Search results for "Mutation."

showing 10 items of 2808 documents

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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Expanding the clinical spectrum of mosaic BRAF skin phenotypes

2021

BRAF postzygotic activating mutations have been found in 50% of cases of syringocystadenoma papilliferum (SCAP)1 and in phacomatosis pigmentokeratotica (PPK)2,3 , also possibly caused by HRAS4 mutations. BRAF is a RAS-activating serine/threonine kinase of the MAP kinase pathway, resulting in cell growth and proliferation. BRAF mutations, particularly p.(Val600Glu), are frequently identified in melanoma and other human cancers5 . We report clinical presentations of three patients with postzygotic BRAF mutations in affected skin, identified by next generation sequencing (NGS).

0301 basic medicineMAPK/ERK pathwayProto-Oncogene Proteins B-rafendocrine system diseases[SDV]Life Sciences [q-bio]DermatologyDNA sequencingSerine030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicinemedicineThreonineneoplasmsComputingMilieux_MISCELLANEOUSSkinKinasebusiness.industryMelanomamedicine.diseasePhenotypedigestive system diseases3. Good health030104 developmental biologyInfectious DiseasesPhenotypeMutationCancer researchbusinessSyringocystadenoma papilliferum
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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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De novo mutations in the X-linked TFE3 gene cause intellectual disability with pigmentary mosaicism and storage disorder-like features

2020

IntroductionPigmentary mosaicism (PM) manifests by pigmentation anomalies along Blaschko’s lines and represents a clue toward the molecular diagnosis of syndromic intellectual disability (ID). Together with new insights on the role for lysosomal signalling in embryonic stem cell differentiation, mutations in the X-linked transcription factor 3 (TFE3) have recently been reported in five patients. Functional analysis suggested these mutations to result in ectopic nuclear gain of functions.Materials and methodsSubsequent data sharing allowed the clustering of de novo TFE3 variants identified by exome sequencing on DNA extracted from leucocytes in patients referred for syndromic ID with or with…

0301 basic medicineMESH: Basic Helix-Loop-Helix Leucine Zipper Transcription Factors[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyIntellectual disabilityTFE3Biology[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsMESH: Intellectual Disability03 medical and health sciencesExon0302 clinical medicineMESH: Whole Exome SequencingMESH: ChildIntellectual disabilityGeneticsmedicineMissense mutationGeneGenetics (clinical)Exome sequencingPigmentary mosaicismMESH: Pathology MolecularGeneticsMESH: AdolescentMESH: HumansAlternative splicingLysosomal metabolismMESH: Child Preschool[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyMESH: Adultmedicine.diseasePhenotypeMESH: InfantMESH: MaleTFE3Storage disorder030104 developmental biologyMESH: Genes X-Linked[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMESH: Young AdultMESH: EpilepsyMESH: MosaicismMESH: Pigmentation DisordersMESH: Female030217 neurology & neurosurgery
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Further delineation of the clinical spectrum of de novo TRIM8 truncating mutations.

2018

IF 2.264; International audience; De novo mutations of the TRIM8 gene, which codes for a tripartite motif protein, have been identified using whole exome sequencing (WES) in two patients with epileptic encephalopathy (EE), but these reports were not sufficient to conclude that TRIM8 was a novel gene responsible for EE. Here we report four additional patients presenting with EE and de novo truncating mutations of TRIM8 detected by WES, and give further details of the patient previously reported by the Epi4K consortium. Epilepsy of variable severity was diagnosed in children aged 2 months to 3.5 years of age. All patients had developmental delay of variable severity with no or very limited la…

0301 basic medicineMaleAdolescentNerve Tissue ProteinsBioinformaticswhole exome sequencing03 medical and health sciencesEpilepsyTripartite MotifGeneticsmedicineHumansTRIM8Amino Acid SequenceChildGeneGenetics (clinical)De novo mutationsExome sequencingbusiness.industrynephrotic syndromeEpileptic encephalopathyInfant NewbornInfantmedicine.diseasePhenotype3. Good health030104 developmental biologyepileptic encephalopathy[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsChild PreschoolMutationFemalebusinessCarrier ProteinsNephrotic syndromeAmerican journal of medical genetics. Part A
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Molecular, clinical and neuropsychological study in 31 patients with Kabuki syndrome and KMT2D mutations

2017

IF 3.326; International audience; Kabuki syndrome (KS-OMIM 147920) is a rare developmental disease characterized by the association of multiple congenital anomalies and intellectual disability. This study aimed to investigate intellectual performance in children with KS and link the performance to several clinical features and molecular data. We recruited 31 children with KMT2D mutations who were 6 to 16 years old. They all completed the Weschler Intelligence Scale for Children, fourth edition. We calculated all indexes: the Full Scale Intellectual Quotient (FSIQ), Verbal Comprehension Index (VCI), Perceptive Reasoning Index (PRI), Processing Speed Index (PSI), and Working Memory Index (WMI…

0301 basic medicineMaleAdolescentVisual impairmentDNA Mutational AnalysisIntelligenceneuropsychologyDisease[SDV.GEN] Life Sciences [q-bio]/GeneticsNeuropsychological Testsgenotype-phenotype correlation03 medical and health sciencesIntensive careIntellectual disabilityGene OrderGeneticsmedicineHumansAbnormalities MultipleChildKMT2D mutationGenetics (clinical)AllelesGenetic Association Studies[SDV.GEN]Life Sciences [q-bio]/GeneticsKabuki syndromebusiness.industryWorking memoryNeuropsychologyWechsler Adult Intelligence Scalemedicine.diseaseHematologic Diseases3. Good healthNeoplasm ProteinsDNA-Binding Proteins030104 developmental biologyPhenotypeVestibular DiseasesGenetic LociFaceMutationFemalemedicine.symptombusinessKabuki syndromeClinical psychology
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Threshold Effects of Circulating Angiopoietin-Like 3 Levels on Plasma Lipoproteins.

2017

Abstract Context Angiopoietin-like 3 (ANGPTL3) deficiency in plasma due to loss-of-function gene mutations results in familial combined hypobetalipoproteinemia type 2 (FHBL2) in homozygotes. However, the lipid phenotype in heterozygotes is much milder and does not appear to relate directly to ANGPTL3 levels. Furthermore, the low-density lipoprotein (LDL) phenotype in carriers of ANGPTL3 mutations is unexplained. Objective To determine whether reduction below a critical threshold in plasma ANGPTL3 levels is a determinant of lipoprotein metabolism in FHBL2, and to determine whether proprotein convertase subtilisin kexin type 9 (PCSK9) is involved in determining low LDL levels in this conditio…

0301 basic medicineMaleApolipoprotein BEndocrinology Diabetes and MetabolismClinical BiochemistryBiochemistryLipoprotein particlePCSK9Cohort StudiesHypobetalipoproteinemiaschemistry.chemical_compoundEndocrinologyANGPTL3biologyChemistryMiddle AgedPedigreeLipoproteins LDLPhenotypeKexinlipids (amino acids peptides and proteins)FemaleANGPTL3; familial combined hypolipidemia; PCSK9Lipoproteins HDLAdultmedicine.medical_specialtyHeterozygoteBlotting Western03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseClinical Research ArticlesAgedAngiopoietin-Like Protein 3Apolipoproteins BCholesterolPCSK9Biochemistry (medical)medicine.disease030104 developmental biologyEndocrinologyAngiopoietin-like ProteinsLDL receptorMultivariate AnalysisMutationbiology.proteinLinear Modelsfamilial combined hypobetalipoproteinemiaHypobetalipoproteinemiaAngiopoietinsLipoprotein
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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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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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