Search results for "Diseases of the blood and blood-forming organs"

showing 10 items of 38 documents

Trabectedin triggers direct and NK-mediated cytotoxicity in multiple myeloma

2019

Background Genomic instability is a feature of multiple myeloma (MM), and impairment in DNA damaging response (DDR) has an established role in disease pathobiology. Indeed, a deregulation of DNA repair pathways may contribute to genomic instability, to the establishment of drug resistance to genotoxic agents, and to the escape from immune surveillance. On these bases, we evaluated the role of different DDR pathways in MM and investigated, for the first time, the direct and immune-mediated anti-MM activity of the nucleotide excision repair (NER)-dependent agent trabectedin. Methods Gene-expression profiling (GEP) was carried out with HTA2.0 Affymetrix array. Evaluation of apoptosis, cell cyc…

0301 basic medicineCancer ResearchCell cycle checkpointNatural killerDNA repairmedicine.medical_treatmentMyelomalcsh:RC254-28203 medical and health sciences0302 clinical medicineMicro-RNAmedicineHumansMolecular BiologyAntineoplastic Agents AlkylatingTrabectedin3D-modelChemistrylcsh:RC633-647.5ResearchMicro-RNAsHematologylcsh:Diseases of the blood and blood-forming organsCell cycleNKG2Dlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensKiller Cells Natural030104 developmental biologyCytokineOncologyApoptosis3D-models030220 oncology & carcinogenesis3D-models; Micro-RNAs; Myeloma; Natural killer; TrabectedinCancer researchDNA fragmentationMultiple Myelomamedicine.drugTrabectedinJournal of Hematology & Oncology
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Multiple myeloma-derived exosomes are enriched of amphiregulin (AREG) and activate the epidermal growth factor pathway in the bone microenvironment l…

2019

Background Multiple myeloma (MM) is a clonal plasma cell malignancy associated with osteolytic bone disease. Recently, the role of MM-derived exosomes in the osteoclastogenesis has been demonstrated although the underlying mechanism is still unknown. Since exosomes-derived epidermal growth factor receptor ligands (EGFR) are involved in tumor-associated osteolysis, we hypothesize that the EGFR ligand amphiregulin (AREG) can be delivered by MM-derived exosomes and participate in MM-induced osteoclastogenesis. Methods Exosomes were isolated from the conditioned medium of MM1.S cell line and from bone marrow (BM) plasma samples of MM patients. The murine cell line RAW264.7 and primary human CD1…

0301 basic medicineCancer ResearchOsteoclastsPlasma cellInterleukin 8ExosomesLigandsMice0302 clinical medicineEpidermal growth factorOsteogenesisMultiple myelomaBone diseaseTumor MicroenvironmentEpidermal growth factor receptorbiologyChemistryAntibodies MonoclonalOsteoblastCell DifferentiationHematologylcsh:Diseases of the blood and blood-forming organslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensErbB Receptorsmedicine.anatomical_structureOncology030220 oncology & carcinogenesislcsh:RC254-282Amphiregulin03 medical and health sciencesAmphiregulinOsteoclastCell Line TumormedicineCell AdhesionAnimalsHumansMolecular BiologyOsteoblastsEpidermal Growth Factorlcsh:RC633-647.5Epidermal growth factor receptorResearchMesenchymal stem cellInterleukin-8Mesenchymal Stem CellsMicrovesiclesExosome030104 developmental biologyRAW 264.7 CellsCancer researchbiology.protein
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Paroxysmal nocturnal haemoglobinuria: When delay in diagnosis and long therapy occurs

2017

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare clonal disorder characterized by hemolytic anemia, bone marrow failure and thrombosis, caused by a somaticmutation in PIG-A gene that results in theabsence of CD55 and CD59, two important complement regulatory proteins. In thispaper, a case of PNH is retrospectively examined looking for clinical and laboratory features, and the entire course of the disease from the onset of the symptoms isdescribed, together with an adequate follow-up over a 7-years treatment period. Inthis case, the not specificity and the limited clinical relevance of the symptoms led to adelay in diagnosis. After thrombosis, Eculizumab therapy has been shown to be effec…

0301 basic medicineHemolytic anemiaPediatricsmedicine.medical_specialtyrenal failureParoxysmal nocturnal haemoglobinuriaparoxysmal nocturnal hemoglobinuriaCase ReportDiseaseCD5903 medical and health sciencesthrombotic eventshemic and lymphatic diseasesMedicineClinical significancebusiness.industrylcsh:RC633-647.5Bone marrow failureHematologylcsh:Diseases of the blood and blood-forming organsEculizumabEculizumabmedicine.diseaseThrombosisparoxysmal nocturnal hemoglo-binuria thrombotic events renal failure Eculizumab030104 developmental biologyParoxysmal nocturnal hemoglobinuriabusinessmedicine.drug
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Phospho-Akt overexpression is prognostic and can be used to tailor the synergistic interaction of Akt inhibitors with gemcitabine in pancreatic cancer

