Search results for "MUTATION"

showing 10 items of 2830 documents

Clinical, immunological, and molecular analysis in a large cohort of patients with X-linked agammaglobulinemia: an Italian multicenter study

2002

A questionnaire-based retrospective clinical and immunological survey was conducted in 73 males with a definite diagnosis of X-linked agammaglobulinemia based on BTK sequence analysis. Forty-four were sporadic and 29 familial cases. At December 2000, the patients' ages ranged from 2 to 33 years; mean age at diagnosis and mean duration of follow-up were 3.5 and 10 years respectively. After the mid-1980s all but 2 were on intravenous immunoglobulin (IVIG) substitution therapy, with residual IgG >500 mg/dl in 94% of the patients at the time of enrollment. Respiratory infections were the most frequent manifestation both prior to diagnosis and over follow-up. Chronic lung disease (CLD) was prese…

Lung DiseasesAdultMalePediatricsmedicine.medical_specialtyGenetic Linkage; Agammaglobulinemia; Humans; Infant Newborn; Protein-Tyrosine Kinases; Child; Child Preschool; X Chromosome; Immunoglobulins Intravenous; Lung Diseases; Adult; Cohort Studies; Chronic Disease; Follow-Up Studies; Adolescent; Mutation; Maleclinical featuresX ChromosomeX-linked agammaglobulinemiaAdolescentGenetic LinkageImmunologyX-linked agammaglobulinemiaImmunoglobulinsX-linked agammaglobulinemia; infections; intravenous immunoglobulin; BTK mutationSepsisCohort StudiesAgammaglobulinemiaImmunopathologyintravenous immunoglobulinEpidemiologymedicineAgammaglobulinaemia Tyrosine KinaseImmunology and AllergyHumansinfectionsChildPreschoolSettore MED/38 - Pediatria Generale e SpecialisticaBTK mutationsbusiness.industryChronic sinusitisInfant NewbornMeningoencephalitisImmunoglobulins IntravenousInfantProtein-Tyrosine Kinasesmedicine.diseaseNewbornBTK mutationagammaglobulinemia; clinical features; BTK mutationsChild PreschoolChronic DiseaseMutationbusinessIntravenousMeningitisCohort studyFollow-Up Studies
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Congenital emphysematous lung disease associated with a novel Filamin A mutation. Case report and literature review

2019

Abstract Background Progressive lung involvement in Filamin A (FLNA)-related cerebral periventricular nodular heterotopia (PVNH) has been reported in a limited number of cases. Case presentation We report a new pathogenic FLNA gene variant (c.7391_7403del; p.Val2464Alafs*5) in a male infant who developed progressive lung disease with emphysematous lesions and interstitial involvement. Following lobar resection, chronic respiratory failure ensued necessitating continuous mechanical ventilation and tracheostomy. Cerebral periventricular nodular heterotopia was also present. Conclusions We report a novel variant of the FLNA gene, associated with a severe lung disorder and PNVH. The lung disord…

Lung DiseasesMalePathologymedicine.medical_specialtyFilaminsmedicine.medical_treatmentChildren; Congenital enphysema; Filamin a; Lung disease; Periventricular nodular heterotopiaCase ReportFilaminKeywords: Filamin a Congenital enphysema Lung disease Children Periventricular nodular heterotopiaFilamin aLung Disorder03 medical and health sciences0302 clinical medicineNeuroimagingLoss of Function Mutation030225 pediatricsmedicineHumansFLNA030212 general & internal medicineLungChildrenCongenital enphysemaGenetic testingMechanical ventilationLungmedicine.diagnostic_testbusiness.industrylcsh:RJ1-570BrainInfantlcsh:Pediatricsrespiratory systemRespiration ArtificialPeriventricular nodular heterotopiamedicine.anatomical_structurePulmonary EmphysemaRespiratory failureLung diseasePediatrics Perinatology and Child HealthRadiography ThoracicRespiratory InsufficiencyTomography X-Ray ComputedbusinessBMC Pediatrics
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Driver mutations and differential sensitivity to targeted therapies: a new approach to the treatment of lung adenocarcinoma

2010

The adenocarcinoma of the lung has recently shown peculiar molecular characteristics, which relate with both carcinogenesis and response to targeted drugs. Several molecular alterations have been defined as "driver mutations". These are responsible for both the initiation and maintenance of the malignancy. The epidermal growth factor receptor (EGFR) pathway is the main regulator of cell function and cancer development. It has a widely defined role in the occurrence of driver mutations. Up till now EGFR gene mutations, KRAS gene mutations and EML4-ALK fusion genes are the most widely recognized alterations involved in both the biology and the clinical management of lung adenocarcinoma. In th…

