Search results for "p16"

showing 10 items of 69 documents

P16INK4A and p15INK4B gene alteration associated with oxidative stress in renal cell carcinomas after the chernobyl accident (pilot study).

2002

Our study was undertaken to better understand the role of G1/S transition abnormalities in the malignant progression of renal cell carcinomas (RCCs), exposed to long-term low doses of ionizing radiation (IR), from patients living in radiocontaminated areas of the Ukraine after the Chernobyl accident. We studied p16 and p15 gene alteration in association with oxidative stress markers, including inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX2). We analyzed 88 samples collected from 22 patients with RCCs and with different exposure to IR. Homozygous deletion of the p16 and p15 genes, as well as hypermethylation of the 5CpG island in the promoter region of the same genes, were…

AdultMalePathologymedicine.medical_specialtyAdolescentCellCell Cycle ProteinsPilot Projectsmedicine.disease_causePolymerase Chain ReactionPathology and Forensic MedicineImmunoenzyme TechniquesCarcinomamedicineBiomarkers TumorHumansMolecular BiologyCarcinoma Renal CellCyclin-Dependent Kinase Inhibitor p16AgedCyclin-Dependent Kinase Inhibitor p15Neoplasm Stagingbiologybusiness.industryTumor Suppressor ProteinsPromoterCell BiologyDNA NeoplasmDNA MethylationMiddle Agedmedicine.diseaseKidney NeoplasmsNitric oxide synthaseOxidative Stressmedicine.anatomical_structureDNA methylationbiology.proteinImmunohistochemistryHistopathologyFemalebusinessRadioactive Hazard ReleaseUkraineOxidative stressPower PlantsDiagnostic molecular pathology : the American journal of surgical pathology, part B
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Increased expression of p16 in both oral and genital lichen planus.

2018

Background Lichen Planus, LP, is an inflammatory disease of possible autoimmune origin affecting mainly oral and genital mucosa and skin. According to the WHO oral LP is considered a potentially malignant disorders. The p16 tumour suppressor protein can act as an inhibitor of cyclin dependent kinases 4 and 6 and thus down regulate cell cycle progression. Since the discovery of p16 several studies have evaluated its expression in various forms of human cancers. The aim of this study was to evaluate and compare the expression of p16 in oral and genital LP and corresponding healthy mucosa. Material and Methods A total of 76 cases of oral LP (OLP), 34 cases of genital LP (GLP), 12 cases of heal…

AdultMalemedicine.medical_specialtyDisease03 medical and health sciences0302 clinical medicinestomatognathic systemMedicineHumansSex organskin and connective tissue diseasesGeneral DentistryCyclin-Dependent Kinase Inhibitor p16AgedAged 80 and overOral Medicine and Pathologyintegumentary systembusiness.industryResearchLichen Planus030206 dentistryMiddle Aged:CIENCIAS MÉDICAS [UNESCO]Dermatologystomatognathic diseasesOtorhinolaryngology030220 oncology & carcinogenesisUNESCO::CIENCIAS MÉDICASSurgeryFemaleGenital Diseases MalebusinessGenital Diseases FemaleGenital lichen planusLichen Planus OralMedicina oral, patologia oral y cirugia bucal
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Up-Regulation of leucocytes Genes Implicated in Telomere Dysfunction and Cellular Senescence Correlates with Depression and Anxiety Severity Scores

2012

BACKGROUND: Major depressive disorder (MDD) is frequently associated with chronic medical illness responsible of increased disability and mortality. Inflammation and oxidative stress are considered to be the major mediators of the allostatic load, and has been shown to correlate with telomere erosion in the leucocytes of MDD patients, leading to the model of accelerated aging. However, the significance of telomere length as an exclusive biomarker of aging has been questioned on both methodological and biological grounds. Furthermore, telomeres significantly shorten only in patients with long lasting MDD. Sensitive and dynamic functional biomarkers of aging would be clinically useful to eval…

