Search results for "Suppressor"

showing 10 items of 532 documents

Use of corticosteroids and immunosuppressive drugs in inflammatory bowel disease: Clinical practice guidelines of the Italian Group for the Study of …

2017

Abstract The two main forms of intestinal bowel disease, namely ulcerative colitis and Crohn’s disease, are not curable but can be controlled by various medical therapies. The Italian Group for the Study of Inflammatory Bowel Disease (IG-IBD) has prepared clinical practice guidelines to help physicians prescribe corticosteroids and immunosuppressive drugs for these patients. The guidelines consider therapies that induce remission in patients with active disease as well as treatment regimens that maintain remission. These guidelines complement already existing guidelines from IG-IBD on the use of biological drugs in patients with inflammatory bowel diseases.

medicine.medical_specialtyIBDDiseaseGuidelineGuidelinesInflammatory bowel diseaseGastroenterologyBiological drugs03 medical and health sciences0302 clinical medicineAdrenal Cortex HormonesInternal medicineMedicalmedicineCorticosteroidCorticosteroidsHumansIn patient030212 general & internal medicineCorticosteroids; Crohn's disease; Guidelines; IBD; Immunosuppressors; Ulcerative colitis; Hepatology; GastroenterologySocieties MedicalCrohn's diseaseSettore MED/12 - GastroenterologiaUlcerative colitiHepatologybusiness.industryImmunosuppressorsRemission InductionGastroenterologyInflammatory Bowel Diseasesmedicine.diseaseInflammatory Bowel DiseasesUlcerative colitisdigestive system diseasesClinical PracticeCrohn's diseaseUlcerative colitisItalyImmunosuppressorCorticosteroids; Crohn's disease; Guidelines; IBD; Immunosuppressors; Ulcerative colitis; Adrenal Cortex Hormones; Humans; Immunosuppressive Agents; Inflammatory Bowel Diseases; Italy; Remission Induction; Societies Medical030211 gastroenterology & hepatologybusinessSocietiesImmunosuppressive Agents
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A girl with an atypical form of ataxia telangiectasia and an additional de novo 3.14Mb microduplication in region 19q12

2011

A 9-year-old girl born to healthy parents showed manifestations suggestive of ataxia telangiectasia (AT), such as short stature, sudden short bouts of horizontal and rotary nystagmus, a weak and dysarthric voice, rolling gait, unstable posture, and atactic movements. She did not show several cardinal features typical of AT such as frequent, severe infections of the respiratory tract. In contrast, she showed symptoms not generally related to AT, including microcephaly, profound motor and mental retardation, small hands and feet, severely and progressively reduced muscle tone with slackly protruding abdomen and undue drooling, excess fat on her upper arms, and severe oligoarthritis. A cranial…

medicine.medical_specialtyMicrocephalyPathologyCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein Serine-Threonine KinasesBiologyShort statureAtaxia Telangiectasia Mutated ProteinsAtaxia TelangiectasiaInternal medicineChromosome DuplicationGene duplicationGeneticsmedicineHumansLymphocytesChildSalivaCerebellar hypoplasiaMetaphaseGenetics (clinical)Mental DisordersTumor Suppressor ProteinsGeneral Medicinemedicine.diseaseDNA-Binding ProteinsEndocrinologyChromosome InversionAtaxia-telangiectasiaChromosomal regionSpeech delayMicrocephalyFemalemedicine.symptomApoptosis Regulatory ProteinsChromosomes Human Pair 19DNA DamageEuropean Journal of Medical Genetics
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Molecular Progression in Unusual Recurrent Non-Pediatric Intracranial Clear Cell Meningioma

