Search results for "Hedgehog Proteins"

showing 10 items of 31 documents

Ligand-dependent Hedgehog pathway activation in Rhabdomyosarcoma : the oncogenic role of the ligands

2017

Altres ajuts: This work was supported by grants from Institut Català d'Oncologia (ICO), Instituto de Salud Carlos III (RTICC-RD12/0036/0016, /0020, /0035, /0057; and PI14/00647), Fundació A BOSCH, Fundació Amics Joan Petit, ajuts predoctorals del VHIR and RIS3CAT grants COMRDI15-1-0014 (ACCIÓ and FEDER). Altres ajuts: FEDER/COMRDI15-1-0014 Rhabdomyosarcoma (RMS) is the most common type of soft tissue sarcoma in children. The Hedgehog (HH) pathway is known to develop an oncogenic role in RMS. However, the molecular mechanism that drives activation of the pathway in RMS is not well understood. The expression of HH ligands was studied by qPCR, western blot and immunohistochemistry. Functional …

0301 basic medicineCancer ResearchsarcomaCarcinogenesisVismodegibRhabdomyosarcoma; Hedgehog; vismodegib; UPR; TRIB3; sarcoma; cancerVismodegib610ApoptosisMice SCIDUPRLigandsMice03 medical and health sciences0302 clinical medicineCell MovementvismodegibRhabdomyosarcomaTumor Cells CulturedmedicinecancerAnimalsHumansHedgehog ProteinsAutocrine signallingRhabdomyosarcomaHedgehogCell ProliferationCancerChemistryTRIB3Sarcomamedicine.diseaseXenograft Model Antitumor AssaysHedgehog signaling pathway3. Good health030104 developmental biologyOncology030220 oncology & carcinogenesisUnfolded protein responseCancer researchFemaleSignal transductionTranslational TherapeuticsSmoothenedHedgehogSignal TransductionTranscription Factorsmedicine.drug
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Opposing Effects of CREBBP Mutations Govern the Phenotype of Rubinstein-Taybi Syndrome and Adult SHH Medulloblastoma

2018

Recurrent mutations in chromatin modifiers are specifically prevalent in adolescent or adult patients with Sonic hedgehog-associated medulloblastoma (SHH MB). Here, we report that mutations in the acetyltransferase CREBBP have opposing effects during the development of the cerebellum, the primary site of origin of SHH MB. Our data reveal that loss of Crebbp in cerebellar granule neuron progenitors (GNPs) during embryonic development of mice compromises GNP development, in part by downregulation of brain-derived neurotrophic factor (Bdnf). Interestingly, concomitant cerebellar hypoplasia was also observed in patients with Rubinstein-Taybi syndrome, a congenital disorder caused by germline mu…

0301 basic medicineCerebellumCrebbp protein mousemetabolism [Cerebellar Neoplasms]acetyltransferase; cerebellum; CREBBP; development; Rubinstein-Taybi syndrome; SHH medulloblastomagenetics [Hedgehog Proteins]MiceNeurotrophic factorsmetabolism [CREB-Binding Protein]Mice KnockoutNeuronsRubinstein-Taybi Syndromepathology [Rubinstein-Taybi Syndrome]CREBBPCREB-Binding ProteinPhenotypegenetics [CREB-Binding Protein]3. Good healthpathology [Cerebellar Neoplasms]acetyltransferasePhenotypemedicine.anatomical_structuregenetics [Rubinstein-Taybi Syndrome]Femalemetabolism [Hedgehog Proteins]Signal TransductionSHH medulloblastomaAdultcerebellumBiologyGeneral Biochemistry Genetics and Molecular BiologyCREBBP; Rubinstein-Taybi syndrome; SHH medulloblastoma; acetyltransferase; cerebellum; development.03 medical and health sciencesGermline mutationAcetyltransferasesmetabolism [Medulloblastoma]medicineAnimalsHumansgenetics [Cerebellar Neoplasms]Hedgehog Proteinsddc:610Cerebellar NeoplasmsdevelopmentMolecular BiologyMedulloblastomaRubinstein–Taybi syndromegenetics [Medulloblastoma]metabolism [Rubinstein-Taybi Syndrome]pathology [Medulloblastoma]Cell Biologymedicine.disease030104 developmental biologyMutationphysiology [CREB-Binding Protein]Cancer researchSHH protein humanCerebellar hypoplasia (non-human)metabolism [Acetyltransferases]CREBBP protein humanMedulloblastomaDevelopmental BiologyCongenital disorderDevelopmental Cell
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The emergence of drug resistance to targeted cancer therapies: Clinical evidence.

