Search results for "Suppressor"

showing 10 items of 532 documents

DNA methylation changes and somatic mutations as tumorigenic events in Lynch syndrome-associated adenomas retaining mismatch repair protein expression

2018

Background: DNA mismatch repair (MMR) defects are a major factor in colorectal tumorigenesis in Lynch syndrome (LS) and 15% of sporadic cases. Some adenomas from carriers of inherited MMR gene mutations have intact MMR protein expression implying other mechanisms accelerating tumorigenesis. We determined roles of DNA methylation changes and somatic mutations in cancer-associated genes as tumorigenic events in LS-associated colorectal adenomas with intact MMR. Methods: We investigated 122 archival colorectal specimens of normal mucosae, adenomas and carcinomas from 57 LS patients. MMR-deficient (MMR-D, n 49) and MMR-proficient (MMR-P, n 18) adenomas were of particular interest and were inter…

0301 basic medicineMaleResearch paperMICROSATELLITE INSTABILITYHYPOMETHYLATIONDNA mismatch repairPHENOTYPEmedicine.disease_causeEpigenesis Genetic0302 clinical medicineCOLORECTAL ADENOMASCDKN2APromoter Regions Geneticcolorectal adenomaDNA methylationLINE-1 methylationTumor suppressorGeneral MedicineMethylationMiddle AgedCANCERTUMORSLynch syndromeDNA-metylaatio3. Good healthDEFICIENCY030220 oncology & carcinogenesisDNA methylationsyöpätauditFemaleColorectal adenomaAdultcongenital hereditary and neonatal diseases and abnormalitiesAdenomatumor suppressorsuolistosyövätColorectal adenomaBiologycomplex mixturesGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesBRAF MUTATIONmedicineHumansLynchin oireyhtymäAgedTumor Suppressor ProteinsMicrosatellite instabilityDNAUNE-1 methylationta3122medicine.diseaseGENEColorectal Neoplasms Hereditary Nonpolyposisdigestive system diseasestumorigenesisCOPY NUMBER030104 developmental biologyLynch syndromeLong Interspersed Nucleotide Elements3121 General medicine internal medicine and other clinical medicineMutationTumorigenesisCancer research3111 BiomedicineTumotigenesismutationCarcinogenesisEBioMedicine
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On the role of cystatin C in cancer progression

2018

Cystatin C (Cyst C) is an endogenous inhibitor of lysosomal cysteine proteinases, which has been shown to play a role in several normal and pathological processes. Interestingly, a growing number of experimental and clinical studies suggest that this inhibitor also appears to be implicated in the malignant progression of various human tumors. However, the role of Cyst C in malignant diseases is still controversial as these studies have highlighted that this protein may function either as tumor suppressor or tumor promoter. The specific mechanisms underlying these opposing effects at present remain murky and are the subject of many current investigations. On the other hand, a complete knowle…

0301 basic medicineMetastasiCysteine proteinaseGeneral Biochemistry Genetics and Molecular BiologyCysteine Proteinase Inhibitorslaw.inventionMetastasisCathepsin03 medical and health sciences0302 clinical medicinelawNeoplasmsMedicineAnimalsHumansCystGeneral Pharmacology Toxicology and PharmaceuticsNeoplasm MetastasisCystatin CCancerCathepsinbiologybusiness.industryCancerProteinase inhibitorsGeneral Medicinemedicine.disease030104 developmental biologyCystatin C030220 oncology & carcinogenesisCancer researchbiology.proteinDisease ProgressionSettore BIO/14 - FarmacologiaSuppressorbusinessFunction (biology)
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The unbalanced p53/SIRT1 axis may impact lymphocyte homeostasis in COVID-19 patients

2021

Abstract Background/objectives A dysregulated inflammatory profile plays an important role in coronavirus disease-2019 (COVID-19) pathogenesis. Moreover, the depletion of lymphocytes is typically associated with an unfavourable disease course. We studied the role and impact of p53 and deacetylase Sirtuin 1 (SIRT1) on lymph-monocyte homeostasis and their possible effect on T and B cell signalling. Methods Gene expression analysis and flow cytometry were performed on peripheral blood mononuclear cells (PBMC) of 35 COVID-19 patients and 10 healthy donors (HD). Inflammatory cytokines, the frequency of Annexin+ cells among CD3+ T cells and CD19+ B cell subsets were quantified. Results PBMC from …

