver: Oxidative stress and the mechanisms of metastatic cell survival.

2020

Abstract Metastatic melanoma is a fatal disease with a rapid systemic dissemination. The most frequent target sites are the liver, bone, and brain. Melanoma metastases represent a heterogeneous cell population, which associates with genomic instability and resistance to therapy. Interaction of melanoma cells with the hepatic sinusoidal endothelium initiates a signaling cascade involving cytokines, growth factors, bioactive lipids, and reactive oxygen and nitrogen species produced by the cancer cell, the endothelium, and also by different immune cells. Endothelial cell-derived NO and H2O2 and the action of immune cells cause the death of most melanoma cells that reach the hepatic microvascul…

0301 basic medicineCancer ResearchEndotheliumCell SurvivalPopulationCellmedicine.disease_cause03 medical and health sciences0302 clinical medicineImmune systemDownregulation and upregulationTumor MicroenvironmentMedicineAnimalsHumansEndotheliumeducationMelanomaeducation.field_of_studybusiness.industryMelanomaLiver Neoplasmsmedicine.diseaseCarcinoma NeuroendocrineOxidative Stress030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisCancer cellCancer researchbusinessOxidation-ReductionOxidative stressSeminars in cancer biology
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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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Introduction of WT-TP53 into pancreatic cancer cells alters sensitivity to chemotherapeutic drugs, targeted therapeutics and nutraceuticals

2018

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive, highly metastatic malignancy and accounts for 85% of pancreatic cancers. PDAC patients have poor prognosis with a five-year survival of only 5–10%. Mutations at the TP53 gene are readily detected in pancreatic tumors isolated from PDAC patients. We have investigated the effects of restoration of wild-type (WT) TP53 activity on the sensitivity of pancreatic cancer cells to: chemotherapy, targeted therapy, as well as, nutraceuticals. Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisp…

0301 basic medicineCancer ResearchPaclitaxelendocrine system diseasesmedicine.medical_treatmentTargeted therapeuticIrinotecanDeoxycytidineTargeted therapyGlycogen Synthase Kinase 303 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorPancreatic cancerGeneticsmedicineHumansDoxorubicinTP53Signal transduction inhibitorneoplasmsMolecular BiologyCell ProliferationCisplatinChemotherapybusiness.industryPancreatic Neoplasmmedicine.diseaseGemcitabinedigestive system diseasesGemcitabinePancreatic NeoplasmsOxaliplatin030104 developmental biologyPaclitaxelchemistryFluorouracil030220 oncology & carcinogenesisCancer researchMolecular MedicineFluorouracilCisplatinbusinessDrug sensitivityHumanSignal Transductionmedicine.drug
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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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Comparative analysis of the effects of a sphingosine kinase inhibitor to temozolomide and radiation treatment on glioblastoma cell lines.

2017

ABSTRACT Glioblastoma multiforme (GBM) exhibits high resistance to the standard treatment of temozolomide (TMZ) combined with radiotherapy, due to its remarkable cell heterogeneity. Accordingly, there is a need to target alternative molecules enhancing specific GBM autocrine or paracrine mechanisms and amplifying the effect of standard treatment. Sphingosine 1-phosphate (S1P) is such a lipid target molecule with an important role in cell invasion and proliferation. Sphingosine kinase inhibitors (SKI) prevent S1P formation and induce increased production of reactive oxygen species (ROS), which may potentiate radiation cytotoxicity. We analyzed the effect of SKI singular versus combined treat…

0301 basic medicineCancer ResearchRadiation-Sensitizing AgentsCell SurvivalCellSphingosine kinaseApoptosistemozolomideBiologyRadiation Tolerancesphingosine kinase inhibition03 medical and health scienceschemistry.chemical_compoundCell Line TumorX-raysmedicineHumansGPx1oxidative stressCytotoxicityAutocrine signallingAntineoplastic Agents AlkylatingPharmacologychemistry.chemical_classificationReactive oxygen speciesTemozolomideSphingosineBrain NeoplasmsDrug SynergismChemoradiotherapyMolecular biologyDacarbazinePhosphotransferases (Alcohol Group Acceptor)030104 developmental biologymedicine.anatomical_structureOncologychemistryCell cultureradiosensitivityCancer researchMolecular MedicineDrug Screening Assays AntitumorGlioblastomamedicine.drugResearch PaperCancer biologytherapy
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Abilities of berberine and chemically modified berberines to interact with metformin and inhibit proliferation of pancreatic cancer cells.

2019

Abstract Pancreatic cancer is devastating cancer worldwide with few if any truly effective therapies. Pancreatic cancer has an increasing incidence and may become the second leading cause of death from cancer. Novel, more effective therapeutic approaches are needed as pancreatic cancer patients usually survive for less than a year after being diagnosed. Control of blood sugar levels by the prescription drug metformin in diseases such as diabetes mellitus has been examined in association with pancreatic cancer. While the clinical trials remain inconclusive, there is hope that certain diets and medications may affect positively the outcomes of patients with pancreatic and other cancers. Other…

0301 basic medicineCancer ResearchSettore MED/09 - Medicina Internaendocrine system diseasesBerberineSignal transduction inhibitorsBlood sugarPharmacologyAMP-Activated Protein KinasesBerberine; PDAC; Signal transduction inhibitors; TP5303 medical and health scienceschemistry.chemical_compound0302 clinical medicineBerberineMETFORMINAPancreatic cancerDiabetes mellitusGeneticsmedicineHumansTP53Signal transduction inhibitorMolecular BiologyCell Proliferationbusiness.industryPDACCancerAMPKmedicine.diseaseMetforminMetforminNeoplasm ProteinsPancreatic Neoplasms030104 developmental biologychemistry030220 oncology & carcinogenesisCancer cellMolecular Medicinebusinessmedicine.drugAdvances in biological regulation
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Inhibition of colon cancer growth by docosahexaenoic acid involves autocrine production of TNFα

2016

IF 7.932; International audience; The omega-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) has anti-inflammatory and anti-cancer properties. Among pro-inflammatory mediators, tumor necrosis factor a (TNF alpha) plays a paradoxical role in cancer biology with induction of cancer cell death or survival depending on the cellular context. The objective of the study was to evaluate the role of TNFa in DHA-mediated tumor growth inhibition and colon cancer cell death. The treatment of human colorectal cancer cells, HCT-116 and HCT-8 cells, with DHA triggered apoptosis in autocrine TNF alpha-dependent manner. We demonstrated that DHA-induced increased content of TNF alpha mRNA occurred thr…

0301 basic medicineCancer ResearchTumoricidal ActionApoptosis[ SDV.CAN ] Life Sciences [q-bio]/CancerMice[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsForkhead Box Protein O3Cell cycle3. Good healthCell biologyGene Expression Regulation NeoplasticAutocrine CommunicationColonic NeoplasmsTumor-Necrosis-FactorTumor necrosis factor alphaProgrammed cell deathDocosahexaenoic AcidsHuman Colorectal-CancerGene-Expression[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiology03 medical and health sciencesGrowth factor receptorLipid-MetabolismGeneticsmedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyCell-DeathPolyunsaturated Fatty-AcidsAutocrine signallingMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyActivated Protein-KinaseTumor Necrosis Factor-alpha[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyInduced ApoptosisCancerHCT116 Cellsmedicine.diseaseXenograft Model Antitumor AssaysMicroRNAs030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsApoptosisCancer cellCancer researchPrevents Breast-Cancer
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