2019

For many decades classical anti-tumor therapies included chemotherapy, radiation and surgery; however, in the last two decades, following the identification of the genomic drivers and main hallmarks of cancer, the introduction of therapies that target specific tumor-promoting oncogenic or non-oncogenic pathways, has revolutionized cancer therapeutics. Despite the significant progress in cancer therapy, clinical oncologists are often facing the primary impediment of anticancer drug resistance, as many cancer patients display either intrinsic chemoresistance from the very beginning of the therapy or after initial responses and upon repeated drug treatment cycles, acquired drug resistance deve…

0301 basic medicineDrugCancer Researchmedicine.drug_classmedicine.medical_treatmentmedia_common.quotation_subjectTranslational researchApoptosisDrug resistanceMonoclonal antibodyBioinformatics03 medical and health sciences0302 clinical medicineNeoplasmsmedicineHumansPharmacology (medical)Hedgehog ProteinsEpigeneticsProtein Kinase Inhibitorsmedia_commonPharmacologyChemotherapybusiness.industryCancerImmunotherapyProtein-Tyrosine Kinasesmedicine.disease030104 developmental biologyInfectious DiseasesOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisbusinessProteasome InhibitorsDrug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy
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Microparticles harbouring Sonic hedgehog morphogen improve the vasculogenesis capacity of endothelial progenitor cells derived from myocardial infarc…

2019

Aims Endothelial progenitor cells (EPC) play a role in endothelium integrity maintenance and regeneration. Decreased numbers of EPC or their impaired function correlates with an increase in cardiovascular events. Thus, EPC are important predictors of cardiovascular mortality and morbidity. Microparticles carrying Sonic hedgehog (Shh) morphogen (MPShh+) trigger pro-angiogenic responses, both in endothelial cells and in ischaemic rodent models. Here, we propose that MPShh+ regulates EPC function, thus enhancing vasculogenesis, and correcting the defects in dysfunctional EPC obtained from acute myocardial infarction (AMI) patients. Methods and results The mechanisms underlying Shh pathway func…

0301 basic medicineEndotheliumNitric Oxide Synthase Type IIIPhysiologyAngiogenesis[SDV]Life Sciences [q-bio]Myocardial InfarctionMice NudeNeovascularization PhysiologicAcute myocardial infarction030204 cardiovascular system & hematologyMicroparticlesZinc Finger Protein GLI103 medical and health sciences0302 clinical medicineVasculogenesisCell-Derived MicroparticlesPhysiology (medical)Paracrine CommunicationVasculogenesismedicineAnimalsHumansHedgehog ProteinsProgenitor cellSonic hedgehogAngiogenic ProteinsCells CulturedComputingMilieux_MISCELLANEOUSEndothelial progenitor cellsbiologybusiness.industryNitric oxideSmoothened ReceptorHedgehog signaling pathwayPatched-1 ReceptorVascular endothelial growth factor A030104 developmental biologymedicine.anatomical_structureCase-Control StudiesKLF2embryonic structuresCancer researchbiology.proteincardiovascular systemCardiology and Cardiovascular MedicinebusinessSignal Transductioncirculatory and respiratory physiology
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Effects of mutations in Wnt/β-catenin, hedgehog, Notch and PI3K pathways on GSK-3 activity—Diverse effects on cell growth, metabolism and cancer

2016

Glycogen synthase kinase-3 (GSK-3) is a serine/threonine kinase that participates in an array of critical cellular processes. GSK-3 was first characterized as an enzyme that phosphorylated and inactivated glycogen synthase. However, subsequent studies have revealed that this moon-lighting protein is involved in numerous signaling pathways that regulate not only metabolism but also have roles in: apoptosis, cell cycle progression, cell renewal, differentiation, embryogenesis, migration, regulation of gene transcription, stem cell biology and survival. In this review, we will discuss the roles that GSK-3 plays in various diseases as well as how this pivotal kinase interacts with multiple sign…

