Search results for " lymphoma"

showing 10 items of 448 documents

Helicobacter pylori and Epstein–Barr Virus Infection in Gastric Diseases: Correlation with IL-10 and IL1RN Polymorphism

2019

Introduction. Helicobacter pylori and Epstein–Barr virus (EBV) infection have recently been shown to be associated with gastric diseases. Polymorphisms in genes encoding cytokines such as interleukin 10 (IL-10) and interleukin 1 Receptor (IL-1RN) influence cytokine secretion levels and appear to contribute to the risk of developing gastroduodenal diseases. To our knowledge, this is the first preliminary study to address the association of coinfection with H. pylori and EBV and their correlation with genetic predisposition in the development of gastric diseases. Methods. Gastric biopsy samples of 96 patients with different gastric diseases were used. Results. Our results showed that the rate…

0301 basic medicineSettore MED/07 - Microbiologia E Microbiologia ClinicaArticle Subjectpolymorphism gastric cancer IL-10Chronic gastritislcsh:RC254-28203 medical and health sciences0302 clinical medicineEBVHelicobactermedicineCagAEpstein–Barr virus infectionbiologybusiness.industryMALT lymphomaHelicobacter pylorimedicine.diseasebiology.organism_classificationlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensdigestive system diseases030104 developmental biologyOncology030220 oncology & carcinogenesisImmunologyCoinfectionCytokine secretionGastritismedicine.symptombusinessResearch ArticleJournal of Oncology
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11q Deletion or ALK Activity Curbs DLG2 Expression to Maintain an Undifferentiated State in Neuroblastoma

2020

High-risk 11q deleted neuroblastomas typically display undifferentiated/poorly differentiated morphology. Neuroblastoma is thought to develop from Schwann cell precursors and undifferentiated neural crest (NC) derived cells. It is therefore vital to understand mechanisms involved in the block of differentiation. We identify an important role for oncogenic ALK-ERK1/2-SP1 signaling in maintenance of undifferentiated NC-derived progenitors via repression of DLG2, a tumor suppressor in neuroblastoma. DLG2 is expressed in the ‘bridge signature’ that represents the transcriptional transition state when neural crest cells or Schwann Cell Precursors become chromaffin cells of the adrenal gland. We …

0301 basic medicineTranscription GeneticCarcinogenesisChromaffin CellsRetinoic acidlaw.inventionNeuroblastomachemistry.chemical_compound0302 clinical medicinelawNerve Growth FactorMedicine and Health Sciencesretinoic acidAnaplastic Lymphoma Kinaselcsh:QH301-705.5NeuronsMice Inbred BALB CNeural crestCell DifferentiationPrognosisCandidate Tumor Suppressor GeneDLG2Up-RegulationCell biologyGene Expression Regulation NeoplasticERKPhenotypeTreatment Outcomemedicine.anatomical_structureFemaleChromosome Deletiontumor suppressorMAP Kinase Signaling SystemSp1 Transcription FactorSchwann cellGenetics and Molecular BiologyTretinoinBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAdrenergic AgentsCell Line TumorNeuroblastomamedicineAnimalsHumansProgenitor cellGenePsychological repressionCell ProliferationChromosomes Human Pair 11Tumor Suppressor Proteinsmedicine.disease030104 developmental biologyALKlcsh:Biology (General)chemistryTrk receptorGeneral BiochemistrySuppressorSchwann CellsGuanylate Kinases030217 neurology & neurosurgerySSRN Electronic Journal
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Active Akt signaling triggers CLL toward Richter transformation via overactivation of Notch1

2021

Abstract Richter’s transformation (RT) is an aggressive lymphoma that occurs upon progression from chronic lymphocytic leukemia (CLL). Transformation has been associated with genetic aberrations in the CLL phase involving TP53, CDKN2A, MYC, and NOTCH1; however, a significant proportion of RT cases lack CLL phase–associated events. Here, we report that high levels of AKT phosphorylation occur both in high-risk CLL patients harboring TP53 and NOTCH1 mutations as well as in patients with RT. Genetic overactivation of Akt in the murine Eµ-TCL1 CLL mouse model resulted in CLL transformation to RT with significantly reduced survival and an aggressive lymphoma phenotype. In the absence of recurren…

