Search results for "Cancer Research"

showing 10 items of 5684 documents

Chemoresistance and chemosensitization in cholangiocarcinoma

2017

One of the main difficulties in the management of patients with advanced cholangiocarcinoma (CCA) is their poor response to available chemotherapy. This is the result of powerful mechanisms of chemoresistance (MOC) of quite diverse nature that usually act synergistically. The problem is often worsened by altered MOC gene expression in response to pharmacological treatment. Since CCA includes a heterogeneous group of cancers their genetic signature coding for MOC genes is also diverse; however, several shared traits have been defined. Some of these characteristics are shared with other types of liver cancer, namely hepatocellular carcinoma and hepatoblastoma. An important goal in modern onco…

0301 basic medicinePharmacologybile ductschemotherapydrug delivery systems0302 clinical medicineChemosensitizationantineoplastic agentsmolecular biologyReceptorhumansreceptor protein-tyrosine kinasesmedia_commonapoptosisgene expression regulationbile duct neoplasmsDrug Resistance Multipletargeted therapiesGene Expression Regulation Neoplasticmultiplebiliary cancer; chemotherapy; liver cancer; multidrug resistance; targeted therapies; antineoplastic agents; apoptosis; bile duct neoplasms; bile ducts; cell survival; cholangiocarcinoma; drug delivery systems; drug resistance multiple; drug resistance; neoplasm; epithelial cells; gene expression regulation neoplastic; genetic therapy; humans; protein kinase inhibitors; receptor protein-tyrosine kinases; signal transduction; treatment outcome; molecular medicine; molecular biology030220 oncology & carcinogenesisHepatocellular carcinomabiliary cancerLiver cancercholangiocarcinomaTyrosine kinasesignal transductionDrugHepatoblastomamedia_common.quotation_subjectcell survivalPharmacological treatmentliver cancer03 medical and health sciencesmultidrug resistancemedicinemolecular medicinedrug resistancebusiness.industrymedicine.diseaseepithelial cellsneoplasticprotein kinase inhibitors030104 developmental biologyDrug Resistance NeoplasmCancer researchtreatment outcomebusinessneoplasmgenetic therapy
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A conditional inducible JAK2V617F transgenic mouse model reveals myeloproliferative disease that is reversible upon switching off transgene expressio…

2019

Aberrant activation of the JAK/STAT pathway is thought to be the critical event in the pathogenesis of the chronic myeloproliferative neoplasms, polycythemia vera, essential thrombocythemia and primary myelofibrosis. The most frequent genetic alteration in these pathologies is the activating JAK2V617F mutation, and expression of the mutant gene in mouse models was shown to cause a phenotype resembling the human diseases. Given the body of genetic evidence, it has come as a sobering finding that JAK inhibitor therapy only modestly suppresses the JAK2V617F allele burden, despite showing clear benefits in terms of reducing splenomegaly and constitutional symptoms in patients. To gain a better …

0301 basic medicinePhysiologyClone (cell biology)Mice0302 clinical medicineAnimal CellsBone MarrowImmune PhysiologyMedicine and Health SciencesBlood and Lymphatic System ProceduresTransgenesBone Marrow TransplantationRegulation of gene expressionMultidisciplinaryQRAnimal ModelsBody FluidsPhenotypesBloodExperimental Organism Systems030220 oncology & carcinogenesisMedicineAnatomyCellular TypesResearch ArticleGenetically modified mousePlateletsTransgeneScienceImmunologyMutation MissenseMice TransgenicMouse ModelsSurgical and Invasive Medical ProceduresBone Marrow CellsBiologyResearch and Analysis Methods03 medical and health sciencesModel OrganismsmedicineGeneticsAnimalsHumansAlleleProgenitor cellMyelofibrosisMolecular Biology TechniquesMolecular BiologyTransplantationMyeloproliferative DisordersBlood CellsEssential thrombocythemiaBiology and Life SciencesCell BiologyJanus Kinase 2medicine.diseaseHematopoietic Stem CellsDisease Models Animal030104 developmental biologyAmino Acid SubstitutionGene Expression RegulationImmune SystemCancer researchAnimal StudiesSpleenCloningPLoS ONE
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Stimulation of natural killer cells with rhCD137 ligand enhances tumor-targeting antibody efficacy in gastric cancer

