0000000000529777

AUTHOR

Amedeo Amedei

0000-0002-6797-9343

showing 4 related works from this author

Mechanisms of environmental chemicals that enable the cancer hallmark of evasion of growth suppression

2015

As part of the Halifax Project, this review brings attention to the potential effects of environmental chemicals on important molecular and cellular regulators of the cancer hallmark of evading growth suppression. Specifically, we review the mechanisms by which cancer cells escape the growth-inhibitory signals of p53, retinoblastoma protein, transforming growth factor-beta, gap junctions and contact inhibition. We discuss the effects of selected environmental chemicals on these mechanisms of growth inhibition and cross-reference the effects of these chemicals in other classical cancer hallmarks.

Cancer ResearchReviewHazardous Substanceschemistry.chemical_compoundNeoplasmsAnimalsHumansMedicinebiologyAnimalbusiness.industryMedicine (all)Retinoblastoma proteinContact inhibitionCancerEnvironmental ExposureGeneral MedicineEnvironmental exposureEvasion (ethics)medicine.diseaseCell biologychemistryHazardous SubstanceImmunologyCancer cellbiology.proteinNeoplasmSignal transductionGrowth inhibitionbusinessHumanSignal TransductionCarcinogenesis
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TpF1 from Treponema pallidum Activates Inflammasome and Promotes the Development of Regulatory T Cells

2011

Abstract Human syphilis is a multistage disease, with diverse and wide-ranging manifestations caused by Treponema pallidum. Despite the fact that a cell-mediated immune response takes part in the course of syphilis, T. pallidum often manages to evade host immunity and, in untreated individuals, may trigger chronic infection. With this study, we demonstrate for the first time, to our knowledge, that Treponema pallidum induces a regulatory T (Treg) response in patients with secondary syphilis and we found that the miniferritin TpF1, produced by the bacterium, is able to expand this response and promote the production of TGF-β. Accordingly, TpF1 stimulates monocytes to release IL-10 and TGF-β,…

AdultMaleMultiprotein complexInflammasomesVirulence FactorsCellsT-LymphocytesImmunologyAdult; Antigens Helminth; Cell Differentiation; Cells Cultured; Down-Regulation; Female; Humans; Inflammasomes; Inflammation Mediators; Male; Middle Aged; Monocytes; Syphilis; T-Lymphocytes Regulatory; Transforming Growth Factor beta; Treponema pallidum; Virulence FactorsDown-RegulationBiologyT-Lymphocytes RegulatoryMonocytesMicrobiologyProinflammatory cytokineImmune systemAntigenTransforming Growth Factor betaHelminthmedicineHumansImmunology and AllergySyphilisTreponema pallidumAntigensCells CulturedCulturedTreponemaCell DifferentiationInflammasomeMiddle Agedbiology.organism_classificationmedicine.diseaseRegulatoryChronic infectionAntigens HelminthImmunologyFemaleSyphilisInflammation Mediatorsmedicine.drugThe Journal of Immunology
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Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead

2015

Goodson, William H. et al.

Cancer ResearchCarcinogenesis[SDV]Life Sciences [q-bio]METHOXYCHLOR-INDUCED ALTERATIONSReviewPharmacologyMESH: Carcinogens EnvironmentalCarcinogenic synergiesChemical mixturesNeoplasmsMESH: AnimalsMESH: NeoplasmsCarcinogenesiRisk assessmentCancerACTIVATED PROTEIN-KINASESMedicine (all)Low dose1. No povertyCumulative effectsBREAST-CANCER CELLSGeneral MedicineEnvironmental exposureMESH: CarcinogenesisBIO/10 - BIOCHIMICAEPITHELIAL-MESENCHYMAL TRANSITION3. Good health[SDV] Life Sciences [q-bio]Environmental CarcinogenesisESTROGEN-RECEPTOR-ALPHARisk assessmentHumanMESH: Environmental ExposureENDOCRINE-DISRUPTING CHEMICALSTARGETING TISSUE FACTOR[SDV.CAN]Life Sciences [q-bio]/CancerBiologyPrototypical chemical disruptorsExposure[SDV.CAN] Life Sciences [q-bio]/CancerEnvironmental healthmedicine[SDV.EE.SANT] Life Sciences [q-bio]/Ecology environment/HealthCarcinogenEnvironmental carcinogenesis[SDV.EE.SANT]Life Sciences [q-bio]/Ecology environment/HealthMESH: HumansAnimalPOLYBROMINATED DIPHENYL ETHERSCancerEnvironmental Exposuremedicine.diseaseMESH: Hazardous SubstancesCarcinogens EnvironmentalMIGRATION INHIBITORY FACTORVASCULAR ENDOTHELIAL-CELLSHazardous SubstanceNeoplasmCarcinogenesis
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Cerebrospinal fluid T-regulatory cells recognize Borrelia burgdorferi NAPA in chronic Lyme borreliosis.

2013

The NapA protein of B. burgdorferi is essential for the persistence of spirochetes in ticks. One of the most intriguing aspects of NapA is its potential to interfere with the host immune system. Here, we investigated the role of the acquired immune responses induced by NapA in the cerebrospinal fluids (CSF) of patients with chronic Lyme borreliosis. We evaluated the cytokine profile induced in microglia cells and CSF T cells following NapA stimulation. We report here that NapA induced a regulatory T (Treg) response in the CSF of patients with chronic Lyme borreliosis and it is able to expand this suppressive response by promoting the production of TGF-β and IL-10 by microglia cells. Collect…

AdultMaleT regChemokineT-LymphocytesT cells; T reg; Borrelia; Lyme; Adult; Bacterial Proteins; Cerebrospinal Fluid; Chemokines CXC; Chronic Disease; Female; Humans; Interleukin-10; Lyme Disease; Male; Microglia; Middle Aged; T-Lymphocytes Regulatory; Transforming Growth Factor betaImmunologyT cellsT-Lymphocytes RegulatoryImmune systemLyme diseaseBacterial ProteinsTransforming Growth Factor betaImmunology and AllergyMedicineHumansBorrelia burgdorferiCerebrospinal FluidPharmacologyNAPACXCLyme DiseasebiologyMicrogliabusiness.industryBorreliaTransforming growth factor betaMiddle Agedbiology.organism_classificationmedicine.diseaseRegulatoryInterleukin-10Interleukin 10medicine.anatomical_structureImmunologyChronic Diseasebiology.proteinLymeFemaleMicrogliaChemokinesbusinessChemokines CXC
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