0301 basic medicineMAPK/ERK pathwaySettore MED/06 - Oncologia MedicaCellular differentiationPI3KTargeted therapyGlycogen Synthase Kinase 3Phosphatidylinositol 3-Kinases0302 clinical medicineGSK-3Neoplasmsbeta CateninGSK-3biologyReceptors NotchKinaseWnt signaling pathwayWnt/beta-cateninCell DifferentiationCell biologyGene Expression Regulation Neoplastic030220 oncology & carcinogenesismTORAkt; GSK-3; Hedgehog; Notch; PI3K; Targeted therapy; Therapy resistance; Wnt/beta-catenin; mTORSignal TransductionBeta-cateninNotchAkt GSK-3 Hedgehog mTOR Notch PI3K Targeted therapy Therapy resistance Wnt/beta-cateninCell Survivalmacromolecular substancesNO03 medical and health sciencesAkt; GSK-3 Hedgehog Notch PI3K Targeted therapy Therapy resistance Wnt/beta-catenin mTORAnimalsHumansHedgehog ProteinsProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayCell ProliferationAktTherapy resistanceAkt; GSK-3; Hedgehog; mTOR; Notch; PI3K; Targeted therapy; Therapy resistance; Wnt/beta-catenin; Molecular Biology; Cell BiologyCell BiologyWnt ProteinsMicroRNAs030104 developmental biologyMutationCancer researchbiology.proteinTumor Suppressor Protein p53Hedgehog
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Pivotal roles of glycogen synthase-3 in hepatocellular carcinoma

2017

Hepatocellular carcinoma (HCC) is one of the most common cancers in the world, and represents the second most frequently cancer and third most common cause of death from cancer worldwide. At advanced stage, HCC is a highly aggressive tumor with a poor prognosis and with very limited response to common therapies. Therefore, there is still the need for new effective and well-tolerated therapeutic strategies. Molecular-targeted therapies hold promise for HCC treatment. One promising molecular target is the multifunctional serine/threonine kinase glycogen synthase kinase 3 (GSK-3). The roles of GSK-3β in HCC remain controversial, several studies suggested a possible role of GSK-3β as a tumor …

0301 basic medicinePathologymedicine.medical_specialtyCancer ResearchCarcinoma HepatocellularEpithelial-Mesenchymal TransitionTumor suppressor geneAntineoplastic Agentsmacromolecular substancesBiologyMetastasisGlycogen Synthase Kinase 303 medical and health sciencesWnt0302 clinical medicineGeneticTransforming Growth Factor betaGSK-3GeneticsmedicineHumansHedgehog ProteinsMolecular Targeted TherapyInsulin-Like Growth Factor IHCCIGFβ-cateninGlycogen synthaseHedgehogMolecular Biologybeta CateninGSK-3Glycogen Synthase Kinase 3 betaReceptors NotchLiver NeoplasmsWnt signaling pathwayCancermedicine.diseaseSurvival Analysisdigestive system diseasesGene Expression Regulation Neoplastic030104 developmental biology030220 oncology & carcinogenesisHepatocellular carcinomabiology.proteinCancer researchMolecular MedicineHedgehogSignal Transduction
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ceRNA Network Regulation of TGF-β, WNT, FOXO, Hedgehog Pathways in the Pharynx of Ciona robusta

2021

The transforming growth factor-β (TGF-β) family of cytokines performs a multifunctional signaling, which is integrated and coordinated in a signaling network that involves other pathways, such as Wintless, Forkhead box-O (FOXO) and Hedgehog and regulates pivotal functions related to cell fate in all tissues. In the hematopoietic system, TGF-β signaling controls a wide spectrum of biological processes, from immune system homeostasis to the quiescence and self-renewal of hematopoietic stem cells (HSCs). Recently an important role in post-transcription regulation has been attributed to two type of ncRNAs: microRNAs and pseudogenes. Ciona robusta, due to its philogenetic position close to verte…

0301 basic medicineascidianpseudogenepseudogeneslcsh:ChemistryTransforming Growth Factor betaProtein Interaction MappingHomeostasisRNA-Seqlcsh:QH301-705.53' Untranslated RegionsSpectroscopyTissue homeostasisForkhead Box Protein O1Wnt signaling pathwayHigh-Throughput Nucleotide Sequencingvirus diseasesGeneral Medicinefemale genital diseases and pregnancy complicationsComputer Science ApplicationsCell biologyNGSStem cellTGF-βCell fate determinationBiologyCatalysisArticleInorganic ChemistryWNT03 medical and health sciencesmicroRNAAnimalsCell LineageHedgehog ProteinsTGF-Physical and Theoretical ChemistryMolecular BiologyHedgehogneoplasmsmiRNA030102 biochemistry & molecular biologyCompeting endogenous RNAOrganic ChemistryfungiComputational BiologyHematopoiesisWnt ProteinsMicroRNAs030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Gene Expression RegulationImmune SystemPharynxFOXOCionaTransforming growth factorInternational Journal of Molecular Sciences
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TCTN3 Mutations Cause Mohr-Majewski Syndrome