2018

Although many anticancer agents for gastric cancer have been developed, the prognosis for many patients remains poor. Recently, costimulatory immune molecules that reactivate antitumor immune responses by utilizing the host immune system have attracted attention as new therapeutic strategies. CD137 is a costimulatory molecule that reportedly potentiates the antitumor activity of tumor-targeting monoclonal antibodies (mAbs) by enhancing antibody-dependent cellular cytotoxicity. However, it remains unclear whether CD137 stimulates tumor-regulatory activity in gastric cancer. In this study, we investigated the antitumor effects of CD137 stimulation on gastric cancer cells administered tumor-ta…

0301 basic medicinePhysiologyCytotoxicityCancer Treatmentlcsh:MedicineNK cellsToxicologyPathology and Laboratory MedicineAntineoplastic Agents ImmunologicalSpectrum Analysis Techniques0302 clinical medicineImmune PhysiologyCellular typeslcsh:ScienceInnate Immune SystemCytotoxicity AssayMultidisciplinarybiologyChemistryImmune cellsCD137Drug SynergismFlow CytometryRecombinant ProteinsUp-RegulationGene Expression Regulation NeoplasticKiller Cells NaturalOncologySpectrophotometry030220 oncology & carcinogenesisCytokinesWhite blood cellsFemaleTumor necrosis factor alphaCytophotometryAntibodyResearch ArticleCell biologyBlood cellsCell Survivalmedicine.drug_classImmunologyAntibodies Monoclonal HumanizedResearch and Analysis MethodsMonoclonal antibody03 medical and health sciencesImmune systemStomach NeoplasmsCell Line TumorGastrointestinal TumorsmedicineHumansSecretionCell ProliferationMedicine and health sciencesBiology and life scienceslcsh:RCancers and NeoplasmsCancerTrastuzumabMolecular Developmentmedicine.diseaseGranzyme BGastric Cancer4-1BB Ligand030104 developmental biologyAnimal cellsImmune SystemCancer cellCancer researchbiology.proteinlcsh:QPhysiological ProcessesDevelopmental BiologyPLOS ONE
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MYC and MCL1 Cooperatively Promote Chemotherapy-Resistant Breast Cancer Stem Cells via Regulation of Mitochondrial Oxidative Phosphorylation

2017

Summary Most patients with advanced triple-negative breast cancer (TNBC) develop drug resistance. MYC and MCL1 are frequently co-amplified in drug-resistant TNBC after neoadjuvant chemotherapy. Herein, we demonstrate that MYC and MCL1 cooperate in the maintenance of chemotherapy-resistant cancer stem cells (CSCs) in TNBC. MYC and MCL1 increased mitochondrial oxidative phosphorylation (mtOXPHOS) and the generation of reactive oxygen species (ROS), processes involved in maintenance of CSCs. A mutant of MCL1 that cannot localize in mitochondria reduced mtOXPHOS, ROS levels, and drug-resistant CSCs without affecting the anti-apoptotic function of MCL1. Increased levels of ROS, a by-product of a…

0301 basic medicinePhysiologyMice NudeTriple Negative Breast NeoplasmsOxidative phosphorylationTumor initiationMitochondrionBiologyOxidative PhosphorylationArticleProto-Oncogene Proteins c-myc03 medical and health sciencesCancer stem cellCell Line TumorAnimalsHumansMCL1Molecular BiologyTriple-negative breast cancerchemistry.chemical_classificationReactive oxygen speciesCell BiologyMitochondria030104 developmental biologychemistryDrug Resistance NeoplasmNeoplastic Stem CellsCancer researchMyeloid Cell Leukemia Sequence 1 ProteinFemaleStem cellReactive Oxygen SpeciesCell Metabolism
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Stem Cells in Pituitary Tumors: Experimental Evidence Supporting Their Existence and Their Role in Tumor Clinical Behavior

2019

Although generally benign, pituitary tumors frequently show local invasiveness and resistance to pharmacological therapy. After the demonstration of the existence of pituitary gland stem cells, over the past decade, the presence of a stem cell subpopulation in pituitary tumors has been investigated, analogous to the cancer stem cell model developed for malignant tumors. This review recapitulates the experimental evidence supporting the existence of a population of stem-like cells in pituitary tumors, focusing on their potential role in tumor initiation, progression, recurrence and resistance to pharmacological therapy.

