Search results for "mutation."

showing 10 items of 2808 documents

The Insulin Receptor Substrate 1 (Irs1) in Intestinal Epithelial Differentiation and in Colorectal Cancer

2012

Colorectal cancer (CRC) is associated with lifestyle factors that affect insulin/IGF signaling, of which the insulin receptor substrate 1 (IRS1) is a key transducer. We investigated expression, localization and pathologic correlations of IRS1 in cancer-uninvolved colonic epithelium, primary CRCs with paired liver metastases and in vitro polarizing Caco2 and HT29 cells. IRS1 mRNA and protein resulted higher, relative to paired mucosa, in adenomas of familial adenomatous polyposis patients and in CRCs that overexpressed c-MYC, ß-catenin, InsRß, and IGF1R. Analysis of IRS1 immunostaining in 24 cases of primary CRC with paired colonic epithelium and hepatic metastasis showed that staining inten…

MalePathologyAnatomy and PhysiologySettore MED/06 - Oncologia MedicaMetastasisIntestinal mucosaInsulin Signaling CascadeMolecular Cell BiologyGastrointestinal CancersBasic Cancer ResearchInsulinIntestinal MucosaInsulin-like Growth FactorCOLON-CARCINOMA-CELLS; GROWTH-FACTOR RECEPTOR; BETA-CATENIN; FACTOR-I; IGF-I; NUCLEAR TRANSLOCATION; ADENOMATOUS POLYPOSIS; STEM-CELL; EXPRESSION; MUTATIONSMultidisciplinarybiologyChemistryQLiver NeoplasmsRCell PolarityCell DifferentiationSignaling CascadesGene Expression Regulation NeoplasticProtein Transportmedicine.anatomical_structureOncologyMedicineFemaleColorectal NeoplasmsHT29 CellsResearch ArticleSignal TransductionAdultendocrine systemmedicine.medical_specialtyColonScienceIRS1 IGF1R colorectal cancerEndocrine SystemGastroenterology and HepatologySignaling PathwaysFamilial adenomatous polyposisHT29 CellsmedicineHumansBiologyAgedInsulin-like growth factor 1 receptorEndocrine Physiologymedicine.diseasedigestive system diseasesEpitheliumIRS1Insulin receptorInsulin Receptor Substrate Proteinsbiology.proteinCancer researchCaco-2 CellsImmunostainingInsulin-Dependent Signal Transduction
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Prognostic significance of K-Ras mutation rate in metastatic colorectal cancer patients

2015

// Bruno Vincenzi 1 , Chiara Cremolini 2 , Andrea Sartore-Bianchi 3 , Antonio Russo 4 , Francesco Mannavola 5 , Giuseppe Perrone 6 , Francesco Pantano 1 , Fotios Loupakis 2 , Daniele Rossini 2 , Elena Ongaro 7 , Erica Bonazzina 3 , Emanuela Dell’Aquila 1 , Marco Imperatori 1 , Alice Zoccoli 1 , Giuseppe Bronte 4 , Giovanna De Maglio 7 , Gabriella Fontanini 8 , Clara Natoli 9 , Alfredo Falcone 2 , Daniele Santini 1 , Andrea Onetti-Muda 6 , Salvatore Siena 3 , Giuseppe Tonini 1 and Giuseppe Aprile 7 1 Department of Medical Oncology, Campus Bio-Medico University of Rome, Rome, Italy 2 Azienda Ospedaliero-Universitaria Pisana, Istituto Toscano Tumori, Pisa, Italy 3 Niguarda Cancer Center, Osped…

MalePathologyColorectal cancerSettore MED/06 - Oncologia MedicaColorectal NeoplasmRetrospective StudieAntineoplastic Combined Chemotherapy ProtocolsTumor Cells Culturededucation.field_of_studyUnivariate analysisBevacizumab; Colorectal cancer; K-Ras; Mutation rate; Prognosis; OncologyLiver NeoplasmsMiddle AgedPrognosisBevacizumabSurvival RateOncologyLiver NeoplasmCohortFemaleK-Ras; mutation rate; colorectal cancer; bevacizumab; prognosisColorectal NeoplasmsK-RasResearch Papermedicine.drugHumanmedicine.medical_specialtyBevacizumabPrognosiMutation ratePopulationBevacizumab; Colorectal cancer; K-Ras; Mutation rate; Prognosis; Antineoplastic Combined Chemotherapy Protocols; Colorectal Neoplasms; Female; Follow-Up Studies; Humans; Liver Neoplasms; Male; Middle Aged; Mutation; Neoplasm Staging; Prognosis; Proto-Oncogene Proteins p21(ras); Real-Time Polymerase Chain Reaction; Retrospective Studies; Survival Rate; Tumor Cells Cultured; OncologyReal-Time Polymerase Chain ReactionFollow-Up StudieProto-Oncogene Proteins p21(ras)Internal medicinemedicineHumanseducationSurvival rateRetrospective StudiesNeoplasm StagingAntineoplastic Combined Chemotherapy Protocolbusiness.industryCancerRetrospective cohort studymedicine.diseaseColorectal cancerK-RaMutationbusinessFollow-Up Studies
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Expanding the clinical spectrum of hereditary fibrosing poikiloderma with tendon contractures, myopathy and pulmonary fibrosis due to FAM111B mutatio…