Lung NeoplasmsOncogene Proteins FusionSettore MED/06 - Oncologia MedicaEGFRGene ExpressionAdenocarcinomaGene mutationmedicine.disease_causeProto-Oncogene Proteins p21(ras)Phosphatidylinositol 3-KinasesPredictive Value of TestsProto-Oncogene ProteinsAntineoplastic Combined Chemotherapy ProtocolsmedicineAdenocarcinoma of the lungHumansRadiology Nuclear Medicine and imagingMolecular Targeted TherapyEpidermal growth factor receptorTyrosine kinase inhibitorsMutationbiologybusiness.industryDriver mutationGeneral MedicineProtein-Tyrosine KinasesPrognosismedicine.diseaseErbB ReceptorsTreatment OutcomeOncologyMutationImmunologyras ProteinsCancer researchbiology.proteinAdenocarcinomaKRASCarcinogenesisbusinessTyrosine kinaseAlgorithmsCancer Treatment Reviews
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Novel therapeutic strategies for patients with NSCLC that do not respond to treatment with EGFR inhibitors

2014

Abstract: Introduction: Treatment with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) yields tumour responses in non-small cell lung cancer (NSCLC) patients harbouring activating EGFR mutations. However, even in long-lasting responses, resistance to EGFR TKIs invariably occurs. Areas covered: This review examines resistance mechanisms to EGFR TKI treatment, which mainly arise from secondary EGFR mutations. Other resistance-inducing processes include mesenchymal-epithelial transition factor (MET) amplification, epithelial-mesenchymal transformation, phenotypic change from NSCLC to small-cell lung carcinoma, and modifications in parallel signalling pathways. Current…

Lung NeoplasmsSettore MED/06 - Oncologia MedicaAfatinibNovel therapeutic strategiesLapatinibmedicine.disease_causeNSCLCT790Mchemistry.chemical_compoundErbB ReceptorsCarcinoma Non-Small-Cell LungAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsHumansRadiology Nuclear Medicine and imagingEpidermal growth factor receptorProtein Kinase InhibitorsEGFR inhibitorsbiologybusiness.industryEGFR mutations; TKI inhibitors resistance; NSCLC; New drugs; Novel therapeutic strategiesGeneral MedicineNew drugEGFR mutationsCombined Modality TherapyDacomitinibrespiratory tract diseasesErbB ReceptorsNew drugsOncologychemistryDrug Resistance NeoplasmCancer researchbiology.proteinKRASHuman medicineEGFR mutationbusinessmedicine.drugTKI inhibitors resistanceCancer Treatment Reviews
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Loss of p53 Attenuates the Contribution of IL-6 Deletion on Suppressed Tumor Progression and Extended Survival in Kras-Driven Murine Lung Cancer

2013

Interleukin-6 (IL-6) is involved in lung cancer tumorigenesis, tumor progression, metastasis, and drug resistance. Previous studies show that blockade of IL-6 signaling can inhibit tumor growth and increase drug sensitivity in mouse models. Clinical trials in non-small cell lung cancer (NSCLC) reveal that IL-6 targeted therapy relieves NSCLC-related anemia and cachexia, although other clinical effects require further study. We crossed IL-6(-/-) mice with Kras(G12D) mutant mice, which develop lung tumors after activation of mutant Kras(G12D), to investigate whether IL-6 inhibition contributes to tumor progression and survival time in vivo. Kras(G12D); IL-6(-/-) mice exhibited increased tumor…

Lung Neoplasmsmedicine.medical_treatmentlcsh:Medicinemedicine.disease_causeMetastasisTargeted therapyMice0302 clinical medicineCarcinoma Non-Small-Cell LungNeoplasm MetastasisPhosphorylationlcsh:Science0303 health sciencesMultidisciplinary3. Good healthGene Expression Regulation Neoplastic030220 oncology & carcinogenesisDisease ProgressionKRASResearch ArticleSignal TransductionSTAT3 Transcription FactorMice TransgenicBiologyProto-Oncogene Proteins p21(ras)03 medical and health sciencesFLOXmedicineAnimalsHumansLung cancerneoplasms030304 developmental biologyChemokine CCL20Interleukin-6Tumor Necrosis Factor-alphalcsh:RCancermedicine.diseaseSurvival Analysisdigestive system diseasesrespiratory tract diseasesDisease Models AnimalTumor progressionMutationCancer researchChemokine CCL19lcsh:QTumor Suppressor Protein p53CarcinogenesisPLoS ONE
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Cell of origin markers identify different prognostic subgroups of lung adenocarcinoma

