Search results for "medicine.disease_cause"

showing 10 items of 6035 documents

Targeting BRAF and RAS in Colorectal Cancer

2021

Simple Summary In colorectal cancer, mutations of the KRAS and BRAF genes are quite common and can contribute to the activation of cell signaling pathways that lead to cell proliferation and differentiation. These processes promote cancer growth, and in some cases, they may cause cells to develop resistance to certain types of treatment, notably EGFR inhibitors. We summarize recent knowledge regarding the effects of KRAS and BRAF mutations in the setting of colorectal cancer and discuss the new therapies under development. Abstract Colorectal cancer (CRC) is still one of the most frequent forms of cancer in the world in terms of incidence. Around 40% of CRC patients carry a mutation of the …

0301 basic medicineMAPK/ERK pathwayCancer ResearchColorectal cancerAngiogenesismedicine.medical_treatmentcolorectal cancerReviewmedicine.disease_causeBRAFTargeted therapy03 medical and health sciences0302 clinical medicineKRASmedicineneoplasmsRC254-282EGFR inhibitorsMutationbusiness.industryNeoplasms. Tumors. Oncology. Including cancer and carcinogensCancertargeted therapymedicine.diseasedigestive system diseases030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchKRASbusinessCancers
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Targeting prohibitins at the cell surface prevents Th17-mediated autoimmunity.

2018

T helper (Th)17 cells represent a unique subset of CD4(+) T cells and are vital for clearance of extracellular pathogens including bacteria and fungi. However, Th17 cells are also involved in orchestrating autoimmunity. By employing quantitative surface proteomics, we found that the evolutionarily conserved prohibitins (PHB1/2) are highly expressed on the surface of both murine and human Th17 cells. Increased expression of PHBs at the cell surface contributed to enhanced CRAF/MAPK activation in Th17 cells. Targeting surface‐expressed PHBs on Th17 cells with ligands such as Vi polysaccharide (Typhim vaccine) inhibited CRAF‐MAPK pathway, reduced interleukin (IL)‐17 expression and ameliorated …

0301 basic medicineMAPK/ERK pathwayMultiple SclerosisT cellCellPopulationAutoimmunityBiologymedicine.disease_causeT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyAutoimmunity03 medical and health sciencesMiceProhibitinsRickettsial VaccinesmedicineAnimalsHumanseducationExtracellular Signal-Regulated MAP KinasesMolecular Biologyeducation.field_of_studyGeneral Immunology and MicrobiologyGeneral NeuroscienceInterleukinFOXP3Forkhead Transcription FactorsArticlesCell biologyRepressor Proteins030104 developmental biologymedicine.anatomical_structureTh17 CellsSignal transductionHeLa CellsSignal TransductionThe EMBO journal
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The Role of ERK Signaling in Experimental Autoimmune Encephalomyelitis

2017

Extracellular signal-regulated kinase (ERK) signaling plays a crucial role in regulating immune cell function and has been implicated in autoimmune disorders. To date, all commercially available inhibitors of ERK target upstream components, such as mitogen-activated protein (MAP) kinase/ERK kinase (MEKs), but not ERK itself. Here, we directly inhibit nuclear ERK translocation by a novel pharmacological approach (Glu-Pro-Glu (EPE) peptide), leading to an increase in cytosolic ERK phosphorylation during T helper (Th)17 cell differentiation. This was accompanied by diminished secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine influencing the encephalitogenicity …

0301 basic medicineMAPK/ERK pathwaymedicine.medical_treatmentCellular differentiationexperimental autoimmune encephalomyelitisLymphocyte Activationmedicine.disease_causemultiple sclerosisAutoimmunitylcsh:ChemistryMice0302 clinical medicineT-Lymphocyte SubsetsPhosphorylationExtracellular Signal-Regulated MAP Kinaseslcsh:QH301-705.5SpectroscopyKinaseExperimental autoimmune encephalomyelitisInterleukinGeneral MedicineComputer Science ApplicationsCell biologyProtein TransportCytokine030220 oncology & carcinogenesisFemaleERK pathwayCell signalingEncephalomyelitis Autoimmune ExperimentalMAP Kinase Signaling SystemT cellsBiologyModels BiologicalArticleCatalysisInorganic Chemistry03 medical and health sciencesmedicineAnimalscell signalingPhysical and Theoretical ChemistryEPE peptideMolecular BiologyT cells; ERK pathway; EPE peptide; experimental autoimmune encephalomyelitis; multiple sclerosis; cell signalingOrganic ChemistryGranulocyte-Macrophage Colony-Stimulating Factormedicine.diseaseDisease Models Animal030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Th17 CellsInternational Journal of Molecular Sciences
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Trends of extended-spectrum β-lactamase-producing Escherichia coli sequence type 131 and its H30 subclone in a French hospital over a 15-year period.

