Search results for "REGIONS"

showing 10 items of 1521 documents

The differential diagnoses of uterine leiomyomas and leiomyosarcomas using DNA and RNA sequencing.

2019

BACKGROUND: Although uterine leiomyomas and leiomyosarcomas are considered biologically unrelated tumors, they share morphologic and histologic characteristics that complicate their differential diagnosis. The long-term therapeutic option for leiomyoma is laparoscopic myomectomy with morcellation, particularly for patients who wish to preserve their fertility. However, because of the potential dissemination of undiagnosed or hidden leiomyosarcoma from morcellation, there is a need to develop a preoperative assessment of malignancy risk. OBJECTIVE: Through an integrated comparative genomic and transcriptomic analysis, we aim to identify differential genetic targets in leiomyomas vs leiomyosa…

LeiomyosarcomaAdultLeiomyosarcomaDNA Copy Number Variationsmedicine.disease_causeMalignancyPolymorphism Single NucleotideDNA sequencinggenomic/transcriptomic profileuterine leiomyosarcomaDiagnosis Differential03 medical and health sciences0302 clinical medicineGene DuplicationmedicineHumans030212 general & internal medicineCopy-number variationGeneAgedMutation030219 obstetrics & reproductive medicineuterine leiomyomaLeiomyomabusiness.industrySequence Analysis RNAGene Expression ProfilingObstetrics and GynecologyHigh-Throughput Nucleotide SequencingGenomicsSequence Analysis DNAMiddle Agedmedicine.diseaseBRCA2body regionsLeiomyomaUterine NeoplasmsCancer researchFGFR4FemaleDifferential diagnosisGene FusionbusinessROS1DNA/RNA sequencingGene DeletionAmerican journal of obstetrics and gynecology
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Immunoexpression of p53 in cutaneous and subcutaneous leiomyosarcomas.

2016

The diagnosis of malignancy in cutaneous and subcutaneous smooth muscle tumors is based on subtle criteria. Therefore, any ancillary technique useful in this differential diagnosis is always welcome. In this report, we study the immunoexpression of p53 in 19 malignant smooth muscle tumors of the skin (15 cutaneous leiomyosarcomas, 2 subcutaneous leiomyosarcomas, and 2 cutaneous metastases of leiomyosarcoma), as well as in 1 leiomyoma with cellular atypia, therefore complementing a previous study on p53 immunoexpression in leiomyomas of the skin. The p53 staining was positive in 12 (63.16%) of 19 leiomyosarcomas. Percentages of immunostaining in the positive cases varied from 2% to 95%. Ten …

LeiomyosarcomaAdultLeiomyosarcomaMalePathologymedicine.medical_specialtySkin NeoplasmsMalignancyPathology and Forensic MedicineDiagnosis Differential030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicinemedicineHumansCutaneous leiomyosarcomaSmooth Muscle TumorAgedAged 80 and overLeiomyomabusiness.industryGeneral MedicineMiddle Agedmedicine.diseaseImmunohistochemistryStainingbody regionsLeiomyoma030220 oncology & carcinogenesisSmooth Muscle TumorUterine NeoplasmsFemaleDifferential diagnosisTumor Suppressor Protein p53businessImmunostainingAnnals of diagnostic pathology
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PML down-regulation in soft tissue sarcomas

2010

To date, little is known concerning the promyelocytic leukemia gene (PML) status in tumors of different origin, and its expression has never been evaluated in soft tissue sarcoma. The aim of the present study is focused on the identification of differences in terms of PML protein expression between different types of soft tissue sarcoma and the corresponding normal surrounding tissue. PML protein expression has been assessed by immunohistochemistry in six different histologic types of soft tissue sarcoma (synovial sarcoma, myofibroblastic sarcoma, angiosarcoma, liposarcoma, pleomorphic sarcoma, and leiomyosarcoma) and in the corresponding normal surrounding tissue. PML resulted significantl…