AgingGene Expressionlcsh:MedicineAnxietySocial and Behavioral Sciences0302 clinical medicineBiomarkers of agingMolecular Cell BiologyLeukocytesPathologyPsychologylcsh:ScienceCellular SenescenceDepression (differential diagnoses)Psychiatry0303 health sciencesMultidisciplinaryDepressionChromosome BiologyGenomicsMiddle AgedTelomereAllostatic loadUp-RegulationTelomeresMental HealthMedicineMajor depressive disorderAnxietyBiomarker (medicine)Femalemedicine.symptomResearch ArticleAdultSenescenceClinical PathologyPsychological StressBiologybehavioral disciplines and activitiesMolecular Genetics03 medical and health sciencesDiagnostic Medicinemental disordersGeneticsmedicineHumansBiologyCyclin-Dependent Kinase Inhibitor p16030304 developmental biologyDepressive Disorder Majorlcsh:RComputational BiologyHuman GeneticsDNAmedicine.diseaseTelomereOxygenGene Expression RegulationImmunologyStathminlcsh:QBiomarkers030217 neurology & neurosurgeryDNA DamagePLoS ONE
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Analysis of TP53, Ki-Ras and P16INK4A promoter methylation as potential prognostic factors in patients with colorectal cancer

2007

AnalysisTP53 Ki-Ras P16INK4A colorectal cancer
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Type 1 diabetic mellitus patients with increased atherosclerosis risk display decreased CDKN2A/2B/2BAS gene expression in leukocytes

2019

Background Type 1 diabetes mellitus (T1DM) patients display increased risk of cardiovascular disease (CVD) and are characterized by a diminished regulatory T (Treg) cell content or function. Previous studies have shown an association between decreased CDKN2A/2B/2BAS gene expression and enhanced CVD. In the present study the potential relationship between CDKN2A/2B/2BAS gene expression, immune cell dysfunction and increased cardiovascular risk in T1DM patients was explored. Methods A cross-sectional study was performed in 90 subjects divided into controls and T1DM patients. Circulating leukocyte subpopulations analysis by flow cytometry, expression studies on peripheral blood mononuclear cel…

Blood Glucose0301 basic medicineendocrine system diseasesCellular differentiationlcsh:Medicine0302 clinical medicineRisk FactorsRAR-related orphan receptor gammaimmune system diseasesLeukocytesIL-2 receptorDiabetisFOXP3Cell DifferentiationGeneral MedicineType 1 diabetes030220 oncology & carcinogenesisCytokinesRNA Long Noncodingmedicine.symptomAdultmedicine.medical_specialtyCD14T cellsInflammationPeripheral blood mononuclear cellGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesInternal medicinemedicineHumansRNA MessengerCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p15Glycated HemoglobinInflammationType 1 diabetesbusiness.industryResearchlcsh:RAtherosclerosismedicine.diseaseCardiovascular riskDiabetes Mellitus Type 1030104 developmental biologyEndocrinologyGene Expression RegulationCase-Control StudiesbusinessJournal of Translational Medicine
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Differences in the mechanisms of growth control in contact-inhibited and serum-deprived human fibroblasts

1997

In the present work we studied mechanisms of growth control in contact-inhibited and serum-deprived human diploid fibroblasts. The observation that the effects on [3H]thymidine incorporation and reduction of retinoblastoma gene product-phosphorylation were additive when contact-inhibition and serum-deprivation were combined led us to the conclusion that the underlying mechanisms might be different. Both contact-inhibition and serum-deprivation led to a strong decrease of cdk4-kinase-activity and cdk2-phosphorylation at Thr 160, while the total amounts of cdk4 and cdk2 remained constant. In contact-inhibited cells, we revealed a strong protein accumulation of the cdk2-inhibitor p27 and a sli…

Cancer ResearchCell Cycle ProteinsProtein Serine-Threonine KinasesRetinoblastoma ProteinCulture Media Serum-FreeS PhaseCyclin D1CyclinsProto-Oncogene ProteinsCDC2-CDC28 KinasesGeneticsmedicineHumansCyclin D1Cyclin D3PhosphorylationCyclin D3FibroblastMolecular BiologyCyclin-Dependent Kinase Inhibitor p16CyclinbiologyCell growthTumor Suppressor ProteinsCyclin-Dependent Kinase 2Cyclin-dependent kinase 2G1 PhaseCyclin-Dependent Kinase 4FibroblastsDiploidyCyclin-Dependent KinasesCulture MediaCell biologymedicine.anatomical_structureCell culturebiology.proteinbiological phenomena cell phenomena and immunitySignal transductionMicrotubule-Associated ProteinsCell DivisionCyclin-Dependent Kinase Inhibitor p27Oncogene
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Analysis of p16 gene and protein status in malignant mixed Müllerian tumors of the uterus

2010

Cancer ResearchP16 genemedicine.anatomical_structureGeneticsCancer researchUterusmedicineBiologyMolecular BiologyMüllerian mimicryCancer Genetics and Cytogenetics
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Novel recombinant GII.P16_GII.13 and GII.P16_GII.3 norovirus strains in Italy.

