Search results for "TREATMENT"

showing 10 items of 17623 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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CXCR7 Reactivates ERK Signaling to Promote Resistance to EGFR Kinase Inhibitors in NSCLC

2019

Abstract Although EGFR mutant–selective tyrosine kinase inhibitors (TKI) are clinically effective, acquired resistance can occur by reactivating ERK. We show using in vitro models of acquired EGFR TKI resistance with a mesenchymal phenotype that CXCR7, an atypical G protein-coupled receptor, activates the MAPK–ERK pathway via β-arrestin. Depletion of CXCR7 inhibited the MAPK pathway, significantly attenuated EGFR TKI resistance, and resulted in mesenchymal-to-epithelial transition. CXCR7 overexpression was essential in reactivation of ERK1/2 for the generation of EGFR TKI–resistant persister cells. Many patients with non–small cell lung cancer (NSCLC) harboring an EGFR kinase domain mutatio…

0301 basic medicineMAPK/ERK pathwayCancer ResearchLung NeoplasmsDrug ResistanceDrug resistanceTransgenicMiceChemokine receptor0302 clinical medicineNeoplasmsCarcinoma Non-Small-Cell LungReceptorsMedicineNon-Small-Cell LungCXCRReceptorLungbeta-ArrestinsCancerEGFR inhibitorsTumorKinaseLung CancerErbB ReceptorsOncology5.1 Pharmaceuticals030220 oncology & carcinogenesisDevelopment of treatments and therapeutic interventionsTyrosine kinaseEpithelial-Mesenchymal TransitionMAP Kinase Signaling SystemOncology and CarcinogenesisMice TransgenicArticleCell LineExperimental03 medical and health sciencesClinical ResearchCell Line TumorAnimalsHumansOncology & CarcinogenesisProtein Kinase InhibitorsReceptors CXCRbusiness.industryCarcinomaNeoplasms Experimentalrespiratory tract diseases030104 developmental biologyProtein kinase domainDrug Resistance NeoplasmMutationCancer researchNeoplasmbusinessCancer Research
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Autocrine CCL5 Effect Mediates Trastuzumab Resistance by ERK Pathway Activation in HER2-Positive Breast Cancer.

2020

Abstract HER2-positive breast cancer is currently managed with chemotherapy in combination with specific anti-HER2 therapies, including trastuzumab. However, a high percentage of patients with HER2-positive tumors do not respond to trastuzumab (primary resistance) or either recur (acquired resistance), mostly due to molecular alterations in the tumor that are either unknown or undetermined in clinical practice. Those alterations may cause the tumor to be refractory to treatment with trastuzumab, promoting tumor proliferation and metastasis. Using continued exposure of a HER2-positive cell line to trastuzumab, we generated a model of acquired resistance characterized by increased expression …

0301 basic medicineMAPK/ERK pathwayCancer ResearchMAP Kinase Signaling SystemReceptor ErbB-2medicine.medical_treatmentMice NudeApoptosisBreast NeoplasmsCCL5Metastasis03 medical and health sciencesMice0302 clinical medicineBreast cancerAntineoplastic Agents ImmunologicalTrastuzumabmedicineBiomarkers TumorTumor Cells CulturedGene silencingAnimalsHumansskin and connective tissue diseasesAutocrine signallingneoplasmsChemokine CCL5Neoadjuvant therapyCell Proliferationbusiness.industryGene Expression ProfilingTrastuzumabmedicine.diseaseXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticAutocrine Communication030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchFemalebusinessmedicine.drugMolecular cancer therapeutics
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RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1 and TP53 pathways and regulatory miRs as therapeutic targets in hepatocellular carcinoma

2019

Introduction: Hepatocellular carcinoma (HCC) is a significant problem globally because of viral infections and the increasing incidence of obesity and fatty liver disease. However, it is difficult to treat because its inherent genetic heterogeneity results in activation of numerous signaling pathways. Kinases have been targeted for decades with varying results, but the development of therapeutic resistance is a major challenge. Areas covered: The key roles of the RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1, TP53 microRNAs (miRs) as therapeutic targets are discussed and we suggests novel approaches for targeting miRs or their downstream targets to combat HCC. We performed literature searches using…

0301 basic medicineMAPK/ERK pathwayCarcinoma HepatocellularHepatocellular carcinmamedicine.medical_treatmentClinical BiochemistryAntineoplastic AgentsmTORC1signal transduction inhibitorsTargeted therapy03 medical and health sciences0302 clinical medicineDrug DiscoverymicroRNAmedicinePTENAnimalsHumanscancerMolecular Targeted TherapyTP53HCCRAS/RAF/MEK/ERKProtein kinase BPI3K/AKT/mTOR pathwaymiRNAPharmacologybiologybusiness.industryKinaseLiver NeoplasmsMirhepatocellular carcinomatargeted therapyGene Expression Regulation NeoplasticMicroRNAssignal transduction inhibitor030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisbiology.proteinCancer researchMolecular MedicinePI3K/PTEN/AKTbusinessSignal Transduction
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Targeting Angiogenesis in Biliary Tract Cancers: An Open Option