LeiomyosarcomaPathologymedicine.medical_specialtyPhysiologysoft tissue tumorSettore MED/06 - Oncologia MedicaClinical BiochemistryDown-RegulationLiposarcomaPromyelocytic Leukemia ProteinPleomorphic LiposarcomaPML sarcomasPromyelocytic leukemia proteinmedicineHumanssarcomasneoplasmsMyxoid liposarcomaPMLbiologybusiness.industrySoft tissue sarcomaTumor Suppressor ProteinsNuclear ProteinsSarcomaCell BiologyAnatomymedicine.diseaseImmunohistochemistrySynovial sarcomabody regionsbiology.proteinSarcomabusinessTranscription Factors
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Functional analysis of the -2548G/A leptin gene polymorphism in breast cancer cells

2009

Leptin is overexpressed in human breast tumors and is produced by breast cancer cells in response to obesity-related stimuli. The leptin promoter polymorphism Lep-2548G/A can be associated with increased leptin secretion by adipocytes and elevated cancer risk. However, molecular mechanisms underlying the link between Lep-2548G/A and breast cancer have never been addressed. Lep-2548G/A is proximal to a binding site for the transcriptional factor Sp1. Furthermore nucleolin, a transcriptional repressor, can bind Sp1 or its consensus site. Consequently, we focused on the impact of Lep-2548G/A on Sp1- and nucleolin-dependent leptin transcription in breast cancer cells. The Lep-2548G/A was identi…

LeptinChromatin ImmunoprecipitationCancer Researchmedicine.medical_specialtyGenotypeSp1 Transcription FactorBlotting WesterneducationAdipokineBreast NeoplasmsBiologyBody Mass IndexBreast cancerInternal medicineTumor Cells CulturedmedicineHumansHypoglycemic AgentsInsulinObesityRNA MessengerPromoter Regions Genetichealth care economics and organizationsPolymorphism GeneticLeptin receptorReverse Transcriptase Polymerase Chain ReactionLeptinRNA-Binding ProteinsCancerPhosphoproteinsmedicine.diseaseEndocrinologyOncologyCancer researchImmunohistochemistryBreast diseaseNucleolinhormones hormone substitutes and hormone antagonistsInternational Journal of Cancer
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Genetic variations of leptin and leptin receptor are associated with body composition changes in response to physical training

2010

Leptin regulates body weight, metabolism, and tissue adaptations to environmental stressors. We examined the association of single nucleotide polymorphism (SNP) of leptin promoter G-2548A (rs7799039) and leptin receptor Gln223Arg (rs1137101) with body composition, plasma leptin levels, and peak oxygen uptake (VO(2)peak) in response to 8 weeks of physical training in 48 male military conscripts. AA homozygotes of leptin promoter SNP-2548 showed higher body fat and BMI values than G allele carriers. Acute exercise decreased leptin levels in G allele carriers, but increased in AA homozygotes. Physical training significantly decreased BMI values and also a tendency for decreased plasma leptin l…

LeptinMalemedicine.medical_specialtyGenotypeClinical BiochemistrySingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideBiochemistryBody Mass IndexYoung AdultOxygen ConsumptionInternal medicinemedicineHumansAllelePromoter Regions GeneticExerciseAllelesLeptin receptorLeptinHomozygotedigestive oral and skin physiologyVO2 maxCell BiologyGeneral MedicineEndocrinologyBlood chemistryHormone receptorBody CompositionReceptors LeptinBody mass indexhormones hormone substitutes and hormone antagonistsCell Biochemistry and Function
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Expression of angiogenic regulators, VEGF and leptin, is regulated by the EGF/PI3K/STAT3 pathway in colorectal cancer cells.

