Search results for " progress."

showing 10 items of 1281 documents

Progressive multifocal encephalopathy in a patient with non-Hodgkin follicular lymphoma

2020

Progressive multifocal leukoencephalopathy (PML) is a rare and often fatal demyelinating disease of the central nervous system caused by John Cunningham virus (JCV). We present a case report of patient with non-Hodgkin follicular lymphoma, who developed PML after hematopoietic stem cell transplantation and rituximab-bendamustine therapy. JCV DNA was proven both in peripheral blood and cerebrospinal fluid. Patient with 4 years history of follicular lymphoma presented with progressing weakness in the right arm and leg and postural instability. Magnetic resonance imaging scans showed bilateral hyperintense lesions in the cerebellum and centrum semiovale consistent with findings in PML. JCV DNA…

Cancer ResearchPathologymedicine.medical_specialtyvirusesmedicine.medical_treatmentEncephalopathyFollicular lymphomaHematopoietic stem cell transplantationImmunocompromised HostCerebrospinal fluidAntineoplastic Combined Chemotherapy ProtocolsCentrum semiovalemedicineDemyelinating diseaseHumansLymphoma Follicularmedicine.diagnostic_testbusiness.industryProgressive multifocal leukoencephalopathyHematopoietic Stem Cell TransplantationLeukoencephalopathy Progressive MultifocalDisease ManagementMagnetic resonance imagingMiddle Agedmedicine.diseaseMagnetic Resonance ImagingTreatment OutcomeOncologyPositron-Emission TomographyFemaleTomography X-Ray ComputedbusinessExperimental Oncology
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Development of resistance towards artesunate in MDA-MB-231 human breast cancer cells.

2011

Breast cancer is the most common cancer and the second leading cause of cancer death in industrialized countries. Systemic treatment of breast cancer is effective at the beginning of therapy. However, after a variable period of time, progression occurs due to therapy resistance. Artesunate, clinically used as anti-malarial agent, has recently revealed remarkable anti-tumor activity offering a role as novel candidate for cancer chemotherapy. We analyzed the anti-tumor effects of artesunate in metastasizing breast carcinoma in vitro and in vivo. Unlike as expected, artesunate induced resistance in highly metastatic human breast cancer cells MDA-MB-231. Likewise acquired resistance led to abol…

Cancer ResearchPhytochemistryPhytopharmacologyCancer TreatmentArtesunateApoptosisElectrophoretic Mobility Shift AssayDrug resistanceNude MiceMetastasischemistry.chemical_compoundMiceMolecular Cell BiologyDrug DiscoveryBreast TumorsBasic Cancer ResearchMedicinebcl-2-Associated X ProteinMultidisciplinaryQRNF-kappa BArtemisininsChemistryOncologyMedicineFemaleMatrix Metalloproteinase 1Breast carcinomamedicine.drugResearch Article570Drugs and DevicesDrug Research and DevelopmentCell SurvivalScienceMice Nude570 Life SciencesBreast NeoplasmsTumor Cell Line610 Medical Sciences MedicineBreast cancerComplementary and Alternative MedicineCell Line TumorAnimalsHumansDoxorubicinBiologyNeoplasm Drug Resistancebusiness.industryCancers and NeoplasmsChemotherapy and Drug Treatmentmedicine.diseaseXenograft Model Antitumor AssaysTranscription Factor AP-1chemistryTumor progressionArtesunateDrug Resistance NeoplasmCancer cellImmunologyEthnopharmacologyCancer researchbusinessPloS one
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Refining sorafenib therapy: lessons from clinical practice

2015

ABSTRACT  Understanding the best use of sorafenib is essential in order to maximize clinical benefit in hepatocellular carcinoma. Based on Phase III and noninterventional study data, as well as our extensive experience, we discuss dose modification in order to manage adverse events, disease response evaluation and how to maximize treatment benefit. Sorafenib should be initiated at the approved dose (400 mg twice daily) and reduced/interrupted as appropriate in order to manage adverse events. Dose modification should be considered before discontinuation. Appropriate tumor response assessment is critical. Focusing on radiologic response may result in premature sorafenib discontinuation; symp…

Cancer ResearchSettore SECS-P/06 - Economia ApplicataAntineoplastic AgentAge FactorChild–Pugh Bpostprogression treatmentresponse assessmentdose modificationClinical Trials as TopicLiver Neoplasmsadverse event managementAge FactorsChild-Pugh Bpostprogression treatmenthepatocellular carcinomaGeneral MedicinePrognosisadverse event management; child–Pugh B; dose modification; elderly hepatocellular carcinoma; mRECIST; postprogression treatment; eal-world data; response assessment; sorafenibelderly hepatocellular carcinomaCombined Modality Therapychild–Pugh BClinical PracticeTreatment OutcomeOncologyLiver Neoplasmeal-world dataHepatocellular carcinomaadverse event managementRetreatmentDisease Progressiondose modificationHumanmedicine.drugPhenylurea CompoundNiacinamideSorafenibmedicine.medical_specialtyCarcinoma HepatocellularDisease ResponsePrognosielderly hepatocellular carcinomaProtein Kinase InhibitorAntineoplastic AgentsmRECISTelderlymRECISTAdverse event management Child–Pugh B dose modification elderly hepatocellular carcinoma mRECIST postprogression treatment real-world data response assessment sorafenibmedicineChild–Pugh BHumansCombined Modality TherapyIntensive care medicineAdverse effectProtein Kinase InhibitorsDose Modificationreal-world databusiness.industryPhenylurea Compoundsmedicine.diseaseDiscontinuationSurgeryreal-world dataresponse assessmentsorafenibbusinessFuture Oncology
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Tumor and its microenvironment: a synergistic interplay.