2017

Abstract: Biliary tract cancers (BTCs) are characterized by a bad prognosis and the armamentarium of drugs for their treatment is very poor. Although the inflammatory status of biliary tract represents the first step in the cancerogenesis, the microenvironment also plays a key role in the pathogenesis of BTCs, promoting tumor angiogenesis, invasion and metastasis. Several molecules, such as vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF), are involved in the angiogenesis process and their expression on tumor samples has been explored as prognostic marker in both cholangiocarcinoma and gallbladder cancer. Recent studies evaluated the genomic landscape of BTCs and…

0301 basic medicineMAPK/ERK pathwayVascular Endothelial Growth Factor AAngiogenesisDrug Evaluation PreclinicalTyrosine kinase inhibitorAngiogenesis InhibitorsReviewFibroblast growth factorCatalysiMetastasisAntineoplastic Agentlcsh:Chemistrychemistry.chemical_compoundangiogenesis0302 clinical medicinetyrosine kinase inhibitorsMolecular Targeted Therapylcsh:QH301-705.5SpectroscopyClinical Trials as TopicMonoclonal antibodieNeovascularization Pathologicvascular endothelial growth factorComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineComputer Science ApplicationsVascular endothelial growth factorGene Expression Regulation NeoplasticAngiogenesiChemistryBiliary Tract NeoplasmsTreatment OutcomeBiliary Tract Neoplasm030220 oncology & carcinogenesismonoclonal antibodiesTyrosine kinaseAngiogenesis InhibitorHumanSignal TransductionProtein Kinase InhibitorAntineoplastic Agentsbiliary tract cancersBiologyModels BiologicalAngiogenesis; Biliary tract cancers; Monoclonal antibodies; Tyrosine kinase inhibitors; Vascular endothelial growth factor; Angiogenesis Inhibitors; Animals; Antineoplastic Agents; Biliary Tract Neoplasms; Clinical Trials as Topic; Drug Evaluation Preclinical; Gene Expression Regulation Neoplastic; Genetic Variation; Humans; Models Biological; Neovascularization Pathologic; Protein Kinase Inhibitors; Signal Transduction; Treatment Outcome; Vascular Endothelial Growth Factor A; Molecular Targeted Therapy; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications1707 Computer Vision and Pattern Recognition; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic ChemistryCatalysisInorganic Chemistry03 medical and health sciencesIn vivomedicineAnimalsHumansPhysical and Theoretical ChemistryGallbladder cancerMolecular BiologyProtein Kinase InhibitorsBiologyAnimalOrganic ChemistryGenetic Variationmedicine.disease030104 developmental biologychemistrylcsh:Biology (General)lcsh:QD1-999Immunologyangiogenesis; biliary tract cancers; monoclonal antibodies; tyrosine kinase inhibitors; vascular endothelial growth factorCancer researchBiliary tract cancerInternational Journal of Molecular Sciences
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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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Neutrophils restrain allergic airway inflammation by limiting ILC2 function and monocyte-dendritic cell antigen presentation

2019

Neutrophil mobilization, recruitment, and clearance must be tightly regulated as overexuberant neutrophilic inflammation is implicated in the pathology of chronic diseases, including asthma. Efforts to target neutrophils therapeutically have failed to consider their pleiotropic functions and the implications of disrupting fundamental regulatory pathways that govern their turnover during homeostasis and inflammation. Using the house dust mite (HDM) model of allergic airway disease, we demonstrate that neutrophil depletion unexpectedly resulted in exacerbated T helper 2 (TH2) inflammation, epithelial remodeling, and airway resistance. Mechanistically, this was attributable to a marked increas…

0301 basic medicineMONOCLONAL-ANTIBODYNeutrophilsmedicine.medical_treatmentImmunologyAntigen presentationINNATE LYMPHOID-CELLSInflammationG-CSFGranulocyteArticleMonocytesAllergic sensitizationDOUBLE-BLINDMice03 medical and health sciences0302 clinical medicineSPUTUMHypersensitivitymedicineAnimalsHumansLymphocytesInflammationAntigen PresentationMice Inbred BALB CScience & Technologybusiness.industryMonocyteInnate lymphoid cellDendritic CellsGeneral MedicineDendritic cellCOLONY-STIMULATING FACTORImmunity Innate3. Good health030104 developmental biologymedicine.anatomical_structureCytokineCXCR2 ANTAGONIST AZD5069030228 respiratory systemImmunologyT-CELLSFemalemedicine.symptombusinessLife Sciences & BiomedicineGRANULOCYTESEVERE ASTHMA
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Unfused Liver Segments: a Case Report of an Unknown Phenotype of the Conradi-Hünermann-Happle Syndrome

