Search results for " Humans"

showing 10 items of 2466 documents

Castration-Induced Downregulation of SPARC in Stromal Cells Drives Neuroendocrine Differentiation of Prostate Cancer.

2021

Abstract Fatal neuroendocrine differentiation (NED) of castration-resistant prostate cancer is a recurrent mechanism of resistance to androgen deprivation therapies (ADT) and antiandrogen receptor pathway inhibitors (ARPI) in patients. The design of effective therapies for neuroendocrine prostate cancer (NEPC) is complicated by limited knowledge of the molecular mechanisms governing NED. The paucity of acquired genomic alterations and the deregulation of epigenetic and transcription factors suggest a potential contribution from the microenvironment. In this context, whether ADT/ARPI induces stromal cells to release NED-promoting molecules and the underlying molecular networks are unestablis…

MaleCancer ResearchStromal cellAnimals Biomarkers Tumor Cell Differentiation Cell Line Tumor Coculture Techniques Endoplasmic Reticulum Chaperone BiP Epigenesis Genetic Gene Expression Regulation Neoplastic Humans Male Mice Mice Inbred C57BL Neuroendocrine Cells Osteonectin Prostatic Neoplasms Stromal Cells Transgenes Tumor Microenvironment Down-RegulationDown-RegulationContext (language use)Settore MED/08 - Anatomia PatologicaNeuroendocrine differentiationEpigenesis GeneticProstate cancerMiceStromaDownregulation and upregulationNeuroendocrine CellsCell Line TumormedicineBiomarkers TumorTumor MicroenvironmentSettore MED/05 - Patologia ClinicaAnimalsHumansOsteonectinEpigeneticsTransgenesEndoplasmic Reticulum Chaperone BiPbusiness.industryMatricellular proteinProstatic NeoplasmsCell Differentiationmedicine.diseaseCoculture TechniquesGene Expression Regulation NeoplasticMice Inbred C57BLOncologyCancer researchStromal CellsbusinessCancer research
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Optimal local control and tolerability of three-dimensional conformal radiation therapy in prostate cancer: A single institutional experience of dose…

2013

Aims To evaluate long-term late side effects, clinical and biochemical relapse in non-metastatic prostate cancer patients treated with dose escalation, from 74 to 78 Gy, by means of three dimensional conformal radiation therapy. Materials and Methods Clinical data of 125 patients with prostate cancer who underwent three-dimensional conformal radiation therapy were retrospectively evaluated. All patients were stratified, according to the NCCN classification, in low, intermediate and high risk, and all of them showed histologically proven adenocarcinoma stage T1–T3 with at least 2 years of follow-up. Late toxicity was analyzed using a modified Radiation Therapy Oncology Group toxicity scale. …

MaleCancer ResearchThree dimensional conformal radiation therapyUrinary BladderUrogenital SystemKaplan-Meier EstimateAdenocarcinomaDisease-Free SurvivalBiomarkers Tumor80 and overHumansLate toxicity; Local control; Prostate cancer; Radiation therapy; Three dimensional conformal radiation therapy; Adenocarcinoma; Aged; Aged 80 and over; Biomarkers Tumor; Disease-Free Survival; Gastrointestinal Tract; Humans; Italy; Kaplan-Meier Estimate; Male; Middle Aged; Neoplasm Staging; Prostate-Specific Antigen; Prostatic Neoplasms; Radiation Injuries; Radiotherapy Dosage; Radiotherapy Conformal; Rectum; Retrospective Studies; Urinary Bladder; Urogenital System; Medicine (all); Oncology; Cancer ResearchRadiation InjuriesAgedNeoplasm StagingRetrospective StudiesAged 80 and overProstate cancerTumorRadiotherapyConformalMedicine (all)RectumProstatic NeoplasmsRadiotherapy DosageGeneral MedicineMiddle AgedProstate-Specific AntigenRadiation therapyGastrointestinal TractItalyOncologyLocal controlRadiotherapy ConformalLate toxicityBiomarkers
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Sequential boost in neoadjuvant irradiation for T3N0-1 rectal cancer: long-term results from a single-center experience.