2017

Background There is increasing evidence of a constitutive activation of Akt in pancreatic ductal adenocarcinoma (PDAC), associated with poor prognosis and chemoresistance. Therefore, we evaluated the expression of phospho-Akt in PDAC tissues and cells, and investigated molecular mechanisms influencing the therapeutic potential of Akt inhibition in combination with gemcitabine. Methods Phospho-Akt expression was evaluated by immunohistochemistry in tissue microarrays (TMAs) with specimens tissue from radically-resected patients (n = 100). Data were analyzed by Fisher and log-rank test. In vitro studies were performed in 14 PDAC cells, including seven primary cultures, characterized for their…

0301 basic medicineOncologyMaleCancer ResearchBiopsyAKT1ApoptosisAkt; Gemcitabine; Pancreatic ductal adenocarcinoma; Synergism; Hematology; Molecular Biology; Oncology; Cancer ResearchDeoxycytidinePancreatic ductal adenocarcinoma0302 clinical medicineCell MovementTumor Cells CulturedGlucose Transporter Type 1medicine.diagnostic_testChemistryCell CyclePancreatic NeoplasmDrug Synergismlcsh:Diseases of the blood and blood-forming organsHematologyCell cycleMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisOncologyAkt; Gemcitabine; Pancreatic ductal adenocarcinoma; Synergism; Aged; Apoptosis; Biopsy; Carcinoma Pancreatic Ductal; Cell Cycle; Cell Movement; Deoxycytidine; Drug Synergism; Female; Glucose Transporter Type 1; Humans; Male; Middle Aged; Pancreatic Neoplasms; Phosphoproteins; Prognosis; Proto-Oncogene Proteins c-akt; RNA Messenger; Spheroids Cellular; Tumor Cells Cultured; Hematology; Molecular Biology; Oncology; Cancer Research030220 oncology & carcinogenesisPhosphoproteinFemalemedicine.drugHumanCarcinoma Pancreatic Ductalmedicine.medical_specialtyPrognosilcsh:RC254-282Flow cytometry03 medical and health sciencesInternal medicinePancreatic cancerSpheroids CellularmedicineHumansRNA MessengerProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayAgedlcsh:RC633-647.5ResearchAktSynergismApoptosimedicine.diseasePhosphoproteinsGemcitabineGemcitabinePancreatic Neoplasms030104 developmental biologyCancer cellCancer researchProto-Oncogene Proteins c-akt
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Immunoistochemical expression of PD-1 and PD-L1 in bone marrow biopsies of patients with acute myeloid leukemia

2020

Background. Haematological and non-haematological malignancies are able to escape the host immune by the capacity to hijack the immune check-points. Several immune check-point molecules are known, such as T cell immunoglobulin mucin-3 (TIM-3), cytotoxic T-cell antigen-4 (CTLA-4), programmed death-1 (PD-1) with its ligand PD-L1 and others.1 The function of these immune check-points is to prevent the damage resulting from an excessive activation of the immune response in the setting of chronic antigenic stimulation, thus leading to autoimmune phenomena, as proved in knock-out mice models. PD-1 is normally present on activated T lymphocytes membrane, acting as a negative costimulatory receptor…

0301 basic medicinemedicine.medical_treatmentvirusesanimal diseaseschemical and pharmacologic phenomena03 medical and health sciences0302 clinical medicinePD-L1Medicinebiologybusiness.industrylcsh:RC633-647.5Myeloid leukemiaHematologyImmunotherapylcsh:Diseases of the blood and blood-forming organsAcute myeloid leukemia Immune check-point blockade Immunotherapy PD-1 PD-L1biochemical phenomena metabolism and nutritionacute myeloid leukemia; immune check-point blockade; PD-1; PD-L1; immunotherapy030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisCancer researchbiology.proteinbacteriaBone marrowbusinessHematology Reports
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Genotypic and Phenotypic Characteristics of Acute Promyelocytic Leukemia Translocation Variants.

2020

Acute promyelocytic leukemia (APL) is a special disease entity of acute myeloid leukemia (AML). The clinical use of all-trans retinoic acid (ATRA) has transformed APL into the most curable form of AML. The majority of APL cases are characterized by the fusion gene PML-RARA. Although the PML-RARA fusion gene can be detected in almost all APL cases, translocation variants of APL have been reported. To date, this is the most comprehensive review of these translocations, discussing 15 different variants. Reviewed genes involved in APL variants include: ZBTB16, NPM, NuMA, STAT5b, PRKAR1A, FIP1L1, BCOR, NABP1, TBLR1, GTF2I, IRF2BP2, FNDC3B, ADAMDTS17, STAT3, and TFG. The genotypic and phenotypic …

Acute promyelocytic leukemiaGenotypeSTAT5BChromosomal translocationFusion geneslcsh:RC254-282Translocation GeneticFusion gene03 medical and health sciences0302 clinical medicineLeukemia Promyelocytic AcuteAcute promyelocytic leukemiaimmune system diseasesMedicineHumansneoplasmsPRKAR1AGeneRARAlcsh:RC633-647.5business.industryMyeloid leukemialcsh:Diseases of the blood and blood-forming organsHematologyGeneral Medicinelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseFusion proteinNeoplasm ProteinsOncology030220 oncology & carcinogenesisCancer researchbusinessChimeric proteins030215 immunologyHematology/oncology and stem cell therapy
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Final Results of a Phase I/II Trial of the Combination Bendamustine and Rituximab With Temsirolimus (BeRT) in Relapsed Mantle Cell Lymphoma and Folli…