2016

Background: Since its description in 1957, Couinaud`s classification of the segmental organization of the liver has remained valid. However, recent investigations by 3-dimensional computed tomography suggest a significant variability of the vascular anatomy and segment volume. Here, we report a surprise finding during the laparoscopic cholecystectomy of a patient with Conradi-Hünermann-Happle syndrome, in whom the liver segments were not fused.
 Case report: Laparoscopic cholecystectomy was performed because of recurrent biliary pancreatitis in a 47 year-old male patient, who had been diagnosed with Conradi-Hünermann-Happle syndrome. Upon direct view, the liver parenchyma appeared norm…

0301 basic medicineMagnetic resonance cholangiopancreatographyPathologymedicine.medical_specialtymedicine.diagnostic_testbusiness.industryBile ductmedicine.medical_treatmentGastroenterologyGenetic disorderMagnetic resonance imagingmedicine.diseasePhenotype03 medical and health sciences030104 developmental biologymedicine.anatomical_structureMedicineCholecystectomyChondrodysplasia punctatabusinessLaparoscopyJournal of Gastrointestinal and Liver Diseases
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Initial serum thyroid peroxidase antibodies and long-term outcomes in SREAT.

2015

Objective To quantify clinical outcome in patients with steroid-responsive encephalopathy and associated autoimmune thyroiditis (SREAT) after the acute phase and explore potential associations of initial serum thyroid peroxidase antibody titers (TPO-Abs) with outcome. Materials and methods Retrospective chart review of patients diagnosed with SREAT between 01/2005 and 05/2014 in a tertiary care center and followed in an affiliated autoimmune outpatient clinic. Outcome was quantified using the extended Glasgow Outcome Scale (GOS-E). We calculated Pearson's correlation coefficients to quantify associations with clinical outcome at follow-up. Results Among 134 patients with encephalopathy of u…

0301 basic medicineMaleAnti-Inflammatory AgentsGlasgow Outcome Scaleblood [Iodide Peroxidase]0302 clinical medicineblood [Hashimoto Disease]blood [Encephalitis]Outpatient clinicHashimoto Diseasebiologytherapy [Hashimoto Disease]Glasgow Outcome Scaletherapy [Encephalitis]therapeutic use [Anti-Inflammatory Agents]General MedicineMiddle Agedblood [Thyroiditis Autoimmune]Magnetic Resonance Imagingtherapy [Thyroiditis Autoimmune]Treatment OutcomeNeurologyEncephalitisFemaleSteroidsImmunosuppressive AgentsAdultmedicine.medical_specialtyEncephalopathyHashimoto DiseaseIodide PeroxidaseAutoimmune thyroiditisanalysis [Autoantibodies]03 medical and health sciencesimmunology [Thyroiditis Autoimmune]Thyroid peroxidaseInternal medicinemedicineHumansddc:610immunology [Encephalitis]therapeutic use [Steroids]AgedAutoantibodiesRetrospective Studiesbusiness.industrytherapeutic use [Methotrexate]Thyroiditis AutoimmuneRetrospective cohort studymedicine.diseasetherapeutic use [Immunosuppressive Agents]immunology [Hashimoto Disease]030104 developmental biologyMethotrexateImmunologybiology.proteinEtiologyNeurology (clinical)businessimmunology [Iodide Peroxidase]030217 neurology & neurosurgeryFollow-Up StudiesActa neurologica Scandinavica
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Six year adalimumab efficacy in steroid-dependent Crohn's disease patients: A prospective single-center real life study.

2016

Abstract Background Adalimumab is effective in the treatment of Crohn's disease. We have already reported data on the efficacy of adalimumab in 110 steroid-dependent patients. At the end of the study 90 patients (64.5%) maintained clinical remission. Aims To assess efficacy and safety of adalimumab after 6 years in patients of the original cohort who responded to treatment. Methods The present study is an extension of the published paper on 90/110 patients. We report results on clinical remission and safety of 6 year maintenance therapy with adalimumab. Results Of the original cohort 90 patients completed the study, 17 were lost to follow-up and 3 died. At the end of follow-up (74.16 ± 10.3…

0301 basic medicineMaleAnti-Inflammatory AgentsKaplan-Meier EstimateSingle CenterInflammatory bowel diseaseInflammatory bowel disease0302 clinical medicineMaintenance therapyCrohn DiseaseLong term therapyProspective Studiesskin and connective tissue diseasesProspective cohort studyMultivariate AnalysiCrohn's diseaseRemission InductionGastroenterologyMiddle AgedCrohn's diseaseAnti-Inflammatory AgentTreatment OutcomeItalyCohort030211 gastroenterology & hepatologyFemaleSteroidsHumanmedicine.drugmusculoskeletal diseasesAdultmedicine.medical_specialtySteroid dependencyMaintenance Chemotherapy03 medical and health sciencesInternal medicinemedicineAdalimumabHumansAdverse effectSteroidHepatologybusiness.industryAdalimumabmedicine.diseaseSurgeryProspective Studie030104 developmental biologyMultivariate AnalysisbusinessDigestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
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