2016

International audience; Sequence type 131 (ST131) is a predominant lineage among extraintestinal pathogenic Escherichia coli. It plays a major role in the worldwide dissemination of E. coli producing extended-spectrum β-lactamases (ESBLs). Here we describe the long-term epidemiology of this clonal group in a French university hospital, where the incidence of ESBL-producing E. coli has increased from 0.018 case per 1000 patient-days in the year 2000 to 0.50 case per 1000 patient-days in 2014. The first of the 141 ST131 isolates was recovered in 2006, and the ST131 clonal group accounted for 18.1% of total ESBL-producing E. coli over the whole period (2000-2014). Subclonal typing showed that …

0301 basic medicineMESH : Escherichia coliMESH : Retrospective StudiesMESH : Multilocus Sequence TypingMESH: beta-LactamasesMESH : GenotypeMultidrug resistancemedicine.disease_causeHospitals UniversityMESH: Genotype[ SDV.MP ] Life Sciences [q-bio]/Microbiology and ParasitologyPharmacology (medical)MESH: IncidenceMESH: Genetic VariationEscherichia coli InfectionsComputingMilieux_MISCELLANEOUSCross InfectionMolecular EpidemiologyExtraintestinal Pathogenic Escherichia coliMESH: Escherichia coliIncidenceIncidence (epidemiology)MESH : beta-LactamasesGeneral MedicinePFGEMESH : IncidenceElectrophoresis Gel Pulsed-Field3. Good healthInfectious DiseasesMESH: Electrophoresis Gel Pulsed-FieldMESH: Multilocus Sequence Typing[SDV.MP]Life Sciences [q-bio]/Microbiology and ParasitologyMESH : Escherichia coli Infections[SDE]Environmental SciencesFranceMESH : Cross InfectionMicrobiology (medical)clone (Java method)Lineage (genetic)GenotypeMESH : Molecular Epidemiology030106 microbiologyBiologybeta-LactamasesMicrobiology03 medical and health sciencesExtended-spectrum β-lactamaseMESH : Genetic VariationEscherichia coliPulsed-field gel electrophoresismedicineHumansMESH: Molecular EpidemiologyTypingMESH : FranceEscherichia coliMESH : Hospitals UniversityRetrospective StudiesMESH : Electrophoresis Gel Pulsed-FieldMESH: Escherichia coli InfectionsMESH: Hospitals UniversityMESH: HumansMESH : HumansGenetic VariationMESH: Cross InfectionMESH: Retrospective Studiesbacterial infections and mycosesMultiple drug resistanceMESH: FranceESBLMultilocus Sequence Typing
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Venlafaxine prevents morphine antinociceptive tolerance: The role of neuroinflammation and the l-arginine-nitric oxide pathway.

2017

Abstract Opioid-induced neuroinflammation and the nitric oxide (NO) signal-transduction pathway are involved in the development of opioid analgesic tolerance. The antidepressant venlafaxine (VLF) modulates NO in nervous tissues, and so we investigated its effect on induced tolerance to morphine, neuroinflammation, and oxidative stress in mice. Tolerance to the analgesic effects of morphine were induced by injecting mice with morphine (50 mg/kg) once a day for three consecutive days; the effect of co-administration of VLF (5 or 40 mg/kg) with morphine was similarly tested in a separate group. To determine if the NO precursor l -arginine hydrochloride ( l -arg) or NO are involved in the effec…

0301 basic medicineMaleArginineAnalgesicPharmacologymedicine.disease_causeNitric oxideProinflammatory cytokine03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineDevelopmental NeurosciencemedicineAnimalsEnzyme InhibitorsNitritesPain Measurementchemistry.chemical_classificationGlutathione PeroxidaseDose-Response Relationship DrugMorphineGlutathione peroxidaseVenlafaxine HydrochlorideBrainMalondialdehydeAnalgesics OpioidDisease Models AnimalOxidative Stress030104 developmental biologyNG-Nitroarginine Methyl EsterNeurologychemistryMorphineAntidepressive Agents Second-GenerationCytokinesLipid PeroxidationMorphine Dependence030217 neurology & neurosurgeryOxidative stressmedicine.drugSignal TransductionExperimental neurology
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Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.