2017

We report a case of a recurrent clear cell meningioma (CCM) in the frontal lobe of the brain of a 67-year-old man. The patient developed three recurrences: at 3, 10, and 12 years after his initial surgery. Histopathology observations revealed a grade 2 CCM with positivity for vimentin and epithelial membrane antigen. Expression of E-cadherin was positive only in the primary tumour and in the first available recurrence. Fluorescence in situ hybridization analyses demonstrated 1p and 14q deletions within the last recurrence. Multiplex ligation-dependent probe amplification studies revealed a heterozygous partial NF2 gene deletion, which progressed to total loss in the last recurrence. The las…

medicine.medical_specialtyPathologyrecurrenceCase ReportVimentin03 medical and health sciences0302 clinical medicineCDKN2ACDKN2BmedicineClear Cell MeningiomaNeoplasmgeneticstumour suppressor genesbiologymedicine.diagnostic_testbusiness.industryintracranial diseaseClear cell meningiomamedicine.diseaseFrontal lobemolecular progressionNF2030220 oncology & carcinogenesisbiology.proteinHistopathologynon-pediatric diseasebusiness030217 neurology & neurosurgeryFluorescence in situ hybridizationCurrent Oncology
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Liver specific deletion of CYLDexon7/8 induces severe biliary damage, fibrosis and increases hepatocarcinogenesis in mice

2012

Background & Aims CYLD is a tumor suppressor gene that is mutated in familial cylindromatosis, an autosomal dominant predisposition to tumors of skin appendages. Reduced CYLD expression has been observed in other tumor entities, including hepatocellular carcinoma. In the present study, we analyzed the role of CYLD in liver homeostasis and hepatocarcinogenesis in vivo . Methods Mice with liver-specific deletion of CYLDexon7/8 ( CYLD FF xAlbCre ) were generated. Liver tissues were histologically analyzed and oval cell activation was investigated. Hepatocarcinogenesis was induced by diethylnitrosamine/phenobarbital (DEN/PB). Microarray expression profiling of livers was performed in untreated …

medicine.medical_specialtyTumor suppressor geneBiliary Tract DiseasesIn Vitro TechniquesBiologymedicine.disease_causeDimethylnitrosamineDeubiquitinating Enzyme CYLDMiceRisk FactorsFibrosisInternal medicinemedicineAnimalsHomeostasisGenetic Predisposition to DiseaseHepatologyLiver NeoplasmsExonsTransforming growth factor betamedicine.diseaseFibrosisMice Mutant StrainsDeubiquitinating Enzyme CYLDMice Inbred C57BLGene expression profilingCysteine EndopeptidasesDisease Models AnimalPhenotypeEndocrinologyLiverPhenobarbitalHepatocellular carcinomaCancer researchbiology.proteinCell activationCarcinogenesisGene DeletionJournal of Hepatology
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Loss of a novel tumor suppressor gene locus at chromosome 8p is associated with leukemic mantle cell lymphoma

2001

Abstract Patients with mantle cell lymphoma (MCL) may present with either nodal or leukemic disease. The molecular determinants underlying this different biologic behavior are not known. This study compared the pattern of genetic abnormalities in patients with nodal and leukemic phases of MCL using comparative genomic hybridization (CGH) and fluorescence in situ hybridization (FISH) for specific gene loci. Although both leukemic and nodal MCL showed similar genomic patterns of losses (involving 6q, 11q22-q23, 13q14, and 17p13) and gains (affecting 3q and 8q), genomic loss of chromosome 8p occurred more frequently in patients with leukemic disease (79% versus 11%,P < .001). Subsequent…

medicine.medical_specialtyTumor suppressor geneImmunologyGenes mycLocus (genetics)Lymphoma Mantle-CellBiologyBiochemistryMYC Gene AmplificationGene duplicationmedicineHumansGenes Tumor SuppressorIn Situ Hybridizationmedicine.diagnostic_testGene AmplificationCytogeneticsNucleic Acid HybridizationCell BiologyHematologyPrognosismedicine.diseaseCancer researchMantle cell lymphomaGene DeletionChromosomes Human Pair 8Fluorescence in situ hybridizationComparative genomic hybridizationBlood
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p53 Involvement in the control of murine hair follicle regression.