0301 basic medicineTumor microenvironmentChronic lymphocytic leukemiaImmunologyNotch signaling pathwayMedizinAggressive lymphomaCell BiologyHematologyBiologymedicine.diseaseBiochemistrySomatic evolution in cancerLymphoma03 medical and health sciencesLeukemia030104 developmental biology0302 clinical medicineimmune system diseaseshemic and lymphatic diseasesmedicineCancer researchneoplasmsProtein kinase B030215 immunology
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T-Cell Lymphoma Clonality by Copy Number Variation Analysis of T-Cell Receptor Genes

2021

Simple Summary T-cells defend the human body from pathogenic invasion via specific recognition by T-cell receptors (TCRs). The TCR genes undergo recombination (rearrangement) in a myriad of possible ways to generate different TCRs that can recognize a wide diversity of foreign antigens. However, in patients with T-cell lymphoma (TCL), a particular T-cell becomes malignant and proliferates, resulting in a population of genetically identical cells with same TCR rearrangement pattern. To help diagnose patients with TCL, a polymerase chain reaction (PCR)-based assay is currently used to determine if neoplastic cells in patient samples are of T-cell origin and bear identical (monoclonal) TCR rea…

0301 basic medicineclone (Java method)Cancer ResearchclonalityBiologylcsh:RC254-282Article03 medical and health sciences0302 clinical medicinemedicineT-cell lymphomaT-cell receptorCopy-number variationcopy number variation analysisGeneWhole genome sequencingwhole genome sequencingT-cell receptorlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseMolecular biology030104 developmental biologyOncology030220 oncology & carcinogenesisT-Cell Receptor GeneMonoclonalT-cell lymphomaClonality Copy number variation analysis T-cell lymphoma T-cell receptor Whole genome sequencingCancers
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Intra-tumour heterogeneity of diffuse large B-cell lymphoma involves the induction of diversified stroma-tumour interfaces

2020

Abstract Background Intra-tumour heterogeneity in lymphoid malignancies encompasses selection of genetic events and epigenetic regulation of transcriptional programs. Clonal-related neoplastic cell populations are unsteadily subjected to immune editing and metabolic adaptations within different tissue microenvironments. How tissue-specific mesenchymal cells impact on the diversification of aggressive lymphoma clones is still unknown. Methods Combining in situ quantitative immunophenotypical analyses and RNA sequencing we investigated the intra-tumour heterogeneity and the specific mesenchymal modifications that are associated with A20 diffuse large B-cell lymphoma (DLBCL) cells seeding of d…

0301 basic medicinediffuse large B-cell lymphoma; digital spatial profiling; intra-tumour heterogeneity; microenvironment; SPARClcsh:MedicineMice0302 clinical medicineimmune system diseaseshemic and lymphatic diseasesTumor MicroenvironmentIn Situ Hybridizationlcsh:R5-920Matricellular proteinGeneral MedicineDiffuse large B-cell lymphomaPrognosisGene Expression Regulation NeoplasticPhenotype030220 oncology & carcinogenesisLymphoma Large B-Cell Diffuselcsh:Medicine (General)Research PaperStromal cellMicroenvironmentTumour heterogeneityBiologySettore MED/08 - Anatomia PatologicaModels BiologicalGeneral Biochemistry Genetics and Molecular BiologyImmunophenotypingGenetic Heterogeneity03 medical and health sciencesImmune systemCell Line TumorBiomarkers TumormedicineAnimalsHumansEpigeneticsSequence Analysis RNAGene Expression Profilinglcsh:RMesenchymal stem cellComputational BiologySPARCDigital spatial profilingmedicine.diseaseIntra-tumour heterogeneityDisease Models Animal030104 developmental biologyCancer researchNeoplastic cellStromal CellsTranscriptomeDiffuse large B-cell lymphoma
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IL-25 dampens the growth of human germinal center-derived B-cell non Hodgkin Lymphoma by curtailing neoangiogenesis