0301 basic medicinePituitary glandrecurrencePharmacological therapyMini ReviewEndocrinology Diabetes and MetabolisminvasivenessPopulation030209 endocrinology & metabolismTumor initiationmedicine.disease_causelcsh:Diseases of the endocrine glands. Clinical endocrinologyresistance03 medical and health sciences0302 clinical medicineEndocrinologyCancer stem cellpituitary tumorsstem cellsmedicineeducationinvasiveness; pituitary tumors; recurrence; resistance; stem cells; tumourigenesiseducation.field_of_studylcsh:RC648-665business.industryPituitary tumorsmedicine.disease030104 developmental biologymedicine.anatomical_structuretumourigenesisCancer researchStem cellCarcinogenesisbusinessFrontiers in Endocrinology
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“Back to a false normality”: new intriguing mechanisms of resistance to PARP inhibitors

2017

Several evidences have shown that BRCA mutations increased tumor-cells sensitivity to PARP inhibitors by synthetic lethality leading to an accelerated development of several compounds targeting the PARP enzymes system as anticancer agents for clinical setting. Most of such compounds have been investigated in ovarian and breast cancer, showing promising efficacy in BRCA-mutated patients. Recently clinical studies of PARP-inhibitors have been extended across different tumor types harboring BRCA-mutations, including also "BRCA-like" sporadic tumors with homologous recombination deficiency (HRD). This review summarizes the biological background underlying PARP-inhibition, reporting the results …

0301 basic medicinePoly ADP ribose polymerasemedicine.medical_treatmentReviewSynthetic lethalityPoly(ADP-ribose) Polymerase Inhibitorsmedicine.disease_causePoly (ADP-Ribose) Polymerase Inhibitorresistance03 medical and health sciences0302 clinical medicineBreast cancerCell Line TumorBRCA1-2AnimalsHumansMedicinePARP inhibitorsBRCA2 ProteinGeneticsMutationChemotherapyBRCA1 Proteinbusiness.industryBRCA1-2; PARP inhibitors; Resistance; Oncologymedicine.diseaseBRCA2 ProteinClinical trialPARP inhibitor030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisMutationCancer researchbusinessOncotarget
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3D polymeric supports promote the growth and progression of anaplastic thyroid carcinoma.

2020

Abstract Anaplastic thyroid carcinoma (ATC) is a rare and aggressive malignancy that accounts for the majority of deaths from all thyroid cancers. ATC exhibits invasiveness and highly resistance to conventional therapies which include cytotoxic chemotherapy, the combination of BRAF and MEK inhibition and, more recently, immunotherapies, that have shown promising but still limited results. A growing knowledge on ATC tumor biology is needed for developing more effective therapies with significant better survival. Researchers have begun to utilize 3D models to culture cancer cells for in vitro studies. In this work, C643 ATC cell line was cultured on polymeric scaffolds with high-interconnecte…

0301 basic medicinePolymersBiophysicsMalignancyStem cell markerThyroid Carcinoma AnaplasticBiochemistryMetastasis03 medical and health sciences0302 clinical medicineCancer stem cellCell Line TumormedicineBiomarkers TumorHumansDoxorubicin3D tumor model Anaplastic thyroid carcinoma Doxorubicin Polymeric scaffold Stem cell markersMolecular BiologyThyroid cancerCell ShapeCell ProliferationTissue Scaffoldsbusiness.industryThyroidCell Biologymedicine.disease030104 developmental biologymedicine.anatomical_structureDoxorubicin030220 oncology & carcinogenesisCancer cellCancer researchDisease ProgressionNeoplastic Stem Cellsbusinessmedicine.drugBiochemical and biophysical research communications
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Dibutyltin(IV) and Tributyltin(IV) Derivatives of meso-Tetra(4 sulfonatophenyl)porphine Inhibit the Growth and the Migration of Human Melanoma Cells.