2018

Strong prognostic markers able to stratify lung adenocarcinoma (ADC) patients are lacking. We evaluated whether a six-immunohistochemical markers panel (TTF1, SP-A, Napsin A, MUC5AC, CDX2 and CK5), defining the putative neoplastic “cell of origin,” allows to identify prognostic subgroups among lung ADC. We screened a large cohort of ADC specimens (2003–2013) from Torino Institutional Repository identifying: (i) marker positivity by immunohistochemistry, (ii) main morphological appearance by light microscopy, (iii) presence of “hotspot” mutations of candidate genes by Sequenom technology. To evaluate possible predictors of survival and time to recurrence, uni- and multivariable-adjusted comp…

Lung adenocarcinomaMorphologyAdultMale0301 basic medicineOncologyBiomarkers; Genetic mutations; Immunohistochemistry; Lung adenocarcinoma; Morphology; Survival analysisPathologymedicine.medical_specialtyCandidate geneCell of originsix-immunohistochemical markers panel (TTF1 SP-A Napsin A MUC5AC CDX2 and CK5)Adenocarcinoma of LungKaplan-Meier Estimategenetic mutationsGene mutationBiologymedicine.disease_causeadenocarcinoma (ADC)survival analysisPathology and Forensic Medicine03 medical and health sciences0302 clinical medicineInternal medicinemorphologyBiomarkers TumormedicineHumansCDX2Survival analysisAgedbiomarkers; genetic mutations; immunohistochemistry; lung adenocarcinoma; morphology; survival analysisbiomarkersSurvival analysisMiddle Agedrespiratory systemPrognosislung adenocarcinomamedicine.diseaseImmunohistochemistryGenetic mutations030104 developmental biology030220 oncology & carcinogenesisimmunohistochemistryAdenocarcinomaImmunohistochemistryFemaleKRASBiomarkersHuman Pathology
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BRAFV600E mutation, TIMP-1 upregulation, and NF-κB activation: closing the loop on the papillary thyroid cancer trilogy.

2011

BRAFV600E is the most common mutation found in papillary thyroid carcinoma (PTC). Tissue inhibitor of metalloproteinases (TIMP-1) and nuclear factor (NF)-κB have been shown to play an important role in thyroid cancer. In particular, TIMP-1 binds its receptor CD63 on cell surface membrane and activates Akt signaling pathway, which is eventually responsible for its anti-apoptotic activity. The aim of our study was to evaluate whether interplay among these three factors exists and exerts a functional role in PTCs. To this purpose, 56 PTC specimens were analyzed for BRAFV600E mutation, TIMP-1 expression, and NF-κB activation. We found that BRAFV600E mutation occurs selectively in PTC nodules an…

MAPK/ERK pathwayAdultMaleProto-Oncogene Proteins B-rafCancer Researchmedicine.medical_specialtyendocrine system diseasesEndocrinology Diabetes and MetabolismThyroid cancer TIMP-1 papillary thyroid cancerMutation MissenseGlutamic AcidGene Expression Regulation EnzymologicSettore MED/13 - EndocrinologiaPapillary thyroid cancerEndocrinologyDownregulation and upregulationInternal medicinemedicineTumor Cells CulturedGene silencingHumansGene Regulatory NetworksNeoplasm InvasivenessThyroid NeoplasmsProtein kinase BThyroid cancerTissue Inhibitor of Metalloproteinase-1ChemistryAkt/PKB signaling pathwayCarcinomaNF-kappa BValineMiddle Agedmedicine.diseaseCarcinoma PapillaryUp-RegulationGene Expression Regulation NeoplasticEndocrinologyCell Transformation NeoplasticOncologyAmino Acid SubstitutionThyroid Cancer PapillaryCancer researchDisease ProgressionFemaleV600ESignal TransductionEndocrine-related cancer
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Emerging MEK inhibitors