2020

Abstract. In this phase I/II study, we explored the combination of Temsirolimus with Bendamustine and Rituximab (BeRT) in patients with relapsed or refractory (r/r) follicular lymphoma (FL) or mantle cell lymphoma (MCL). Patients with 1 to 3 previous therapies received Bendamustine (90 mg/m2, day 1 + 2) and Rituximab (375 mg/m2, day 1) with Temsirolimus in doses from 25 to 75 mg in phase I and 50 mg Temsirolimus in phase II, added on day 1, 8, 15 of a 28 days cycle. The primary endpoint of the phase II was ORR at the end of treatment. Overall, 39 (29 MCL, 10 FL) patients were included. Median age was 71 years and median pretreatment number was 2. Grade 3/4 non-hematologic adverse events wer…

Bendamustinemedicine.medical_specialtyCancer ResearchLeukopeniabusiness.industrylcsh:RC633-647.5Follicular lymphomaHematologylcsh:Diseases of the blood and blood-forming organsNeutropeniamedicine.diseaseGastroenterology002TemsirolimusArticleRegimenInternal medicinehemic and lymphatic diseasesmedicineMantle cell lymphomaRituximabmedicine.symptombusinessmedicine.drugHemaSphere
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Anticoagulation in splanchnic and cerebral vein thrombosis: Still groping in the dark.

2020

Cerebral veinsmedicine.medical_specialtybusiness.industrymedicine.drug_classSplanchnic Circulation10031 Clinic for Angiology2720 HematologyAnticoagulantanticoagulantvenous thromboembolism610 Medicine & healthHematologyCerebral vein thrombosisbleedingcerebral veinsplanchnic circulationsInternal medicineCardiologyCommentaryMedicineDiseases of the blood and blood-forming organsRC633-647.5businessSplanchnicVenous thromboembolismResearch and practice in thrombosis and haemostasis
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Granulocyte–Colony Stimulating Factor plus Plerixafor in Patients with β-thalassemia Major Results in the Effective Mobilization of Primitive CD34+ C…

2017

Successful gene therapy for β-thalassemia requires optimal numbers of autologous gene-transduced hematopoietic stem and progenitor cells (HSPCs) with high repopulating capacity. Previous studies suggested superior mobilization in these patients by the combination of granulocyte–colony stimulating factor (G-CSF) plus plerixafor over single agents. We mobilized four adult patients using G-CSF+plerixafor to assess the intra-individual variation of the circulating CD34+ cells number and subtypes preand post-plerixafor administration. The procedure was well-tolerated and the target cell dose of ≥8×10 6 CD34+ cells/kg was achieved in three of them with one apheresis procedure. The addition of ple…

Mobilizationbusiness.industryCD34+ cells expression profilingCd34 cellsPlerixaforGenetic enhancementβ-thalassemia; CD34 cells expression profiling; G-CSF plerixafor mobilization; gene therapygene therapySettore MED/15 - Malattie Del SangueGranulocyte colony-stimulating factorSettore BIO/18 - Geneticagene therapy.β-thalassemiaGene expressionImmunologyCancer researchG-CSF+plerixafor mobilizationMedicineDiseases of the blood and blood-forming organsIn patientβ-thalassemia; CD34+ cells expression profiling; G-CSF+plerixafor mobilization; gene therapyRC633-647.5businessβ thalassemia majormedicine.drugThalassemia Reports
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The mTOR Inhibitor Temsirolimus Added to Rituximab Combined With Dexamethasone, Cytarabine, and Cisplatinum (R-DHAP) for the Treatment of Patients Wi…

2021

There is a high need for novel treatment options in relapsed and refractory diffuse large B-cell lymphoma. Single agent mammalian target of rapamycin (mTOR) inhibitor treatment has shown promising efficacy in this entity. Here, we report on the results of the mTOR-inhibitor temsirolimus combined to standard rituximab-DHAP salvage regimen in a prospective, multicenter, phase II, open-label study. The STORM regimen consisted of rituximab 375 mg/m(2) (day 2) and DHAP (dexamethasone 40 mg day 3-6, cisplatinum 100 mg/m(2) day 3, cytarabine 2 × 2  g/m(2) day 4) with temsirolimus added on day 1 and 8 of a 21-day cycle, with 2 to 4 cycles planned. In part I, dose levels of 25, 50, 75, and 100 mg fo…

OncologyCancer Researchmedicine.medical_specialtybusiness.industryHematology002ArticleTemsirolimusddc:TransplantationRegimenRefractoryInternal medicineDHAPmedicineCytarabineDiseases of the blood and blood-forming organsRituximabRC633-647.5businessDexamethasonemedicine.drug
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