2015

Background Hereditary Fibrosing Poikiloderma (HFP) with tendon contractures, myopathy and pulmonary fibrosis (POIKTMP [MIM 615704]) is a very recently described entity of syndromic inherited poikiloderma. Previously by using whole exome sequencing in five families, we identified the causative gene, FAM111B (NM_198947.3), the function of which is still unknown. Our objective in this study was to better define the specific features of POIKTMP through a larger series of patients. Methods Clinical and molecular data of two families and eight independent sporadic cases, including six new cases, were collected. Results Key features consist of: (i) early-onset poikiloderma, hypotrichosis and hypoh…

MalePathologyMyopathyPulmonary FibrosisMedicine/Public HealthCell Cycle ProteinsGrowthHypotrichosisContracturesTendons030207 dermatology & venereal diseases0302 clinical medicineFibrosisPulmonary fibrosisSerineGenetics(clinical)Pharmacology (medical)TrypsinExomeChildGenetics (clinical)FAM111BSkinMedicine(all)0303 health sciencesMicroscopyMuscle WeaknessMusclesSkin Diseases GeneticGeneral MedicineMiddle AgedMagnetic Resonance ImagingMuscle atrophy3. Good healthMuscular AtrophyTissuesLiverChild PreschoolFemalemedicine.symptomAdultmedicine.medical_specialtyContractureAdolescentMolecular Sequence DataPoikiloderma03 medical and health sciencesPoikilodermaMuscular DiseasesmedicineHumansAdiposisAmino Acid SequenceCysteineExocrine pancreatic insufficiencyMyopathyMuscle Skeletal030304 developmental biologyMuscle contractureHypohidrosisSclerosisbusiness.industryResearchInfantProteinsmedicine.diseaseFibrosisGenesMutationSkin AbnormalitiesHypotrichosisExocrine Pancreatic Insufficiencybusiness
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BRAF-V600E expression in precursor versus differentiated dendritic cells defines clinically distinct LCH risk groups.

2014

BRAF-V600E expression is identified in hematopoietic progenitor and precursor myeloid dendritic cells in patients with high-risk LCH, and enforced expression of BRAF-V600E in CD11c+ cells recapitulates a high-risk LCH-like phenotype in mice.

MalePathologyendocrine system diseasesCellular differentiationCD34Antigens CD34Mice0302 clinical medicineLangerhans cell histiocytosisBone MarrowRisk FactorsImmunology and Allergyskin and connective tissue diseasesChild0303 health sciencesCell Differentiation3. Good healthHistiocytosismedicine.anatomical_structurePhenotypeTreatment Outcome030220 oncology & carcinogenesisChild PreschoolAntigens Surface2723 Immunology and AllergyFemaleProto-Oncogene Proteins B-rafmedicine.medical_specialtyImmunologyCD11c610 Medicine & healthBiologyArticle03 medical and health sciencesGermline mutationmedicineAnimalsHumansCell LineageGenetic Predisposition to DiseaseLectins C-TypeProgenitor cellneoplasms030304 developmental biology2403 ImmunologyHistocompatibility Antigens Class II302InfantCorrectionDendritic Cellsmedicine.diseaseHematopoietic Stem Cellsdigestive system diseasesCD11c Antigenenzymes and coenzymes (carbohydrates)Histiocytosis Langerhans-CellMannose-Binding Lectins10032 Clinic for Oncology and HematologyMutationBone marrowThe Journal of experimental medicine
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A European family with histidine 58 transthyretin mutation in familial amyloid polyneuropathy