0301 basic medicineMicrobiology (medical)Male030106 microbiologyInflammationInfectious and parasitic diseasesRC109-216CD19ArticleProinflammatory cytokineBLNK Inflammation03 medical and health sciences0302 clinical medicineSirtuin 1Lymphocyte homeostasismedicineHomeostasisHumans030212 general & internal medicineLymphocytesInterleukin-7 receptorB cellAgedInflammationBLNKbiologySirtuin 1SARS-CoV-2COVID-19p53/SIRT1General MedicineIL-7RMiddle Agedmedicine.anatomical_structureInfectious DiseasesSettore MED/38 - PEDIATRIA GENERALE E SPECIALISTICABLNK; COVID-19; IL-7R; inflammation; p53/SIRT1ImmunologyB-cell linkerbiology.proteinCytokinesFemalemedicine.symptomTumor Suppressor Protein p53
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An Inflammatory Profile Correlates With Decreased Frequency of Cytotoxic Cells in Coronavirus Disease 2019

2020

Abstract Increased production of inflammatory cytokines and myeloid-derived suppressor cells occurs in patients with coronavirus disease 2019. These inversely correlated with perforin-expressing natural killer (NK) and CD3+ T cells. We observed a lower number of perforin-expressing NK cells in intensive care unit (ICU) patients compared with non-ICU patients, suggesting an impairment of the immune cytotoxic arm as a pathogenic mechanism.

0301 basic medicineMicrobiology (medical)medicine.medical_treatmentMDSCInflammationchemical and pharmacologic phenomenaNK cellsProinflammatory cytokineNatural killer cell03 medical and health sciences0302 clinical medicineImmune systemmedicineCytotoxic T cellcytotoxic cellcytotoxic cellsbiologybusiness.industryCOVID-19COVID-19; cytotoxic cells; inflammation; MDSC; NK cells030104 developmental biologymedicine.anatomical_structureCytokineInfectious DiseasesPerforinSettore MED/38 - PEDIATRIA GENERALE E SPECIALISTICAinflammation030220 oncology & carcinogenesisImmunologybiology.proteinMyeloid-derived Suppressor Cellmedicine.symptombusinessClinical Infectious Diseases
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Mechanisms of viral mutation

2016

The remarkable capacity of some viruses to adapt to new hosts and environments is highly dependent on their ability to generate de novo diversity in a short period of time. Rates of spontaneous mutation vary amply among viruses. RNA viruses mutate faster than DNA viruses, single-stranded viruses mutate faster than double-strand virus, and genome size appears to correlate negatively with mutation rate. Viral mutation rates are modulated at different levels, including polymerase fidelity, sequence context, template secondary structure, cellular microenvironment, replication mechanisms, proofreading, and access to post-replicative repair. Additionally, massive numbers of mutations can be intro…

0301 basic medicineMutation rateEvolutionMutation ratevirusesGenome ViralReviewBiologyVirus ReplicationGenetic diversityVirus03 medical and health sciencesCellular and Molecular NeuroscienceMolecular BiologySuppressor mutationRecombination GeneticPharmacologyGeneticsCell BiologyResistance mutationVirologyReplication fidelityVirusPost-replicative repair030104 developmental biologyViral replicationViral evolutionMutationVirusesMutation (genetic algorithm)Dynamic mutationMolecular MedicineHyper-mutationCellular and Molecular Life Sciences
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Mesenchymal Transition of High-Grade Breast Carcinomas Depends on Extracellular Matrix Control of Myeloid Suppressor Cell Activity

2016

SummaryThe extracellular matrix (ECM) contributes to the biological and clinical heterogeneity of breast cancer, and different prognostic groups can be identified according to specific ECM signatures. In high-grade, but not low-grade, tumors, an ECM signature characterized by high SPARC expression (ECM3) identifies tumors with increased epithelial-to-mesenchymal transition (EMT), reduced treatment response, and poor prognosis. To better understand how this ECM3 signature is contributing to tumorigenesis, we expressed SPARC in isogenic cell lines and found that SPARC overexpression in tumor cells reduces their growth rate and induces EMT. SPARC expression also results in the formation of a h…