2001

p53 is a transcription factor mediating a variety of biological responses including apoptotic cell death. p53 was recently shown to control apoptosis in the hair follicle induced by ionizing radiation and chemotherapy, but its role in the apoptosis-driven physiological hair follicle regression (catagen) remains to be elucidated. Here, we show that p53 protein is strongly expressed and co-localized with apoptotic markers in the regressing hair follicle compartments during catagen. In contrast to wild-type mice, p53 knockout mice show significant retardation of catagen accompanied by significant decrease in the number of apoptotic cells in the hair matrix. Furthermore, p53 null hair follicles…

medicine.medical_specialtyTumor suppressor genemedicine.medical_treatmentDown-RegulationApoptosisBiologyPathology and Forensic MedicineTelogen effluviumMiceBcl-2-associated X proteinDownregulation and upregulationInternal medicineProto-Oncogene ProteinsmedicineAnimalsbcl-2-Associated X ProteinMice Knockoutintegumentary systemGrowth factorAlopecia areatamedicine.diseaseHair follicleCell biologyUp-RegulationMice Inbred C57BLEndocrinologymedicine.anatomical_structureInsulin-Like Growth Factor Binding Protein 3Proto-Oncogene Proteins c-bcl-2Knockout mousebiology.proteinCommentaryFemaleTumor Suppressor Protein p53Hair FollicleThe American journal of pathology
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Generating p53-specific cytotoxic T lymphocytes by recombinant adenoviral vector-based vaccination in mice, but not man.

2002

Mutations and aberrant expression of the p53 tumor suppressor protein are the most frequent molecular alterations in human malignancy. Peptides derived from the wild-type (wt) p53 protein and presented by major histocompatibility complex (MHC) molecules for T lymphocyte recognition are believed to serve as universal tumor-associated antigens for cancer immunotherapy. We studied the immunogeneicity of a recombinant replication-defective adenoviral vector encoding human full-length wt p53 (rAd/hup53) in human leukocyte antigen (HLA)-A2K(b)-transgenic (Tg) mice and man. The generation of p53 epitope-specific cytotoxic T lymphocytes (CTLs) in p53-proficient and p53-deficient A2K(b)-Tg mice was …

medicine.medical_treatmentGenetic VectorsEpitopes T-LymphocyteMice TransgenicPilot ProjectsHuman leukocyte antigenBiologyMajor histocompatibility complexCancer VaccinesEpitopeAdenoviridaeMiceImmune systemCancer immunotherapyAntigenSpecies SpecificityNeoplasmsHLA-A2 AntigenGeneticsmedicineCytotoxic T cellAnimalsHumansTreatment FailureMolecular BiologyT lymphocyteGenetic TherapyGenes p53Self ToleranceImmunologybiology.proteinMolecular MedicineTumor Suppressor Protein p53T-Lymphocytes CytotoxicGene therapy
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Epigenetic siRNA and Chemical Screens Identify SETD8 Inhibition as a Therapeutic Strategy for p53 Activation in High-Risk Neuroblastoma

2017

Given the paucity of druggable mutations in high-risk neuroblastoma (NB), we undertook chromatin-focused small interfering RNA and chemical screens to uncover epigenetic regulators critical for the differentiation block in high-risk NB. High-content Opera imaging identified 53 genes whose loss of expression led to a decrease in NB cell proliferation and 16 also induced differentiation. From these, the secondary chemical screen identified SETD8, the H4K20me1 methyltransferase, as a druggable NB target. Functional studies revealed that SETD8 ablation rescued the pro-apoptotic and cell-cycle arrest functions of p53 by decreasing p53K382me1, leading to activation of the p53 canonical pathway. I…