2016

Purpose To evaluate the influence of radiation dose on tumor regression grade (TRG) and sphincter preservation rate in a series of cT3N0-1 rectal cancer patients treated with neoadjuvant chemoradiotherapy (CT-RT) with or without a sequential radiation boost. Materials and methods Between May 2002 and September 2013, 116 cases were eligible for retrospective evaluation. Radiotherapy was delivered for a total dose of 45 Gy (no boost arm) or 50.4 Gy (boost arm). TRG was evaluated with the Dworak scale. Results Median follow-up was 62 months (range, 12-138 months). The 5-year overall survival and local control rates were 72% and 93%, respectively. Fifty-five patients (47%) were treated with a s…

MaleCancer ResearchTime FactorsTumor downsizingColorectal cancermedicine.medical_treatmentAnal CanalKaplan-Meier EstimateSingle Center030218 nuclear medicine & medical imaging0302 clinical medicineAdjuvantNeoadjuvant therapyDigestive System Surgical ProceduresTumor Regression GradeIleostomyMedicine (all)Colorectal cancer; Radiation therapy; Tumor downsizing; Adenocarcinoma; Adult; Aged; Anal Canal; Antineoplastic Agents; Capecitabine; Chemoradiotherapy; Digestive System Surgical Procedures; Female; Fluorouracil; Follow-Up Studies; Gastrointestinal Tract; Humans; Ileostomy; Kaplan-Meier Estimate; Male; Middle Aged; Neoadjuvant Therapy; Neoplasm Staging; Organ Sparing Treatments; Radiotherapy Dosage; Radiotherapy Adjuvant; Rectal Neoplasms; Retrospective Studies; Time Factors; Treatment Outcome; Urogenital System; Medicine (all); Oncology; Cancer ResearchRadiotherapy DosageGeneral MedicineChemoradiotherapyMiddle AgedNeoadjuvant TherapyRadiation therapyTreatment OutcomeOncology030220 oncology & carcinogenesisFemaleRadiologyFluorouracilmedicine.drugAdultmedicine.medical_specialtyUrogenital SystemAntineoplastic AgentsAdenocarcinomaCapecitabine03 medical and health sciencesmedicineHumansCapecitabineAgedNeoplasm StagingRetrospective StudiesRadiotherapybusiness.industryRectal Neoplasmsmedicine.diseaseColorectal cancerRadiation therapyGastrointestinal TractConcomitantRadiotherapy AdjuvantbusinessOrgan Sparing TreatmentsChemoradiotherapyFollow-Up StudiesTumori
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Loss of function mutation in the palmitoyl-transferase HHAT leads to syndromic 46,XY disorder of sex development by impeding Hedgehog protein palmito…

2014

The Hedgehog (Hh) family of secreted proteins act as morphogens to control embryonic patterning and development in a variety of organ systems. Post-translational covalent attachment of cholesterol and palmitate to Hh proteins are critical for multimerization and long range signaling potency. However, the biological impact of lipid modifications on Hh ligand distribution and signal reception in humans remains unclear. In the present study, we report a unique case of autosomal recessive syndromic 46,XY Disorder of Sex Development (DSD) with testicular dysgenesis and chondrodysplasia resulting from a homozygous G287V missense mutation in the hedgehog acyl-transferase (HHAT) gene. This mutation…

MaleCancer Research[SDV]Life Sciences [q-bio]medicine.disease_causeCell Fate DeterminationMiceTestisMorphogenesisMissense mutationddc:576.5Genetics (clinical)MutationHomozygoteCell DifferentiationHedgehog signaling pathwayPedigreeCell biologyFemaleSignal transductionSignal TransductionResearch Articlemedicine.medical_specialtylcsh:QH426-470LipoylationMolecular Sequence DataMutation MissenseBiologyPalmitoylationHHATInternal medicineGeneticsmedicineAnimalsHumansHedgehog ProteinsAmino Acid SequenceMolecular BiologyHedgehogEcology Evolution Behavior and SystematicsDisorder of Sex Development 46XY[ SDV ] Life Sciences [q-bio]Sequence Homology Amino AcidBiology and Life SciencesSex Determinationlcsh:GeneticsEndocrinology46 XY Disorders of Sex Development/*genetics; Acyltransferases/chemistry/*genetics/metabolism; Amino Acid Sequence; Animals; Female; Hedgehog Proteins/*metabolism; Homozygote; Humans; Lipoylation/*genetics; Male; Mice; Molecular Sequence Data; *Mutation Missense; Pedigree; Sequence Homology Amino Acid; Signal Transduction/*genetics; Testis/embryologyLipid modificationAcyltransferasesDevelopmental Biology
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Detection and clinical implications of a novel BCR-ABL1 E12A2 insertion/deletion in a CML patient expressing the E13A2 isoform