2014

Novel norovirus strains are continuously emerging worldwide. Molecular investigation and phylogenetic analysis identified GII.P16 recombinant noroviruses from the stools of four Italian children with gastroenteritis. The capsid gene was characterized as either GII.13 or GII.3. The GII.P16_GII.13 Italian strains were closely related to German strains involved in a large outbreak in the second half of 2012 and the Italian strains are the first recorded occurrence of GII.P16_GII.13 in Europe.

Cancer ResearchSettore MED/07 - Microbiologia E Microbiologia ClinicaGenotypevirusesMolecular Sequence DataBiologymedicine.disease_causelaw.inventionfluids and secretionslawVirologymedicineCluster AnalysisHumansGenePhylogenyCaliciviridae InfectionsRecombination GeneticNoroviruPhylogenetic treeGastroenteritiNorovirusvirus diseasesOutbreakGII.P16_GII.3InfantSequence Analysis DNAVirologyRecombinationGastroenteritisInfectious DiseasesCapsidItalyChild PreschoolRecombinant DNANorovirusRNA ViralCapsid ProteinsGII.P16_GII.13Virus research
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Bmi1 and Cell of Origin Determinants of Brain Tumor Phenotype

2007

Glioblastomas frequently express oncogenic EGFR and loss of the Ink4a/Arf locus. Bmi1, a positive regulator of stem cell self renewal, may be critical to drive brain tumor growth. In this issue of Cancer Cell, Bruggeman and colleagues suggest that brain tumors with these molecular alterations can be initiated in both neural precursor and differentiated cell compartments in the absence of Bmi1; however, tumorigenicity is reduced, and tumors contain fewer precursor cells. Surprisingly, tumors appear less malignant when initiated in precursor cells. Bmi1-deficient tumors also had fewer neuronal lineage cells, suggesting a role for Bmi1 in determination of cell lineage and tumor phenotype.

Cancer ResearchTime FactorsCell of originCellular differentiationBrain tumormacromolecular substancesBiologyMiceProto-Oncogene ProteinsPrecursor cellmedicineAnimalsHumansCyclin-Dependent Kinase Inhibitor p16Cell ProliferationNeoplasm StagingMice KnockoutNeuronsPolycomb Repressive Complex 1Brain NeoplasmsCell growthStem CellsNuclear ProteinsCell DifferentiationNeoplasms ExperimentalCell Biologymedicine.diseaseStem Cell Self-RenewalErbB ReceptorsGene Expression Regulation NeoplasticRepressor ProteinsCell Transformation NeoplasticPhenotypeOncologyBMI1AstrocytesMutationCancer cellCancer researchGlioblastomaSignal TransductionCancer Cell
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Delayed ageing through damage protection by the Arf/p53 pathway.

2007

The tumour-suppressor pathway formed by the alternative reading frame protein of the Cdkn2a locus (Arf) and by p53 (also called Trp53) plays a central part in the detection and elimination of cellular damage, and this constitutes the basis of its potent cancer protection activity. Similar to cancer, ageing also results from the accumulation of damage and, therefore, we have reasoned that Arf/p53 could have anti-ageing activity by alleviating the load of age-associated damage. Here we show that genetically manipulated mice with increased, but otherwise normally regulated, levels of Arf and p53 present strong cancer resistance and have decreased levels of ageing-associated damage. These obser…

Cell signalingAgingTime FactorsTumor suppressor geneLongevityBiologymedicine.disease_causeAntioxidantsTranscriptomeMiceCDKN2ANeoplasmsmedicineAnimalsCells CulturedCyclin-Dependent Kinase Inhibitor p16MultidisciplinaryCell cycleFibroblastsCell biologyOxidative StressAgeingDisease SusceptibilitySignal transductionTumor Suppressor Protein p53Oxidative stressNature
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