2010

IMPORTANCE OF THE FIELD: The Ras/Raf/MEK/ERK pathway is often activated by genetic alterations in upstream signaling molecules. Integral components of this pathway such as Ras and B-Raf are also activated by mutation. The Ras/Raf/MEK/ERK pathway has profound effects on proliferative, apoptotic and differentiation pathways. This pathway can often be effectively silenced by MEK inhibitors. AREAS COVERED BY THIS REVIEW: This review will discuss targeting of MEK which could lead to novel methods to control abnormal proliferation which arises in cancer and other proliferative diseases. This review will cover the scientific literature from 1980 to present and is a follow on from a review which fo…

MAPK/ERK pathwayCell signalingAntineoplastic Agentsmedicine.disease_causemekerkEnzyme activatorNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsHumansPharmacology (medical)Protein phosphorylationProtein Kinase InhibitorsMEK inhibitorsCell ProliferationCancerPharmacologyapoptosis; cancer; erk; kinases; mek; mek inhibitors; proliferative disorders; protein phosphorylation; signal transductionproliferative disordersMutationKinasebusiness.industryapoptosisApoptosiCancerDrugs InvestigationalMAP Kinase Kinase Kinasesmedicine.diseaseprotein phosphorylationCell biologyEnzyme ActivationTreatment OutcomekinasesChemotherapy AdjuvantRadiotherapy AdjuvantSignal transductionbusinesssignal transductionExpert Opinion on Emerging Drugs
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Coupling of endothelin receptors to the ERK/MAP kinase pathway. Roles of palmitoylation and G(alpha)q.

2001

Endothelins are potent mitogens that stimulate extracellular signal-regulated kinases (ERK/MAP kinases) through their cognate G-protein-coupled receptors, ET(A) and ET(B). To address the role of post-translational ET receptor modifications such as acylation on ERK activation and to identify relevant downstream effectors coupling the ET receptor to the ERK signaling cascades we have constructed a panel of palmitoylation-deficient ET receptor mutants with differential G(alpha) protein binding capacity. Endothelin-1 stimulation of wild-type ET(A) or ET(B) induced a fivefold to sixfold increase in ERK in COS-7 and CHO cells whereas full-length nonpalmitoylated ET(A) and ET(B) mutants failed to …

MAPK/ERK pathwayGs alpha subunitInsectaMAP Kinase Signaling SystemBlotting WesternMolecular Sequence DataPalmitic AcidSRC Family Tyrosine KinaseBiochemistryCell LineCricetinaeArrestinTumor Cells CulturedAnimalsHumansAmino Acid SequenceReceptorMitogen-Activated Protein Kinase 1KinaseChemistryReceptors EndothelinCell MembraneHeterotrimeric GTP-Binding ProteinsCell biologyEnzyme ActivationErbB ReceptorsType C PhospholipasesCOS CellsMutationcardiovascular systemMutagenesis Site-DirectedPhosphorylationGTP-Binding Protein alpha Subunits Gq-G11Mitogen-Activated Protein KinasesProto-oncogene tyrosine-protein kinase SrcEuropean journal of biochemistry
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Synthesis and biological evaluation of cycloalkylidene carboxylic acids as novel effectors of Ras/Raf interaction.

2002

The protooncogenes Ras and Raf play important roles in signal transduction pathways regulated by mitogen-activated protein kinases. Mutations of Ras that arrest the protein in its active state are frequently implicated in tumor formation. We used Ras and Raf proteins in the yeast two-hybrid system to search for natural or synthesized substances capable of modulating Ras/Raf interaction by specifically binding to one of the interacting partners. We found that cycloalkylidene carboxylic acids enhanced Ras/Raf interaction by acting on the cysteine-rich domain of Raf. Several analogues of the active substance 2-cyclohexylidene propanoic acid were synthesized and the importance of the semicyclic…

MAPK/ERK pathwayMagnetic Resonance SpectroscopyCarboxylic acidSaccharomyces cerevisiaeAmino Acid MotifsCarboxylic AcidsAnti-apoptotic Ras signalling cascadeTwo-Hybrid System TechniquesDrug DiscoveryHumansHRASProtein kinase Achemistry.chemical_classificationbiologyChemistryKinasebiology.organism_classificationProtein Structure TertiaryProto-Oncogene Proteins c-rafBiochemistryModels ChemicalMutationMutagenesis Site-Directedras ProteinsMolecular MedicineSignal transductionPlasmidsProtein BindingJournal of medicinal chemistry
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