2019

Background/Aim: The Philadelphia chromosome is the most frequent cytogenetic abnormality in chronic myelogenous (CML). More than 95% of CML patients are diagnosed with the e13a2 or e14a2 BCR-ABL1 fusion transcripts while, in about 1% of these individuals, the break generates the e1a2 rearrangement. Furthermore, about 5% of CML patients are diagnosed with rare BCR-ABL1 fusion transcripts, such as e19a2, e8a2, e13a3, e14a3, e1a3 and e6a2. However, there is limited evidence concerning the clinical and prognostic implications of these infrequent oncogenic variants for CML patients receiving tyrosine kinase inhibitors (TKIs). Case Report: We describe a novel atypical e12a2 insertion/deletion (In…

MaleCancer Researchbcr-ablFusion Proteins bcr-ablBCR-ABL1; CML; E12a2; E13a2; Nilotinib; Ponatinib; TKIs; Antineoplastic Combined Chemotherapy Protocols; Fusion Proteins bcr-abl; Humans; INDEL Mutation; Imidazoles; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Protein Isoforms; Pyridazines; Pyrimidines; Treatment Outcomechemistry.chemical_compoundExon0302 clinical medicineINDEL Mutationhemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsProtein IsoformsChronicCMLLeukemiaPonatinibImidazolesGeneral MedicineMiddle AgedTKIPyridazinesTreatment OutcomeOncology030220 oncology & carcinogenesisPonatinibPyridazineTyrosine kinaseINDEL MutationE13a2Humanmedicine.drugPhiladelphia chromosome03 medical and health sciencesMyelogenousLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansImidazoleAntineoplastic Combined Chemotherapy Protocolbusiness.industryBreakpointProtein IsoformFusion Proteinsmedicine.diseaseNilotinibBCR-ABL1PyrimidinesPyrimidinechemistryNilotinibTKIsCancer researchBCR-ABL PositivebusinessE12a2Myelogenous
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Detection of translocations affecting the BCL6 locus in B cell non-Hodgkin's lymphoma by interphase fluorescence in situ hybridization

2001

Structural alterations in 3q27 affecting the BCL6 locus are among the most frequent changes in B-NHL. The aim of the present study was to establish an interphase-FISH assay for the detection of all diverse BCL6 translocations in B-NHL. Two different approaches were tested, one using a PAC-clone spanning the major breakpoint region (MBR) of BCL6 (span-assay), and another using two BAC clones flanking the MBR (flank-assay). Interphase FISH with the span-assay detected the various BCL6 translocations in seven B-NHL cell lines. The dual-color flank-assay was evaluated in two laboratories independently: in normal controls, the cutoff level for false-positive signals was 2.6%, whereas the cutoff …

MaleCancer Researchmedicine.medical_specialtyLymphoma B-CellLymphomaMolecular Sequence DataTranslocationChromosomal translocationLocus (genetics)BiologyTranslocation GeneticFluorescenceChromosomesGeneticimmune system diseaseshemic and lymphatic diseasesmedicineHumansIn Situ Hybridization FluorescenceIn Situ HybridizationGeneticsGene Rearrangementmedicine.diagnostic_testBase SequenceBreakpointCytogeneticsB-CellBase Sequence; Chromosome Banding; Female; Gene Rearrangement; Humans; In Situ Hybridization Fluorescence; Karyotyping; Lymphoma B-Cell; Male; Molecular Sequence Data; Chromosomes Human Pair 3; Translocation GeneticHematologyGene rearrangementmedicine.diseaseMolecular biologyChromosome BandingOncologyChromosome 3KaryotypingPair 3FemaleChromosomes Human Pair 3TrisomyFluorescence in situ hybridizationHuman
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Association of a functional deficit of the BKCa channel, a synaptic regulator of neuronal excitability, with autism and mental retardation

2006

International audience; Objective: Autism is a complex, largely genetic psychiatric disorder. In the majority of cases, the cause of autism is not known, but there is strong evidence for a genetic etiology. To identify candidate genes, the physical mapping of balanced chromosomal aberrations is a powerful strategy, since several genes have been characterized in numerous disorders. In this study, the authors analyzed a balanced reciprocal translocation arising de novo in a subject with autism and mental retardation. Method: The authors performed the physical mapping of the balanced 9q23/ 10q22 translocation by fluorescent in situ hybridization experiments using bacterial artificial chromosom…