2009

Both leptin and vascular endothelial growth factor (VEGF) are growth and angiogenic cytokines that are upregulated in different types of cancer and have been implicated in neoplastic progression. Here we investigated the molecular mechanism by which leptin and VEGF expression are regulated in colon cancer by epidermal growth factor (EGF). In colon cancer cell line HT-29, EGF induced the binding of signal transducer and activator transcription 3 (STAT3) to STAT3 consensus motifs within the VEGF and leptin promoters and stimulated leptin and VEGF mRNA and protein synthesis. All these EGF effects were significantly blocked when HT-29 cells were treated with an inhibitor of the phosphoinositide…

LeptinSTAT3 Transcription FactorVascular Endothelial Growth Factor ASmall interfering RNAPhysiologyColorectal cancerClinical BiochemistryNeovascularization PhysiologicEGF/PI3K/STAT3colorectal cancerchemistry.chemical_compoundPhosphatidylinositol 3-KinasesEpidermal growth factormedicineHumansLY294002Gene SilencingRNA MessengerSTAT3Promoter Regions GeneticPI3K/AKT/mTOR pathwayCell NucleusbiologyEpidermal Growth FactorChemistryLeptinangiogenic regulators VEGF leptinCell Biologymedicine.diseaseUp-RegulationVascular endothelial growth factorGene Expression Regulation NeoplasticCancer researchbiology.proteinColorectal NeoplasmsHT29 Cellshormones hormone substitutes and hormone antagonistsProtein Binding
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Insulin-dependent leptin expression in breast cancer cells.

2008

Abstract Pathologic conditions associated with hyperinsulinemia, such as obesity, metabolic syndrome, and diabetes, seem to increase the risk of breast cancer. Here, we studied molecular mechanisms by which insulin activates the expression of leptin, an obesity hormone that has been shown to promote breast cancer progression in an autocrine or paracrine way. Using MDA-MB-231 breast cancer cells, we found that (a) insulin stimulated leptin mRNA and protein expression, which was associated with increased activation of the leptin gene promoter; (b) insulin increased nuclear accumulation of transcription factors hypoxia inducible factor (HIF)-1α and Sp1 and their loading on the leptin promoter;…

LeptinTranscriptional ActivationCancer Researchmedicine.medical_specialtySmall interfering RNAChromatin ImmunoprecipitationSp1 Transcription FactorBlotting WesternFluorescent Antibody TechniqueBreast NeoplasmsEnzyme-Linked Immunosorbent AssayBiologyParacrine signallingPhosphatidylinositol 3-Kinasesbreast cancerInternal medicinemedicineHyperinsulinemiaTumor Cells CulturedHumansHypoglycemic AgentsInsulinRNA MessengerRNA Small InterferingAutocrine signallingLuciferasesPromoter Regions GeneticTranscription factorCell NucleusMitogen-Activated Protein Kinase 1Gene knockdownLeptin receptorMitogen-Activated Protein Kinase 3Reverse Transcriptase Polymerase Chain ReactionLeptinmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaEndocrinologyOncologyCancer researchFemalehormones hormone substitutes and hormone antagonistsCancer research
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Effects of PPARγ agonists on the expression of leptin and vascular endothelial growth factor in breast cancer cells.

2013

The obesity hormone leptin has been implicated in breast cancer development. Breast cancer cells express the leptin receptor and are able to synthesize leptin in response to obesity-related stimuli. Furthermore, leptin is a positive regulator of vascular endothelial growth factor (VEGF) and high levels of both proteins are associated with worse prognosis in breast cancer patients. Peroxisome proliferator-activated receptor γ (PPARγ) ligands are therapeutic agents used in patient with Type 2 diabetes and obesity which have recently been studied for their potential anti-tumor effect. Here, we studied if these compounds, ciglitazone and GW1929, can affect the expression of leptin and VEGF in b…