2012

Orofaciodigital syndromes (OFDSs) consist of a group of heterogeneous disorders characterized by abnormalities in the oral cavity, face, and digits and associated phenotypic abnormalities that lead to the delineation of 13 OFDS subtypes. Here, by a combined approach of homozygozity mapping and exome ciliary sequencing, we identified truncating TCTN3 mutations as the cause of an extreme form of OFD associated with bone dysplasia, tibial defect, cystic kidneys, and brain anomalies (OFD IV, Mohr-Majewski syndrome). Analysis of 184 individuals with various ciliopathies (OFD, Meckel, Joubert, and short rib polydactyly syndromes) led us to identify four additional truncating TCTN3 mutations in un…

AdolescentFoot Deformities CongenitalMolecular Sequence DataCiliopathiesJoubert syndromeYoung AdultFetusReportCerebellumGLI3medicineGeneticsHumansExomeHedgehog ProteinsGenetics(clinical)Sonic hedgehogChildExomeGenetics (clinical)Adaptor Proteins Signal TransducingCystic kidneyGeneticsBase SequencebiologyHomozygoteIntracellular Signaling Peptides and ProteinsMembrane ProteinsCiliary transition zoneSequence Analysis DNAOrofaciodigital Syndromesmedicine.diseaseCleft PalateCiliopathyPhenotypeMutationbiology.proteinApoptosis Regulatory ProteinsHand Deformities CongenitalSignal TransductionThe American Journal of Human Genetics
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Cemiplimab in locally advanced basal cell carcinoma after hedgehog inhibitor therapy: an open-label, multi-centre, single-arm, phase 2 trial.

2021

Summary Background Before February, 2021, there was no standard treatment regimen for locally advanced basal cell carcinoma after first-line hedgehog inhibitor (HHI) therapy. Cemiplimab, a PD-1 antibody, is approved for treatment of advanced cutaneous squamous cell carcinoma and has shown clinical activity as monotherapy in first-line non-small-cell lung cancer. Here, we present the primary analysis data of cemiplimab in patients with locally advanced basal cell carcinoma after HHI therapy. Methods We did an open-label, multicentre, single-arm, phase 2 trial across 38 outpatient clinics, primarily at academic medical centres, in Canada, Europe, and the USA. Eligible patients (aged ≥18 years…

AdultMalemedicine.medical_specialtySkin NeoplasmsPyridinesProgrammed Cell Death 1 ReceptorVismodegibAntibodies Monoclonal Humanized030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicineInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineCarcinomaClinical endpointOutpatient clinicHumansBasal cell carcinomaAnilidesHedgehog ProteinsLung cancerImmune Checkpoint InhibitorsAgedbusiness.industryStandard treatmentMiddle Agedmedicine.diseaseRegimenOncologyCarcinoma Basal CellDrug Resistance Neoplasm030220 oncology & carcinogenesisFemaleNeoplasm Recurrence LocalSettore MED/35 - MALATTIE CUTANEE E VENEREEbusinessmedicine.drugThe Lancet. Oncology
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Long‐term efficacy and safety of sonidegib in patients with advanced basal cell carcinoma: 42‐month analysis of the phase II randomized, double‐blind…

2019

Background: Basal cell carcinomas (BCCs) exhibit aberrant activation of the hedgehog pathway. Sonidegib is a hedgehog pathway inhibitor approved for the treatment of locally advanced BCC (laBCC) and metastatic BCC (mBCC) based on primary results of the BOLT study [Basal Cell Carcinoma Outcomes with LDE225 (sonidegib) Treatment]. Objectives: This is the final 42-month analysis of the BOLT study, evaluating the efficacy and safety of sonidegib. Methods: Adults with no prior hedgehog pathway inhibitor therapy were randomized in a 1 : 2 ratio to sonidegib 200 mg or 800 mg once daily. Treatment continued for up to 42 months or until disease progression, unacceptable toxicity, death, study termin…

AdultOncologymedicine.medical_specialtySkin NeoplasmsPyridinesmedicine.medical_treatmentAntineoplastic AgentsDermatologySonidegiblaw.invention030207 dermatology & venereal diseases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRandomized controlled triallawInternal medicinemedicineCarcinomaHumansHedgehog ProteinsBasal cell carcinomaAdverse effectbusiness.industryBiphenyl Compoundsmedicine.diseaseRadiation therapyClinical trialBiphenyl compoundchemistryCarcinoma Basal CellbusinessBritish Journal of Dermatology
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