Search results for "medicine.disease_cause"

showing 10 items of 6035 documents

NGS‐based liquid biopsy profiling identifies mechanisms of resistance to ALK inhibitors: a step toward personalized NSCLC treatment

2021

Despite impressive and durable responses, nonsmall cell lung cancer (NSCLC) patients treated with anaplastic lymphoma kinase (ALK) inhibitors (ALK‐Is) ultimately progress due to development of resistance. Here, we have evaluated the clinical utility of circulating tumor DNA (ctDNA) profiling by next‐generation sequencing (NGS) upon disease progression. We collected 26 plasma and two cerebrospinal fluid samples from 24 advanced ALK‐positive NSCLC patients at disease progression to an ALK‐I. These samples were analyzed by NGS and digital PCR. A tool to retrieve variants at the ALK locus was developed (VALK tool). We identified at least one resistance mutation in the ALK locus in ten (38.5%) p…

0301 basic medicineCancer ResearchLung NeoplasmsEML4-ALKAntineoplastic AgentsEML4‐ALKmedicine.disease_causeNSCLCIDH2Circulating Tumor DNA03 medical and health sciencesALK-TKI0302 clinical medicineCarcinoma Non-Small-Cell LungMAP2K1hemic and lymphatic diseasesALK‐TKIGeneticsmedicineHumansAnaplastic lymphoma kinaseAnaplastic Lymphoma KinaseDigital polymerase chain reactionPrecision MedicineLiquid biopsyProtein Kinase InhibitorsneoplasmsResearch ArticlesRC254-282MutationCrizotinibliquid biopsybusiness.industryHigh-Throughput Nucleotide SequencingNeoplasms. Tumors. Oncology. Including cancer and carcinogensGeneral MedicineResistance mutation3. Good health030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisNGSMutationCancer researchMolecular MedicinebusinessResearch Articlemedicine.drugMolecular Oncology
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Myeloid Cell-Derived Reactive Oxygen Species Induce Epithelial Mutagenesis

2017

Increased oxidative stress has been suggested to initiate and promote tumorigenesis by inducing DNA damage and to suppress tumor development by triggering apoptosis and senescence. The contribution of individual cell types in the tumor microenvironment to these contrasting effects remains poorly understood. We provide evidence that during intestinal tumorigenesis, myeloid cell-derived H2O2 triggers genome-wide DNA mutations in intestinal epithelial cells to stimulate invasive growth. Moreover, increased reactive oxygen species (ROS) production in myeloid cells initiates tumor growth in various organs also in the absence of a carcinogen challenge in a paracrine manner. Our data identify an i…

0301 basic medicineCancer ResearchMyeloidDNA damageApoptosismedicine.disease_causeMice03 medical and health sciencesParacrine signallingmedicineAnimalsMyeloid Cellschemistry.chemical_classificationReactive oxygen speciesTumor microenvironmentChemistryEpithelial CellsHydrogen PeroxideCell BiologyMice Mutant StrainsCell biologyOxidative Stress030104 developmental biologymedicine.anatomical_structureOncologyMutagenesisMutationTumor necrosis factor alphaReactive Oxygen SpeciesCarcinogenesisOxidative stressDNA DamageSignal TransductionCancer Cell
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Parthenolide and DMAPT exert cytotoxic effects on breast cancer stem-like cells by inducing oxidative stress, mitochondrial dysfunction and necrosis

2016

Triple-negative breast cancers (TNBCs) are aggressive forms of breast carcinoma associated with a high rate of recidivism. In this paper, we report the production of mammospheres from three lines of TNBC cells and demonstrate that both parthenolide (PN) and its soluble analog dimethylaminoparthenolide (DMAPT) suppressed this production and induced cytotoxic effects in breast cancer stem-like cells, derived from dissociation of mammospheres. In particular, the drugs exerted a remarkable inhibitory effect on viability of stem-like cells. Such an effect was suppressed by N-acetylcysteine, suggesting a role of reactive oxygen species (ROS) generation in the cytotoxic effect. Instead z-VAD, a ge…