2018

Interleukin (IL)-25, a member of the IL-17 cytokine superfamily, is produced by immune and non-immune cells and exerts type 2 pro-inflammatory effects in vitro and in vivo. The IL-25 receptor(R) is composed of the IL-17RA/IL-17RB subunits. Previous work showed that germinal centre (GC)-derived B-cell non Hodgkin lymphomas (B-NHL) expressed IL-17AR, formed by IL-17RA and IL-17RC subunits, and IL-17A/IL-17AR axis promoted B-NHL growth by stimulating neoangiogenesis. Here, we have investigated expression and function of IL-25/IL-25R axis in lymph nodes from human GC-derived B-NHL, i.e. Follicular Lymphoma (FL,10 cases), Diffuse Large B Cell Lymphoma (6 cases) and Burkitt Lymphoma (3 cases). Tu…

0301 basic medicinelcsh:Immunologic diseases. AllergyPathologymedicine.medical_specialtyAngiogenesismedicine.medical_treatmentImmunologyFollicular lymphomalcsh:RC254-282Angiogenesis; B lymphocytes; B-NHL; Cytokines; IL-25; Tumor immunology; Immunology and Allergy; Immunology; Oncology03 medical and health sciencesangiogenesisIL-25immune system diseaseshemic and lymphatic diseasesmedicineImmunology and AllergyCytokineOriginal ResearchB lymphocyteChemistryGerminal centerInterleukinmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenscytokinesLymphomaAngiogenesi030104 developmental biologyCytokineOncologyCancer researchB-Cell Non-Hodgkin LymphomaTumor immunologyB-NHLb lymphocyteslcsh:RC581-607Diffuse large B-cell lymphoma
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Hepatic B cell leukemia-3 promotes hepatic steatosis and inflammation through insulin-sensitive metabolic transcription factors.

2016

Background & Aims The pathomechanisms underlying non-alcoholic fatty liver disease (NAFLD) and the involved molecular regulators are incompletely explored. The nuclear factor-kappa B (NF-κB)-cofactor gene B cell leukemia-3 ( Bcl-3 ) plays a critical role in altering the transcriptional capacity of NF-κB – a key inducer of inflammation – but also of genes involved in cellular energy metabolism. Methods To define the role of Bcl-3 in non-alcoholic steatohepatitis (NASH), we developed a novel transgenic mouse model with hepatocyte-specific overexpression of Bcl-3 ( Bcl-3 Hep ) and employed a high-fat, high-carbohydrate dietary feeding model. To characterize the transgenic model, deep RNA seque…

0301 basic medicinemedicine.medical_specialtyCirrhosisCarcinoma Hepatocellularmedicine.medical_treatmentBiology03 medical and health sciencesLiver diseaseMice0302 clinical medicineB-Cell Lymphoma 3 ProteinInternal medicineProto-Oncogene ProteinsmedicineAnimalsHumansInsulinInflammationHepatologyInsulinLiver cellFatty liverLiver Neoplasmsmedicine.disease030104 developmental biologyEndocrinology030220 oncology & carcinogenesisLipogenesisSteatohepatitisSteatosisTranscription FactorsJournal of hepatology
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Safety and Clinical Activity of Temsirolimus in Combination with Rituximab and DHAP in Patients with Relapsed or Refractory Diffuse Large B-Cell Lymp…

2016

Abstract Purpose. To evaluate the safety, tolerability and efficacy of the combination of the mTOR inhibitor Temsirolimus and a standard salvage regimen (R-DHAP) in patients with relapsed or refractory diffuse large cell B-Cell lymphoma (DLBCL). Methods. This is a prospective, multicenter, phase II, open-label study. Patients with relapsed or refractory DLBCL with a maximum of two prior treatment lines were eligible. The STORM regimen consisted of Rituximab 375 mg/m² (day 2) and DHAP (Dexamethasone 40mg day 3-6, Cisplatine 100 mg/m² day 3, Cytarabine 2x2 g/m² day 4) with Temsirolimus added on day 1 and 8 of a 21 d cycle, with 2-4 cycles planned. In part I, dose levels of 25, 50, 75 and 100 …