2019

Melanoma is the most aggressive and deadly form of skin cancer, which is largely due to its propensity to metastasize. Therefore, with the aim to inhibit the growth and the metastatic dissemination of melanoma cells and to provide a novel treatment option, we studied the effects of the melanoma treatment with two organotin(IV) complexes of the meso-tetra(4-sulfonato-phenyl)porphine, namely (Bu2Sn)2TPPS and (Bu3Sn)4TPPS. In particular, we showed that nanomolar concentrations of (Bu2Sn)2TPPS and (Bu3Sn)4TPPS are sufficient to inhibit melanoma cell growth, to increase the expression of the full-length poly (ADP-ribose) polymerase (PARP-1), to induce the cell cycle arrest respectively at G2/M a…

0301 basic medicinePorphyrinsCellAntineoplastic AgentsApoptosisorganotin(IV)migrationArticleBRAF03 medical and health sciences0302 clinical medicineCyclin D1Cell MovementCell Line Tumormelanoma; organotin(IV); cellular growth; BRAF; cell cycle; migrationmedicinemelanomaHumansSTAT3Cell ProliferationDose-Response Relationship DrugMolecular StructurebiologyCell growthChemistryMelanomaCell migrationCell Cycle CheckpointsGeneral Medicinecellular growthCell cyclemedicine.disease030104 developmental biologymedicine.anatomical_structureFocal Adhesion Kinase 1030220 oncology & carcinogenesisbiology.proteinCancer researchcell cycleSkin cancerSignal Transduction
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Metformin decreases progerin expression and alleviates pathological defects of Hutchinson–Gilford progeria syndrome cells

2016

Hutchinson–Gilford progeria syndrome (HGPS) is a rare genetic disorder that causes systemic accelerated aging in children. This syndrome is due to a mutation in the LMNA gene that leads to the production of a truncated and toxic form of lamin A called progerin. Because the balance between the A-type lamins is controlled by the RNA-binding protein SRSF1, we have hypothesized that its inhibition may have therapeutic effects for HGPS. For this purpose, we evaluated the antidiabetic drug metformin and demonstrated that 48 h treatment with 5 mmol/l metformin decreases SRSF1 and progerin expression in mesenchymal stem cells derived from HGPS induced pluripotent stem cells (HGPS MSCs). The effect …

0301 basic medicinePremature agingcongenital hereditary and neonatal diseases and abnormalitiesAgingArticleLMNA03 medical and health sciencesProgeria0302 clinical medicinemedicineInduced pluripotent stem cellProgeriaintegumentary systembusiness.industryGenetic disordernutritional and metabolic diseasesmedicine.diseaseProgerinMetformin030104 developmental biology030220 oncology & carcinogenesisCancer researchGeriatrics and GerontologybusinessLaminmedicine.drugnpj Aging and Mechanisms of Disease
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Neuroendocrine differentiation in a large series of genetically-confirmed Ewing’s sarcoma family tumor: Does it provide any diagnostic or prognostic …

2021

Given the potential for neuroendocrine differentiation in Ewing's sarcoma family of tumors (ESFT), we aimed to determine neuroendocrine expression in a large series of genetically-confirmed ESFT and its prognostic significance in clinically-localised neoplasms (n = 176). Slides prepared from tissue microarrays were stained for Insulinoma-associated protein 1 (INSM1), CD56, chromogranin-A and synaptophysin. INSM1 expression was present in 59% of ESFT, while synaptophysin, chromogranin-A and CD56 were expressed in only 13%, 8% and 5% of ESFT, respectively. Histological subtypes were only significantly correlated with INSM1 (p = 0.032) or CD56 (p = 0.016) immunoexpression. Regarding prognosis,…

0301 basic medicinePrognostic factorLung NeoplasmsSynaptophysinSarcoma EwingNeuroendocrine differentiationPathology and Forensic Medicine03 medical and health sciences0302 clinical medicineBiomarkers TumormedicineHumansTissue microarraybiologybusiness.industryEwing's sarcomaLarge seriesChromogranin ACell DifferentiationCell Biologymedicine.diseaseCarcinoma NeuroendocrineRepressor Proteins030104 developmental biology030220 oncology & carcinogenesisSynaptophysinbiology.proteinCancer researchSarcomabusinessPathology - Research and Practice
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