2019

Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of…

0301 basic medicineMaleCancer ResearchBiopsyL-amp GB EGFR-low amplified glioblastomamedicine.disease_causewt wildtypeMYBPC3 myosin-binding protein C0302 clinical medicineHIC1 hypermethylated in cancer 1Gene duplicationIn Situ Hybridization FluorescenceIDH2 isocitrate dehydrogenase 2MutationRB-pat RB signaling pathwayEGFRvIII epidermal growth factor receptor variant number IIIPAH phenylalanine hydroxylaseGBM glioblastoma IDH-wildtype (glioblastoma multiforme primary glioblastoma).ANOVA ANalysis Of VArianceN-amp GB EGFR-no amplified glioblastomaMiddle AgedCDKN2A cyclin-dependent kinase inhibitor 2Alcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisPrimary tumorImmunohistochemistryH-amp GB EGFR-high amplified glioblastomaErbB ReceptorsTKR-pat tyrosine-kinase receptors signaling pathway030220 oncology & carcinogenesisDisease ProgressionCDK6 cyclin-dependent kinase 6CDH1 Cadherin 1FemaleCREM cAMP response element modulatorIHC immunohistochemistryAdultOriginal articleDNA Copy Number VariationsCDKN1B cyclin-dependent kinase inhibitor 1BBiologyRARB retinoic acid receptor betaCNS central nervous systemlcsh:RC254-282IDH1 isocitrate dehydrogenase 1BCL2 B-cell cll/ lymphoma 2CNAs copy number algerationsWHO World Health Organization03 medical and health sciencesYoung Adultp53-pat p53 signaling pathwaymedicineBiomarkers TumorTMA tissue microarrayPTENHumansProtein kinase BPI3K/AKT/mTOR pathwaySurvival analysisAgedGenetic heterogeneityGene AmplificationGFAP glial fibrillary acidic proteinMLPA multiplex ligation-dependent probe amplificationmedicine.diseaseFISH fluorescence in situ hibridizationSurvival AnalysisCDKN2B cyclin-dependent kinase inhibitor 2BPTEN phosphatase and tensin homologEGFR epidermal growth factor receptorCNV-load load of copy number variations030104 developmental biologyMutationPARK2 parkinCancer researchbiology.proteinTCGA The Cancer Genome AtlasLARGE1 acetylglucosaminyltransferase-like protein 1GlioblastomaCHD7 Chromodomain Helicase DNA Binding Protein 7DAPI 4′6-diamidino-2-phenylindoleNeoplasia (New York, N.Y.)
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Treatment patterns for metastatic colorectal cancer in Spain

2020

Abstract Purpose The primary aim of this retrospective study was to describe the treatment patterns according to the type of treatment received by patients with metastatic colorectal cancer (mCRC) in Spain. Methods This was a retrospective, observational, multicenter study performed by 33 sites throughout Spain that included consecutive patients aged 18 years or older who had received or were receiving treatment for mCRC. Results At the time of inclusion, of the 873 evaluable patients, 507 (58%) had received two lines, 235 (27%) had received three lines, 106 (12%) had received four lines, and the remaining patients had received up to ten lines. The most frequent chemotherapy schemes were th…

0301 basic medicineMaleCancer ResearchColorectal cancermedicine.medical_treatmentmedicine.disease_causeTargeted therapy0302 clinical medicineFOLFOXAntineoplastic Combined Chemotherapy ProtocolsKRAS/BRAF mutation statusMolecular Targeted TherapyNeoplasm MetastasisCàncerTreatment patternsGeneral MedicineMiddle AgedTreatment OutcomeOncology030220 oncology & carcinogenesisFOLFIRIMetastaticFemaleKRASGuideline AdherenceColorectal NeoplasmsCàncer Pacientsmedicine.drugResearch ArticleProto-Oncogene Proteins B-rafmedicine.medical_specialtyProto-Oncogene Proteins p21(ras)03 medical and health sciencesInternal medicinemedicineHumansAgedRetrospective StudiesClinical practice guidelineChemotherapybusiness.industryRetrospective cohort studymedicine.diseaseColorectal cancerdigestive system diseases030104 developmental biologySpainMutationObservational studybusiness
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A multidimensional network approach reveals microRNAs as determinants of the mesenchymal colorectal cancer subtype

2016

Colorectal cancer (CRC) is a heterogeneous disease posing a challenge for accurate classification and treatment of this malignancy. There is no common genetic molecular feature that would allow for the identification of patients at risk for developing recurrences and thus selecting patients who would benefit from more stringent therapies still poses a major clinical challenge. Recently, an international multicenter consortium (CRC Subtyping Consortium) was established aiming at the classification of CRC patients in biologically homogeneous CRC subtypes. Four consensus molecular subtypes (CMSs) were identified, of which the mesenchymal CMS4 presented with worse prognosis signifying the impor…