MaleCandidate geneChromosomes Artificial BacterialIndolesDNA Mutational AnalysisRegulatorChromosomal translocationautism mental retardation KCNMA1 genelarge conductance Ca(2+)-activated K(+) (BK(Ca)) channel synaptic transmission chromosomal translocationSynaptic TransmissionTranslocation GeneticPair 10CA2+-ACTIVATED K+ CHANNELSCloning MolecularChildLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMUTATIONIn Situ HybridizationIn Situ Hybridization FluorescenceReverse Transcriptase Polymerase Chain ReactionBacterialChromosome MappingETIOLOGYPsychiatry and Mental healthArtificialKCNMA1 Gene[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]HaploinsufficiencyPsychologyChromosomes Human Pair 9POTASSIUM CHANNELSHumanPair 9Autistic Disorder; Child; Chromosome Aberrations; Chromosome Mapping; Chromosomes; Artificial; Bacterial; Chromosomes; Human; Pair 10; Chromosomes; Human; Pair 9; Cloning; Molecular; DNA Mutational Analysis; Humans; In Situ Hybridization; Fluorescence; Indoles; Intellectual Disability; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits; Male; Reverse Transcriptase Polymerase Chain Reaction; Synaptic Transmission; Translocation; GeneticTranslocationNeurotransmissionChromosomesFluorescenceGeneticIntellectual DisabilitymedicineHumansAutistic DisorderRELEASEChromosome AberrationsCOMPLEXChromosomes Human Pair 10MolecularAutistic Disorder; Child; Chromosome Aberrations; Chromosome Mapping; Chromosomes Artificial Bacterial; Chromosomes Human Pair 10; Chromosomes Human Pair 9; Cloning Molecular; DNA Mutational Analysis; Humans; In Situ Hybridization Fluorescence; Indoles; Intellectual Disability; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits; Male; Reverse Transcriptase Polymerase Chain Reaction; Synaptic Transmission; Translocation GeneticPERVASIVE DEVELOPMENTAL DISORDERSmedicine.diseaseDevelopmental disorderINDIVIDUALSLARGE-CONDUCTANCEAutismSCREENNeuroscience[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyCloning
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The genomic and clinical landscape of fetal akinesia

2020

International audience; Fetal akinesia has multiple clinical subtypes with over 160 gene associations, but the genetic etiology is not yet completely understood.Methods: In this study, 51 patients from 47 unrelated families were analyzed using next-generation sequencing (NGS) techniques aiming to decipher the genomic landscape of fetal akinesia (FA).Results: We have identified likely pathogenic gene variants in 37 cases and report 41 novel variants. Additionally, we report putative pathogenic variants in eight cases including nine novel variants. Our work identified 14 novel disease-gene associations for fetal akinesia: ADSSL1, ASAH1, ASPM, ATP2B3, EARS2, FBLN1, PRG4, PRICKLE1, ROR2, SETBP1…

MaleCandidate geneMyopathyVARIANTSFetal akinesiaMESH: Ryanodine Receptor Calcium Release Channel0302 clinical medicineMESH: ChildGuanine Nucleotide Exchange FactorsMESH: Guanine Nucleotide Exchange FactorsExomeCopy-number variationChildExomeMESH: High-Throughput Nucleotide SequencingGenetics (clinical)GeneticsArthrogryposisArthrogryposis0303 health sciencesMESH: Infant NewbornMESH: Genetic Predisposition to DiseaseHigh-Throughput Nucleotide SequencingRNA-Binding ProteinsMESH: Infant3. Good healthFetal DiseasesCopy-number variationMESH: Fetal DiseasesMESH: Young AdultChild PreschoolASAH1FemaleMESH: DNA Copy Number Variationsmedicine.symptomAdultGENETICSAdolescentDNA Copy Number VariationsMESH: Trans-ActivatorsMESH: ArthrogryposisBiologyASPMYoung Adult03 medical and health sciencesMuscular DiseasesmedicineHumansGenetic Predisposition to DiseaseGene030304 developmental biologyMESH: Adolescent[SDV.MHEP.PED]Life Sciences [q-bio]/Human health and pathology/PediatricsMESH: HumansMUTATIONSMESH: Child PreschoolInfant NewbornMESH: Muscular DiseasesInfantNEMALINE MYOPATHYRyanodine Receptor Calcium Release ChannelMESH: Adultmedicine.diseaseCongenital myopathyMESH: MaleMESH: RNA-Binding Proteins[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsDISTAL ARTHROGRYPOSISTrans-ActivatorsMESH: Female030217 neurology & neurosurgery
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Sex differences in anthracycline-induced cardiotoxicity: the benefits of estrogens

2019

Anthracyclines are the cornerstone for many oncologic treatments, but their cardiotoxicity has been recognized for several decades. Female subjects, especially before puberty and adolescence, or after menopause, seem to be more at increased risk, with the prognostic impact of this sex issue being less consistent compared to other cardiovascular risk factors. Several studies imply that sex differences could depend on the lack of the protective effect of sex hormones against the anthracycline-initiated damage in cardiac cells, or on differential mitochondria-related oxidative gene expression. This is also reflected by the results obtained with different diagnostic methods, such as cardiovascu…