1997

1. IntroductionMore than 50 mutations of the transthyretin (TTR) [1]molecule resulting in different clinical forms of amyloidosisincluding familial amyloid polyneuropathy (FAP) havebeen reported to date. Within this FAP spectrum severaltransthyretin mutations are more frequent, others are rare.One mutation, the codon 58 histidine for leucine has pre-viously been recorded only in American subjects (Mary-land/German type), originally reported in a large kinship[2,3] and in another family from Ohio [4]. In the originaldescription of the Maryland/German type of amyloidosis[2], it was stated that the early immigrants in this pedigreewere from the Rhine river area, "nearly all of them from thelef…

MalePathologymedicine.medical_specialtyAtaxiaAmyloid Neuropathiesmedicine.disease_causeAtrophyLeucineGermanymedicineHumansPoint MutationPrealbuminHistidineCodonGenetics (clinical)Genes DominantMutationDysesthesiabiologybusiness.industryPoint mutationAmyloidosisMiddle Agedmedicine.diseaseUnited StatesTransthyretinNeurologyPediatrics Perinatology and Child Healthbiology.proteinNeurology (clinical)medicine.symptomRestriction fragment length polymorphismbusinessNeuromuscular Disorders
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SIL1 mutations and clinical spectrum in patients with Marinesco-Sjogren syndrome.

2013

Marinesco-Sjogren syndrome is a rare autosomal recessive multisystem disorder featuring cerebellar ataxia, early-onset cataracts, chronic myopathy, variable intellectual disability and delayed motor development. More recently, mutations in the SIL1 gene, which encodes an endoplasmic reticulum resident co-chaperone, were identified as the main cause of Marinesco-Sjogren syndrome. Here we describe the results of SIL1 mutation analysis in 62 patients presenting with early-onset ataxia, cataracts and myopathy or combinations of at least two of these. We obtained a mutation detection rate of 60% (15/25) among patients with the characteristic Marinesco-Sjogren syndrome triad (ataxia, cataracts, m…

MalePathologymedicine.medical_specialtyAtaxiaultrastructure [Muscle Skeletal]SIL1 protein humanAdolescentMarinesco–Sjögren syndromeDNA Mutational Analysisgenetics [Mutation]Bioinformaticsmedicine.disease_causepathology [Muscle Skeletal]physiopathology [Spinocerebellar Degenerations]Cataractspathology [Brain]Intellectual disabilitymedicineGuanine Nucleotide Exchange FactorsHumansddc:610MyopathyMuscle SkeletalCells CulturedRetrospective StudiesSpinocerebellar DegenerationsFamily HealthMutationB-LymphocytesCerebellar ataxiabusiness.industryBrainmedicine.diseasegenetics [Guanine Nucleotide Exchange Factors]Magnetic Resonance Imaging10124 Institute of Molecular Life Sciencesgenetics [Spinocerebellar Degenerations]2728 Neurology (clinical)pathology [Spinocerebellar Degenerations]Mutationultrastructure [Brain]570 Life sciences; biologyAllelic heterogeneityFemaleNeurology (clinical)Neurosciences & Neurologymedicine.symptombusinessBrain : a journal of neurology
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Portal Vein Thrombosis in a Preterm Newborn with Mutation of the MTHFR and PAI-1 Genes and Sepsis by Candida parapsilosis

2016

Objective This report discusses the role of both congenital and acquired risk factors in the pathogenesis of portal vein thrombosis (PVT). Study Design We describe the clinical management and treatment of PVT in a preterm newborn with a homozygous mutation of the methylenetetrahydrofolate reductase (MTHFR) and plasminogen activator inhibitor-1 (PAI-1) genes and sepsis by Candida parapsilosis. Results Although literature data suggest a minor role of genetic factors in thrombophilia in the case of only one mutation, we hypothesize that combined thrombophilic genetic defects may have a cumulative effect and significantly increase the thrombotic risk. Conclusion It could be appropriate to incl…

MalePathologymedicine.medical_specialtyCandida parapsilosis030204 cardiovascular system & hematologyBioinformaticsCandida parapsilosisThrombophiliaSepsisPathogenesis03 medical and health sciences0302 clinical medicineSepsis030225 pediatricsPlasminogen Activator Inhibitor 1medicineHumansMethylenetetrahydrofolate Reductase (NADPH2)Venous ThrombosisPolymorphism GeneticbiologyPortal Veinbusiness.industryCandidiasisInfant NewbornAnticoagulantsFactor VObstetrics and Gynecologyportal thrombosis fungal infection gene polymorphismmedicine.diseasebiology.organism_classificationPortal vein thrombosisSurgical Procedures OperativeMethylenetetrahydrofolate reductaseMutationPediatrics Perinatology and Child Healthbiology.proteinGene polymorphismbusinessPlasminogen activatorAmerican Journal of Perinatology
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Complexity of the Hereditary Motor and Sensory Neuropathies