0301 basic medicineCancer ResearchNecrosismedicine.disease_causeCancer -- Treatmentchemistry.chemical_compoundOnium CompoundsMedicineCytotoxic T cellBreast -- CancerMembrane Potential Mitochondrialchemistry.chemical_classificationSuperoxideMitochondrial DNAMitochondriaNeoplastic Stem CellsFemaleOriginal Articlemedicine.symptomOligopeptidesSesquiterpenesCell SurvivalNF-E2-Related Factor 2ImmunologyBreast NeoplasmsReal-Time Polymerase Chain Reaction03 medical and health sciencesCellular and Molecular NeuroscienceDownregulation and upregulationCell Line TumorHumansParthenolideparthenolide cancer stem cell triple-negative breast cancer reactive oxygen species nuclear factor erythroid 2-related factor 2Fluorescent DyesReactive oxygen speciesbusiness.industryAcetophenonesNADPH OxidasesCell BiologyCell nuclei -- AbnormalitiesOxidative Stress030104 developmental biologychemistryApocyninImmunologyCancer researchReactive Oxygen SpeciesbusinessOxidative stressTranscription FactorsCell Death & Disease
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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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Thymic Hyperplasia with Lymphoepithelial Sialadenitis (LESA)-Like Features: Strong Association with Lymphomas and Non-Myasthenic Autoimmune Diseases.

2021

Thymic hyperplasia (TH) with lymphoepithelial sialadenitis (LESA)-like features (LESA-like TH) has been described as a tumor-like, benign proliferation of thymic epithelial cells and lymphoid follicles. We aimed to determine the frequency of lymphoma and autoimmunity in LESA-like TH and performed retrospective analysis of cases with LESA-like TH and/or thymic MALT-lymphoma. Among 36 patients (21 males) with LESA-like TH (age 52 years, 32&ndash

0301 basic medicineCancer ResearchPathologymedicine.medical_specialtyPure red cell aplasia610 Medicine & healthautoimmune diseaselymphomathymitismedicine.disease_causelcsh:RC254-282SclerodermaArticleAutoimmunitysurgery03 medical and health sciences0302 clinical medicinethymusimmune system diseaseshemic and lymphatic diseasesmedicineddc:610Autoimmune diseasebusiness.industryLESAimagingHyperplasialcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseLESA; autoimmune disease; imaging; lymphoma; myasthenia; pathology; surgery; thymic epithelial tumor; thymitis; thymusSialadenitisMyasthenia gravis3. Good healthLymphomamyasthenia030104 developmental biologyOncologythymic epithelial tumor030220 oncology & carcinogenesis570 Life sciences; biologypathologybusiness
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Repurposing of plant alkaloids for cancer therapy: Pharmacology and toxicology.

2019

Drug repurposing (or repositioning) is an emerging concept to use old drugs for new treatment indications. Phytochemicals isolated from medicinal plants have been largely neglected in this context, although their pharmacological activities have been well investigated in the past, and they may have considerable potentials for repositioning. A grand number of plant alkaloids inhibit syngeneic or xenograft tumor growth in vivo. Molecular modes of action in cancer cells include induction of cell cycle arrest, intrinsic and extrinsic apoptosis, autophagy, inhibition of angiogenesis and glycolysis, stress and anti-inflammatory responses, regulation of immune functions, cellular differentiation, a…

0301 basic medicineCancer ResearchPhytochemicalsContext (language use)Antineoplastic AgentsPharmacologymedicine.disease_causeMetastasis03 medical and health sciences0302 clinical medicineAlkaloidsNeoplasmsDrug DiscoveryToxicity TestsmedicineAnimalsHumansRepurposingCardiotoxicitybusiness.industryDrug Repositioningmedicine.diseaseDrug repositioning030104 developmental biology030220 oncology & carcinogenesisCancer cellbusinessCarcinogenesisGenotoxicitySeminars in cancer biology
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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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Phosphoproteome Profiling Reveals Multifunctional Protein NPM1 as part of the Irradiation Response of Tumor Cells