MaleCardiac & Cardiovascular SystemsMagnetic Resonance Spectroscopyand protection from anthracycline cardiotoxicitymedicine.disease_causeBioinformaticsRisk FactorsAnthracycline cardiotoxicityGender differenceGender differencesAnthracyclinesGonadal Steroid Hormones1102 Cardiorespiratory Medicine and HaematologyAMERICAN SOCIETYCardioprotectionSex CharacteristicsHeartPrognosisMitochondriaMenopauseEchocardiographyReperfusion InjuryHEART-FAILUREAnthracycline cardiotoxicity; Gender differences; Pathophysiology monitoring and protection from anthracycline cardiotoxicity; Anthracyclines; Biomarkers; Cardiotonic Agents; Cardiotoxicity; Echocardiography; Female; Gonadal Steroid Hormones; Heart; Heart Failure; Humans; Magnetic Resonance Spectroscopy; Male; Mitochondria; Nuclear Medicine; Oxidative Stress; Prognosis; Reperfusion Injury; Risk Factors; Sex CharacteristicsFemaleCardiology and Cardiovascular MedicineLife Sciences & BiomedicinePOSITION PAPERCARDIAC DYSFUNCTIONCardiotonic AgentsAnthracyclineSPECKLE-TRACKINGIschemiaDRUG CARDIOTOXICITYPathophysiologymedicineHumansCHILDHOOD-CANCER SURVIVORSBREAST-CANCERPathophysiology monitoring and protection from anthracycline cardiotoxicityHeart FailureCardiotoxicityScience & Technologybusiness.industryWORKING GROUPmedicine.diseaseCardiotoxicityOxidative StressmonitoringCardiovascular System & HematologyHeart failureCardiovascular System & CardiologyRISK-FACTORSNuclear MedicinebusinessOxidative stressAnthracycline cardiotoxicity; Gender differences; Pathophysiology monitoring and protection from anthracycline cardiotoxicityBiomarkersHormone
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Changes in intracortical circuits of the human motor cortex following theta burst stimulation of the lateral cerebellum

2008

Objective: The cerebellum takes part in several motor functions through its influence on the motor cortex (M1). Here, we applied the theta burst stimulation (TBS) protocol, a novel form of repetitive Transcranial Magnetic Stimulation (rTMS) over the lateral cerebellum. The aim of this study was to test whether TBS of the lateral cerebellum could be able to modulate the excitability of the contralateral M1 in healthy subjects. Methods: Motor-evoked potentials (MEPs) amplitude, short intracortical inhibition (SICI), long intracortical inhibition (LICI) and short intracortical facilitation (SICF) were tested in the M1 before and after cerebellar continuous TBS (cTBS) or intermittent TBS (iTBS)…

MaleCerebellumTime FactorsTranscranial magnetic stimulation; Cerebellum; Intracortical inhibition; Connectivity; Theta burst stimulation; TMSmedicine.medical_treatmentCTBSFunctional LateralityIntracortical inhibitionCONNECTIVITYNeck MusclesTheta burst stimulationCerebellumTheta RhythmEvoked PotentialsYoung Adult; Theta Rhythm; Analysis of Variance; Neck Muscles; Differential Threshold; Humans; Cerebellum; Electromyography; Hand; Neural Inhibition; Electric Stimulation; Motor Cortex; Evoked Potentials Motor; Adult; Psychomotor Performance; Transcranial Magnetic Stimulation; Time Factors; Female; Functional Laterality; MaleMotor CortexTranscranial Magnetic StimulationSensory SystemsNeck Musclemedicine.anatomical_structureNeurologyMotorCerebellar cortexFemaleSettore MED/26 - NeurologiaPrimary motor cortexPsychologyHumanMotor cortexAdultTime FactorFRONTAL CORTEXDifferential ThresholdSensory systemNOYoung AdultPARIETAL CORTEXPhysiology (medical)medicineHumansAnalysis of VarianceSettore M-PSI/02 - Psicobiologia E Psicologia FisiologicaElectromyographyNeural InhibitionEvoked Potentials MotorHandElectric StimulationTranscranial magnetic stimulationElectrophysiologyCerebellum; Connectivity; Intracortical inhibition; Theta burst stimulation; TMS; Transcranial magnetic stimulation;TMSNeurology (clinical)NeurosciencePsychomotor Performance
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