0301 basic medicineMyeloidMDSCGene Expressionmedicine.disease_causeT-Lymphocytes RegulatoryPolyethylene GlycolsExtracellular matrixMiceBreast cancerMyeloid CellsOsteonectinMast Cellslcsh:QH301-705.5Mice KnockoutAntigen PresentationMice Inbred BALB CEMTepithelial to mesenchymal transitionBreast cancer; COX-2; CXCL12; ECM; EMT; G-CSF; GM-CSF; MDSC; SPARC; aminobisphosphonates; cyclooxygenase-2; epithelial to mesenchymal transition; extracellular matrix; granulocyte colony-stimulating factor; granulocyte-macrophage colony-stimulating factor; myeloid-derived suppressor cellsCXCL12Granulocyte macrophage colony-stimulating factormedicine.anatomical_structurecyclooxygenase-2granulocyte-macrophage colony-stimulating factorFemalegranulocyte colony-stimulating factormedicine.drugEpithelial-Mesenchymal Transitionextracellular matrixAntineoplastic AgentsBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaG-CSFGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpithelial–mesenchymal transitionECMMesenchymal stem cellSPARCGM-CSFCOX-2myeloid-derived suppressor cellsXenograft Model Antitumor AssaysIsogenic human disease modelsaminobisphosphonates030104 developmental biologylcsh:Biology (General)CelecoxibDoxorubicinImmunologyCancer researchMyeloid-derived Suppressor CellaminobisphosphonateNeoplasm GradingCarcinogenesisCell Reports
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Myeloid cells as orchestrators of the tumor microenvironment: novel targets for nanoparticular cancer therapy.

2016

Macrophages, myeloid-derived suppressor cells and tolerogenic dendritic cells are central players of a heterogeneous myeloid cell population, with the ability to suppress innate and adaptive immune responses and thus to promote tumor growth. Their influx and local proliferation are mainly induced by the cancers themselves, and their numbers in the tumor microenvironment and the peripheral blood correlate with decreased survival. Therapeutic targeting these innate immune cells, either aiming at their elimination or polarization toward tumor suppressive cells is an attractive novel approach to control tumor progression and block metastasis. We review the current understanding of cancer immun…

0301 basic medicineMyeloidPolymersmedicine.medical_treatmentPopulationBiomedical EngineeringMedicine (miscellaneous)BioengineeringDevelopmentBiology03 medical and health sciences0302 clinical medicineImmune systemNeoplasmsmedicineTumor MicroenvironmentAnimalsHumansGeneral Materials ScienceMyeloid CellsRNA Small InterferingeducationCancer immunologyeducation.field_of_studyTumor microenvironmentDrug CarriersInnate immune systemMacrophagesMyeloid-Derived Suppressor CellsImmunotherapyDendritic CellsImmunity Innate030104 developmental biologymedicine.anatomical_structureTumor progression030220 oncology & carcinogenesisImmunologyNanoparticlesImmunotherapyNanomedicine (London, England)
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Accumulation of MDSC and Th17 Cells in Patients with Metastatic Colorectal Cancer Predicts the Efficacy of a FOLFOX-Bevacizumab Drug Treatment Regimen

2016

Abstract Host immunity controls the development of colorectal cancer, and chemotherapy used to treat colorectal cancer is likely to recruit the host immune system at some level. Athough preclinical studies have argued that colorectal cancer drugs, such as 5-fluorouracil (5-FU) and oxaliplatin, exert such effects, their combination as employed in the oncology clinic has not been evaluated. Here, we report the results of prospective immunomonitoring of 25 metastatic colorectal cancer (mCRC) patients treated with a first-line combination regimen of 5-FU, oxaliplatin, and bevacizumab (FOLFOX–bevacizumab), as compared with 20 healthy volunteers. Before this therapy was initiated, T regulatory ce…