2015

Early-onset hereditary motor and sensory neuropathies are rare diseases representing a broad clinical and genetic spectrum. Without a notable familial history, the clinical diagnosis is complicated because acquired causes of peripheral neuropathy, such as inflammatory neuropathies, neuropathies with toxic causes, and nutritional deficiencies, must be considered. We examined the clinical, electrophysiological, and pathologic manifestations of a boy with an initial diagnosis of chronic inflammatory demyelinating polyneuropathy. The progression of the disease despite treatment led to a suspicion of hereditary motor and sensory neuropathy. Genetic testing revealed the presence of the MPZ p.D90…

MalePathologymedicine.medical_specialtyChronic inflammatory demyelinating polyneuropathySensory systemDiseaseBioinformaticsSural NervemedicineHumansGenetic testingmedicine.diagnostic_testbusiness.industrymedicine.diseasePhenotypePeripheral neuropathyChild PreschoolClinical diagnosisMutationPediatrics Perinatology and Child HealthMutation (genetic algorithm)Disease ProgressionNeurology (clinical)Hereditary Sensory and Motor NeuropathybusinessHereditary motor and sensory neuropathyMyelin P0 ProteinHeLa CellsJournal of Child Neurology
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DJ-1 mutations and parkinsonism-dementia-amyotrophic lateral sclerosis complex.

2005

Mutations in DJ-1 gene have been recently shown to cause autosomal recessive early-onset Parkinson’s disease (EOPD) in a large Dutch family and in a small consanguineous Italian family.1 Subsequent to this initial finding, several additional DJ-1 mutations were identified in subjects with EOPD.2–6 We describe a family from southern Italy with three brothers affected by a complex disorder characterized by early-onset parkinsonism-dementia-amyotrophic lateral sclerosis (EOPD-D-ALS). The analysis of the DJ-1 gene showed a novel homozygous mutation (E163K) in exon 7 and a novel homozygous mutation (g.168_185dup) in the promoter region of this gene in living affected subjects

MalePathologymedicine.medical_specialtyDNA Mutational AnalysisProtein Deglycase DJ-1Glutamic AcidGene mutationParkinsonismmedicine.disease_causeDISEASEPARK7GUAMExonMucoproteinsDegenerative diseaseParkinsonian DisordersmedicineHumansDementiaRNA MessengerAmyotrophic lateral sclerosisGeneFamily HealthOncogene ProteinsGeneticsMutationReverse Transcriptase Polymerase Chain Reactionbusiness.industryParkinsonismAmyotrophic Lateral SclerosisIntracellular Signaling Peptides and ProteinsExonsDEGENERATIONBlotting Northernmedicine.diseaseGENEINCLUSIONSNeurologyMutationAmyotrophic LateralFemaleDementiaNeurology (clinical)TAUbusiness
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Biological aggressiveness evaluation in prostate carcinomas: immunohistochemical analysis of PCNA and p53 in a series of Gleason 6 (3+3) adenocarcino…

2003

We selected 63 prostate tumors with Gleason's grade 6 (3+3), commonly showing both tubular and cribrous patterns. We compared in both patterns the expression of two of the most used biologic markers: PCNA and p53, with the aim to verify the validity of the Gleason's grading system to compare the morphologic grade with biologic aggressiveness and prognostic value. We did not find any statistical difference in the protein immunopositivity, indicating that both patterns could have identical biologic behaviour; then we confirmed the validity of Gleason's system for considering both tubular and cribrous patterns as an intermediate grade of tumoral differentiation. Moreover, we found a linear rel…

MalePathologymedicine.medical_specialtyHistologyProliferative indexBiophysicsStatistical differenceSettore MED/08 - Anatomia PatologicaAdenocarcinomaBiologyP53 MutationProstateProliferative index; Prostate cancerogenesis; Tumoral differentiation; Tumoral prognosis; Cell Biology; Anatomy; Animal Science and Zoology; Developmental BiologyProliferating Cell Nuclear AntigenBiomarkers TumormedicineHumansProstate tumorsIntermediate Gradelcsh:QH301-705.5Tumoral differentiationBiologic markerProstatic NeoplasmsCell BiologyImmunohistochemistryProliferating cell nuclear antigenmedicine.anatomical_structurelcsh:Biology (General)Prostate cancerogenesibiology.proteinImmunohistochemistryTumoral prognosiAnimal Science and ZoologyAnatomyTumor Suppressor Protein p53Developmental BiologyEuropean Journal of Histochemistry
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