LeptinVascular Endothelial Growth Factor APhysiologySettore MED/06 - Oncologia MedicaClinical BiochemistryLigandschemistry.chemical_compoundCell MovementPromoter Regions Geneticskin and connective tissue diseasesReceptorGENE-EXPRESSIONLeptindigestive oral and skin physiologyVEGFGene Expression Regulation NeoplasticVascular endothelial growth factorROSIGLITAZONEACTIVATED-RECEPTOR-GAMMAMCF-7 CellsPIOGLITAZONEFemalemedicine.medical_specialtyCell SurvivalSp1 Transcription FactorBLADDER-CANCERBreast NeoplasmsBiologyBenzophenonesBreast cancerCiglitazoneInternal medicinemedicineHumansRNA MessengerViability assayBinding SitesLeptin receptorDose-Response Relationship DrugCell BiologyIN-VITROmedicine.diseaseTRANSACTIVATIONDIABETIC-PATIENTSPPAR gammaEndocrinologychemistryTyrosineTHIAZOLIDINEDIONESACTIVATED-RECEPTOR-GAMMA; BLADDER-CANCER; IN-VITRO; DIABETIC-PATIENTS; GENE-EXPRESSION; VEGF; PIOGLITAZONE; THIAZOLIDINEDIONES; TRANSACTIVATION; ROSIGLITAZONEHormone
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Genetic and Biochemical Analysis of PadR-padC Promoter Interactions during the Phenolic Acid Stress Response in Bacillus subtilis 168

2011

ABSTRACT Bacillus subtilis 168 is resistant to phenolic acids by expression of an inducible enzyme, the phenolic acid decarboxylase (PadC), that decarboxylates these acids into less toxic vinyl derivatives. In the phenolic acid stress response (PASR), the repressor of padC , PadR, is inactivated by these acids. Inactivation of PadR is followed by a strong expression of padC . To elucidate the functional interaction between PadR and the padC promoter, we performed (i) footprinting assays to identify the region protected by PadR, (ii) electrophoretic mobility shift assays (EMSAs) with a modified padC promoter protected region to determine the interacting sequences, and (iii) random mutagenesi…

Leucine zipperMutantRepressorElectrophoretic Mobility Shift AssayGenetics and Molecular BiologyBacillus subtilisBiologyMicrobiologyProtein Structure Secondary03 medical and health scienceschemistry.chemical_compoundBacterial ProteinsStress PhysiologicalBacillus subtilis 168Hydroxybenzoates[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyPromoter Regions GeneticMolecular Biology030304 developmental biology2. Zero hungerchemistry.chemical_classification0303 health sciences030306 microbiologyMutagenesisPhenolic acidGene Expression Regulation Bacterialbiology.organism_classificationMolecular biologyFootprintingEnzymechemistryBiochemistryBacillus subtilisProtein Binding
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Cigarette smoke increases BLT2 receptor functions in bronchial epithelial cells: in vitro and ex vivo evidence

2013

Summary Leukotriene B4 (LTB4) is a neutrophil chemotactic molecule with important involvement in the inflammatory responses of chronic obstructive pulmonary disease (COPD). Airway epithelium is emerging as a regulator of innate immune responses to a variety of insults including cigarette smoke, the major risk factor for COPD. In this study we have explored whether cigarette smoke extracts (CSE) or soluble mediators present in distal lung fluid samples (mini-bronchoalveolar lavages) from smokers alter the expression of the LTB4 receptor 2 (BLT2) and peroxisome proliferator-activated receptor-α (PPAR-α) in bronchial epithelial cells. We also evaluated the effects of CSE on the expression of i…

Leukotriene B4NeutrophilsImmunologyIntercellular Adhesion Molecule-1Blotting WesternReceptors Leukotriene B4Peroxisome proliferator-activated receptorSettore MED/41 - AnestesiologiaInflammationBronchiBiologychronic obstructive pulmonary diseasechemistry.chemical_compoundTobaccoacute lung injiurybronchial epithelial cellleukotriene B4.medicineCell AdhesionImmunology and AllergyHumansPPAR alphaReceptorPromoter Regions GeneticCells Culturedchemistry.chemical_classificationInnate immune systemPlant Extractscigarette smokeSmokingEpithelial CellsOriginal Articlesrespiratory systemFlow CytometryIntercellular Adhesion Molecule-1Neutrophiliarespiratory tract diseasesacute lung injiury; bronchial epithelial cells; cigarette smoke; chronic obstructive pulmonary disease; inflammation; leukotriene B4.STAT1 Transcription FactorchemistryinflammationImmunologyRespiratory epitheliumRNA Interferencemedicine.symptomBronchoalveolar Lavage FluidProtein Binding
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