2019

To fight resistances to radiotherapy, the understanding of escape mechanisms of tumor cells is crucial. The aim of this study was to identify phosphoproteins that are regulated upon irradiation. The comparative analysis of the phosphoproteome before and after irradiation brought nucleophosmin (NPM1) into focus as a versatile phosphoprotein that has already been associated with tumorigenesis. We could show that knockdown of NPM1 significantly reduces tumor cell survival after irradiation. NPM1 is dephosphorylated stepwise within 1 hour after irradiation at two of its major phosphorylation sites: threonine-199 and threonine-234/237. This dephosphorylation is not the result of a fast cell cycl…

0301 basic medicineCancer ResearchProgrammed cell deathOriginal articleNucleoplasmCell cycle checkpointChemistryNucleolusmedicine.disease_causelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenslcsh:RC254-282Cell biologyDephosphorylation03 medical and health sciences030104 developmental biology0302 clinical medicineOncologyCytoplasm030220 oncology & carcinogenesismedicineCarcinogenesisIntracellularTranslational Oncology
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HDAC1 and HDAC2 integrate the expression of p53 mutants in pancreatic cancer.

2015

Mutation of p53 is a frequent genetic lesion in pancreatic cancer being an unmet clinical challenge. Mutants of p53 have lost the tumour-suppressive functions of wild type p53. In addition, p53 mutants exert tumour-promoting functions, qualifying them as important therapeutic targets. Here, we show that the class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of p53 mutants in human and genetically defined murine pancreatic cancer cells. Our data reveal that the inhibition of these HDACs with small molecule HDAC inhibitors (HDACi), as well as the specific genetic elimination of HDAC1 and HDAC2, reduce the expression of mutant p53 mRNA and protein levels. We fur…

0301 basic medicineCancer ResearchProteasome Endopeptidase ComplexMutantHistone Deacetylase 2Histone Deacetylase 1Biologymedicine.disease_causeMolecular oncologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicePancreatic cancerGeneticsmedicineAnimalsHumansRNA MessengerPromoter Regions GeneticMolecular BiologyRegulation of gene expressionMice KnockoutMutationWild typeCancerProto-Oncogene Proteins c-mdm2medicine.diseaseGenes p53HDAC13. Good healthGene Expression Regulation NeoplasticHistone Deacetylase InhibitorsPancreatic NeoplasmsDisease Models Animal030104 developmental biologyMutationCancer researchOncogene
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Normal vs cancer thyroid stem cells: the road to transformation

2015

Recent investigations in thyroid carcinogenesis have led to the isolation and characterisation of a subpopulation of stem-like cells, responsible for tumour initiation, progression and metastasis. Nevertheless, the cellular origin of thyroid cancer stem cells (SCs) remains unknown and it is still necessary to define the process and the target population that sustain malignant transformation of tissue-resident SCs or the reprogramming of a more differentiated cell. Here, we will critically discuss new insights into thyroid SCs as a potential source of cancer formation in light of the available information on the oncogenic role of genetic modifications that occur during thyroid cancer develop…

0301 basic medicineCancer ResearchThyroid GlandBiologymedicine.disease_causeMalignant transformationMetastasis03 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALECancer stem cellGeneticsmedicineHumansThyroid Neoplasmsthyroid stem cellsMolecular BiologyThyroid cancerThyroidCancerThyroid Cancer Stem Cells Cancer Stem Cells Oncogenes Metastasismedicine.diseaseCell Transformation Neoplastic030104 developmental biologymedicine.anatomical_structureImmunologyNeoplastic Stem CellsCancer researchStem cellCarcinogenesisOncogene
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