0301 basic medicineOncologyCancer ResearchOrganoplatinum CompoundsColorectal cancermedicine.medical_treatmentLeucovorinKaplan-Meier EstimatePolymerase Chain ReactionSuppressor-Cells[ SDV.CAN ] Life Sciences [q-bio]/Cancer0302 clinical medicineFOLFOXAntineoplastic Combined Chemotherapy ProtocolsProspective StudiesProgressionFlow Cytometry3. Good healthBevacizumabOncology030220 oncology & carcinogenesisFluorouracilColorectal Neoplasmsmedicine.drugmedicine.medical_specialtyBevacizumabT-Cells[SDV.CAN]Life Sciences [q-bio]/CancerDisease-Free Survival03 medical and health sciencesInternal medicinemedicineCarcinomaHumansChemotherapyTumorsInflammationChemotherapyAntitumor Immunitybusiness.industryMyeloid-Derived Suppressor CellsCarcinomaCancermedicine.diseasedigestive system diseasesOxaliplatinRegimen030104 developmental biologyTherapiesImmunologyTh17 CellsPoor-Prognosisbusiness
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Baseline Splenic Volume as a Prognostic Biomarker of FOLFIRI Efficacy and a Surrogate Marker of MDSC Accumulation in Metastatic Colorectal Carcinoma

2020

Background: Predictive biomarkers of response to chemotherapy plus antiangiogenic for metastatic colorectal cancer (mCRC) are lacking. The objective of this study was to test the prognostic role of splenomegaly on baseline CT scan. Methods: This study is a sub-study of PRODIGE-9 study, which included 488 mCRC patients treated by 5-fluorouracil, leucovorin and irinotecan (FOLFIRI) and bevacizumab in first line. The association between splenic volume, and PFS and OS was evaluated by univariate and multivariable Cox analyses. The relation between circulating monocytic Myeloid derived suppressor cells (mMDSC) and splenomegaly was also determined. Results: Baseline splenic volume &gt

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyBevacizumabColorectal cancermedicine.medical_treatment[SDV]Life Sciences [q-bio]MDSClcsh:RC254-282Article03 medical and health sciences0302 clinical medicineInternal medicineMedicinePrognostic biomarkerprognostic biomarkerChemotherapysplenomegalybusiness.industrySurrogate endpointmetastatic colorectal cancerlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasedigestive system diseases3. Good healthIrinotecan030104 developmental biologyOncology030220 oncology & carcinogenesisMyeloid-derived Suppressor CellFOLFIRIcirculating monocytic myeloid derived suppressor cellsbusinessmedicine.drugCancers
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Schlafen-11 (SLFN11): a step forward towards personalized medicine in small-cell lung cancer?

2018

Purpose Both temozolomide (TMZ) and poly (ADP-ribose) polymerase (PARP) inhibitors are active in small-cell lung cancer (SCLC). This phase II, randomized, double-blind study evaluated whether addition of the PARP inhibitor veliparib to TMZ improves 4-month progression-free survival (PFS). Patients and Methods A total of 104 patients with recurrent SCLC were randomly assigned 1:1 to oral veliparib or placebo 40 mg twice daily, days 1 to 7, and oral TMZ 150 to 200 mg/m

0301 basic medicineOncologyMaleLung NeoplasmsDNA Mutational AnalysisPoly (ADP-Ribose) Polymerase-1Placebos0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsPromoter Regions GeneticDNA Modification MethylasesAged 80 and overStandard treatmentNuclear ProteinsMiddle AgedNeoplastic Cells CirculatingImmunohistochemistryhumanitiesEditorialOncology030220 oncology & carcinogenesisFemaleNon small cellAdultmedicine.medical_specialtyMEDLINEAggressive disease03 medical and health sciencesText miningDouble-Blind MethodInternal medicinemedicineBiomarkers TumorTemozolomideHumansLung cancerneoplasmsAntineoplastic Agents AlkylatingAgedbusiness.industryTumor Suppressor ProteinsDNA Methylationmedicine.diseaseSmall Cell Lung Carcinomarespiratory tract diseases030104 developmental biologyDNA Repair EnzymesBenzimidazolesPersonalized medicinebusiness
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