p530301 basic medicineCancer ResearchSmall interfering RNAMethyltransferaseCellular differentiationDruggabilityBiologyArticleEpigenesis GeneticNeuroblastoma03 medical and health sciences0302 clinical medicineNeuroblastomamedicineHumansEpigeneticsRNA Small InterferingGeneCell ProliferationsiRNA screenCell growthQuinazolineCell DifferentiationdifferentiationHistone-Lysine N-Methyltransferasemedicine.diseaseSETD8030104 developmental biologyOncology030220 oncology & carcinogenesisQuinazolinesCancer researchdifferentiation; epigenetics; neuroblastoma; p53; SETD8; siRNA screen; Oncology; Cell Biology; Cancer ResearchTumor Suppressor Protein p53epigeneticHuman
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Expression of p63, p53 and ki-67 in patients with cervical intraepithelial neoplasia

2017

Objective: Cervical intraepithelial neoplasia (CIN) is a dysplastic process in cervical squamous epithelium and carries a risk of progression to cervical cancer. The aim of this study was to compare expression of three biomarkers named p53, p63 and Ki-67 in patients with various grades of cervical intraepithelial neoplasia and in a control group. Material and Method: 58 patients were enrolled in the study. Each patient underwent a colposcopy-guided biopsy of the cervix. Immunostaining for markers (p53, p63 and Ki-67) was performed on tissue samples of normal cases (n=10), CIN I (n=20), CIN II (n=14), and CIN III (n=14). Results: Our study showed a significant increase of the expression of t…

p530301 basic medicineUterine Cervical Neoplasmsurologic and male genital diseasesGastroenterology0302 clinical medicineYoung adultCervical cancerp63medicine.diagnostic_testbiologyvirus diseasesMiddle AgedImmunohistochemistryfemale genital diseases and pregnancy complicationsKoilocytesurgical procedures operativemedicine.anatomical_structure030220 oncology & carcinogenesisKi-67Disease ProgressionKi-67ImmunohistochemistryFemalelcsh:RB1-214Adultmedicine.medical_specialtyAdolescentCervical intraepithelial neoplasiaPathology and Forensic MedicineYoung Adult03 medical and health sciencesInternal medicineBiopsyBiomarkers Tumorlcsh:PathologymedicineHumansneoplasmsCervixCervical intraepithelial neoplasiabusiness.industryMembrane ProteinsUterine Cervical Dysplasiamedicine.diseaseKi-67 Antigen030104 developmental biologybiology.proteinTumor Suppressor Protein p53businessTurkish Journal of Pathology
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Influence of aryl hydrocarbon- (Ah) receptor and genotoxins on DNA repair gene expression and cell survival of mouse hepatoma cells

2009

The aryl hydrocarbon receptor (AhR) mediates toxicity of a variety of environmental pollutants such as polycyclic aromatic hydrocarbons (PAHs) and dioxins. However, the underlying mechanisms and genetic programmes regulated by AhR to cause adverse effects but also to counteract poisoning are still poorly understood. Here we analysed the effects of two AhR ligands, benzo[a]pyrene (B[a]P), a DNA damaging tumour initiator and promotor and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a pure tumour promoter, on cell survival and on nucleotide excision repair (NER) gene expression. NER deals with so called "bulky" DNA adducts including those generated by enzymatically activated B[a]P. Therefore, t…

p53Aryl hydrocarbon receptor nuclear translocatorDNA RepairTumor suppressor geneCell SurvivalDNA damageDNA repairBlotting WesternDNA-Directed DNA Polymerasecis-PlatinBiologyToxicologyMiceLiver Neoplasms ExperimentalCell Line TumorGene expressionAnimals2378-Tetrachlorodibenzo-p-dioxinGeneAryl hydrocarbon receptorGene Expression ProfilingAryl Hydrocarbon Receptor Nuclear TranslocatorGenes p53Aryl hydrocarbon receptorMolecular biologyNucleotide excision repairBenzo[a]pyreneGene Expression RegulationReceptors Aryl HydrocarbonBiochemistrybiology.proteinEnvironmental PollutantsMutagensNucleotide excision repairToxicology
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