0301 basic medicineMaleCancer ResearchEpithelial-Mesenchymal TransitionGene regulatory networkComputational biologyBiologymedicine.disease_causeEpigenesis Genetic03 medical and health sciencesMolecular Biology; Cancer Research; GeneticsCell Line TumormicroRNAmedicineGeneticsHumansGene Regulatory NetworksEpigeneticsPromoter Regions GeneticMolecular BiologyRegulation of gene expressionCancerComputational BiologyDNA Methylationmedicine.diseasePrognosisSubtyping3. Good healthGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologyPhenotypeMultigene FamilyDNA methylationCancer researchFemaleOriginal ArticleCarcinogenesisColorectal NeoplasmsTranscriptomeOncogene
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Exome-wide somatic mutation characterization of small bowel adenocarcinoma

2018

Small bowel adenocarcinoma (SBA) is an aggressive disease with limited treatment options. Despite previous studies, its molecular genetic background has remained somewhat elusive. To comprehensively characterize the mutational landscape of this tumor type, and to identify possible targets of treatment, we conducted the first large exome sequencing study on a population-based set of SBA samples from all three small bowel segments. Archival tissue from 106 primary tumors with appropriate clinical information were available for exome sequencing from a patient series consisting of a majority of confirmed SBA cases diagnosed in Finland between the years 2003–2011. Paired-end exome sequencing was…

0301 basic medicineMaleCancer ResearchMICROSATELLITE INSTABILITYColorectal canceroncogenesReceptor ErbB-2medicine.disease_causeCOLORECTAL-CANCERACTIVATIONCohort Studies0302 clinical medicineAnimal CellsAdenocarcinomasMedicine and Health SciencesExomeFrameshift MutationExomeGenetics (clinical)Exome sequencingAged 80 and overSMALL-INTESTINEeducation.field_of_study1184 Genetics developmental biology physiologyCELIAC-DISEASENonsense MutationMiddle Aged3. Good healthsyöpägeenitOncology030220 oncology & carcinogenesissyöpätauditFemaleSIGNALING PATHWAYKRASCellular TypesResearch ArticleAdultProto-Oncogene Proteins B-raflcsh:QH426-470SEQUENCING DATAImmune CellsNonsense mutationPopulationImmunologyAntigen-Presenting CellsComputational biologysuolistosyövätBiologyAdenocarcinomata3111CarcinomasFrameshift mutation03 medical and health sciencesGermline mutationQUALITY-CONTROLGenetiikka kehitysbiologia fysiologia - Genetics developmental biology physiologySyöpätaudit - CancersIntestinal NeoplasmsmedicineGeneticsPoint MutationHumanseducationMolecular BiologyEcology Evolution Behavior and SystematicsAgedColorectal CancerBiology and Life SciencesCancers and Neoplasmscancerous diseasesCell Biologymedicine.diseaseta3122mutationsCOMPREHENSIVE MOLECULAR CHARACTERIZATIONlcsh:Genetics030104 developmental biologyMutationSomatic Mutationbowel cancer3111 BiomedicinemutaatiotHIGH-RESOLUTIONPLoS Genetics
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Phase II study of necitumumab plus modified FOLFOX6 as first-line treatment in patients with locally advanced or metastatic colorectal cancer

2016

Background:This single-arm phase II study investigated the EGFR monoclonal antibody necitumumab plus modified FOLFOX6 (mFOLFOX6) in first-line treatment of locally advanced or metastatic colorectal cancer (mCRC).Methods:Patients received 800-mg intravenous necitumumab (day 1; 2-week cycles), followed by oxaliplatin 85 mg m -2, folinic acid 400 mg m -2, and 5-fluorouracil (400 mg m -2 bolus then 2400 mg m -2 over 46 h). Radiographic evaluation was performed every 8 weeks until progression. Primary endpoint was objective response rate.Results:Forty-four patients were enrolled and treated. Objective response rate was 63.6% (95% confidence interval 47.8-77.6); complete response was observed in …

0301 basic medicineMaleCancer ResearchOrganoplatinum CompoundsLeucovorinPhases of clinical researchmedicine.disease_causeGastroenterology0302 clinical medicineadvanced colorectal cancerAntineoplastic Combined Chemotherapy ProtocolsClinical endpointNeoplasm MetastasisNecitumumabModified FOLFOX6Aged 80 and overnecitumumabAntibodies MonoclonalMiddle AgedOxaliplatinTreatment OutcomeOncologyFluorouracil030220 oncology & carcinogenesisFemaleKRASFluorouracilColorectal Neoplasmsmedicine.drugAdultmedicine.medical_specialtyEGFRNeutropeniamodified FOLFOX6Antibodies Monoclonal HumanizedDisease-Free SurvivalProto-Oncogene Proteins p21(ras)03 medical and health sciencesFolinic acidInternal medicinemedicineKRASHumansAdvanced colorectal cancerAgedbusiness.industrymedicine.diseaseSurvival AnalysisSurgeryOxaliplatinCancérologie030104 developmental biologyClinical StudybusinessNecitumumabBritish Journal of Cancer
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