0301 basic medicinemedicine.medical_specialtyImmunologyNeutropeniaBiochemistry03 medical and health sciences0302 clinical medicineMedian follow-upInternal medicinemedicineLeukopeniabusiness.industryCell BiologyHematologymedicine.diseaseTemsirolimusSurgeryRegimen030104 developmental biologyTolerability030220 oncology & carcinogenesisRituximabmedicine.symptombusinessDiffuse large B-cell lymphomamedicine.drugBlood
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A practical algorithmic approach to mature aggressive B cell lymphoma diagnosis in the double/triple hit era. Selecting cases, matching clinical bene…

2019

An accurate diagnosis of clinically distinct subgroups of aggressive mature B cell lymphomas is crucial for the choice of proper treatment. Presently, precise recognition of these disorders relies on the combination of morphological, immunophenotypical, and cytogenetic/molecular features. The diagnostic workup in such situations implies the application of costly and time-consuming analyses, which are not always required, since an intensified treatment option is reasonably reserved to fit patients. The Italian Group of Haematopathology proposes herein a practical algorithm for the diagnosis of aggressive mature B cell lymphomas based on a stepwise approach, aimed to select cases deserving mo…

0301 basic medicinemedicine.medical_specialtyMatching (statistics)Lymphoma B-CellLymphomadouble hitComputer scienceMYCDouble hitFluorescencePathology and Forensic MedicineImmunophenotyping03 medical and health sciences0302 clinical medicineFISHDiagnosismedicinePractical algorithmHumansIntensive care medicineB-cell lymphomaMolecular BiologyIn Situ HybridizationIn Situ Hybridization FluorescenceHGBLBrief ReportB-CellTreatment optionsCorrectionDiagnosis; DLBCL; Double hit; FISH; HGBL; MYC; Humans; Immunophenotyping; In Situ Hybridization Fluorescence; Lymphoma B-Cell; AlgorithmsCell BiologyGeneral MedicineDiagnosis DLBCL Double hit FISH HGBL MYCmedicine.diseaseDiagnosis; DLBCL; double hit; FISH; HGBL; MYCOptimal managementMolecular analysis030104 developmental biology030220 oncology & carcinogenesisDLBCLPosition paperProper treatmentAlgorithmsDiagnosiHuman
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The B-cell receptor in control of tumor B-cell fitness: Biology and clinical relevance

2019

Surface expression of a functional B cell antigen receptor (BCR) is essential for the survival and proliferation of mature B cells. Most types of B-cell lymphoproliferative disorders retain surface BCR expression, including B-cell non-Hodgkin lymphomas (B-NHL) and chronic lymphocytic leukemia (CLL). Targeting BCR effectors in B-NHL cell lines in vitro has indicated that this signaling axis is crucial for malignant B cell growth. This has led to the development of inhibitors of BCR signaling, which are currently used for the treatment of CLL and several B-NHL subtypes. Recent studies based on conditional BCR inactivation in a MYC-driven mouse B-cell lymphoma model have revisited the role of …

0301 basic medicinetumor cell fitnessChronic lymphocytic leukemiaImmunologyB-cell receptorPopulationReceptors Antigen B-CellLymphoproliferative disorderslymphomaBiologyMice03 medical and health sciences0302 clinical medicineimmune system diseaseshemic and lymphatic diseasesB-cell receptorTumor MicroenvironmentmedicineAnimalsHumansImmunology and AllergyeducationHematologic NeoplasmB cellBCR inhibitorB-Lymphocyteseducation.field_of_studyAnimalB-Lymphocytebreakpoint cluster regionB-cell receptor; BCR inhibitors; c-MYC; lymphoma; lymphoma resistance; tumor cell fitnesslymphoma resistancemedicine.diseaseLymphoproliferative DisordersLymphomaBCR inhibitorsPhenotype030104 developmental biologymedicine.anatomical_structurec-MYCtumor cell fitneCell cultureLymphoproliferative DisorderHematologic NeoplasmsCancer researchHumanSignal Transduction030215 immunology
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