2013

The mutual and interdependent interaction between tumor and its microenvironment is a crucial topic in cancer research. Recently, it was reported that targeting stromal events could improve efficacies of current therapeutics and prevent metastatic spreading. Tumor microenvironment is a "complex network" of different cell types, soluble factors, signaling molecules and extracellular matrix components, which orchestrate the fate of tumor progression. As by definition, cancer stem cells (CSCs) are proposed to be the unique cell type able to maintain tumor mass and survive outside the primary tumor at metastatic sites. Being exposed to environmental stressors, including reactive oxygen species …

Cancer ResearchStromal cellEpithelial-Mesenchymal TransitionAngiogenesisCell SurvivalBiologyCancer stem cellCell MovementNeoplasmsmedicineTumor MicroenvironmentAnimalsHumansEpithelial–mesenchymal transitionNeoplasm MetastasisStem Cell NicheHypoxiaTumor microenvironmentNeovascularization Pathologicmedicine.diseaseAngiogenesis CAFs CAMs CRC CSCs ECM EMT GSH HIF Hypoxia MMPs ROS Tumor microenvironment VEGF cancer stem cells cancer-associated fibroblasts cancer-associated macrophages colorectal cancer epithelial mesenchymal transition extracellular matrix hypoxia-inducible factor matrix metalloproteinase reactive oxygen species reduced glutathione vascular endothelial growth factorPrimary tumorTumor progressionImmunologyCancer researchNeoplastic Stem CellsCancer-Associated FibroblastsOxidation-ReductionSignal Transduction
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Tumor-intrinsic and -extrinsic roles of c-Kit: mast cells as the primary off-target of tyrosine kinase inhibitors.

2011

c-Kit tyrosine kinase receptor and its ligand stem cell factor have multiple functions during development, whereas in adulthood they are mostly needed for stem cell (SC) maintenance and mast cell (MC) biology. c-Kit plays an essential tumor-cell-intrinsic role in many types of cancer, either providing the tumorigenic force when aberrantly activated or conferring stem-like features characterizing the most aggressive variants. A tumor-cell-extrinsic role occurs through c-Kit-dependent accessory cells (such as MCs) that infiltrate tumors and deeply influence their progression. c-Kit-targeted therapy with tyrosine kinase inhibitors (TKIs) may ideally work against both tumor and stromal cells. H…

Cancer ResearchStromal cellStem cell factorAntineoplastic AgentsBiologyc-kit; mast cells; mouse mutants; off-target; tyrosine kinase inhibitorsReceptor tyrosine kinaseMicec-KitNeoplasmstyrosine kinase inhibitorsGeneticsmedicineAnimalsHumansNeoplasm InvasivenessMast CellsMolecular BiologyProtein Kinase InhibitorsStem Cell Factormouse mutantsNeovascularization PathologicMast cellRatsProto-Oncogene Proteins c-kitmedicine.anatomical_structureTumor progressionmast cells.biology.proteinCancer researchStem cellTyrosine kinasePlatelet-derived growth factor receptoroff-targetMastocytosisOncogene
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Dendritic cells as mediators of tumor-induced tolerance in metastatic melanoma.

1997

Escape from immune surveillance is critical for tumor progression in metastatic melanoma. We assessed the function of melanoma-derived dendritic cells (DCs) in patients presenting simultaneously with responding (rM) or progressing (pM) melanoma metastases. These rare coincidences allowed us to compare syngeneically the function of tumor DCs. CD83+ DCs were purified freshly from large responding (rDCs) or progressing (pDCs) metastases following chemo-immunotherapy. rDCs were 5 times more potent inducers of allogeneic T-cell proliferation than the pDCs that were used as control. Phenotypic analysis showed a marked depression of CD86 expression on pDCs. Culture supernatants from pM showed prod…

Cancer ResearchT-LymphocytesImmune toleranceImmune systemAntigens CDAntigens NeoplasmAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansAntigen-presenting cellMelanomaCD86Membrane Glycoproteinsbusiness.industryMelanomaInterferon-alphahemic and immune systemsDendritic cellDendritic Cellsmedicine.diseaseInterleukin-10Neoplasm ProteinsTolerance inductionOncologyTumor progressionImmunologyCytokinesInterleukin-2Tumor EscapeB7-2 AntigenCisplatinbusinessCell DivisionInternational journal of cancer
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Abstract A24: Bone marrow hematopoietic adaptation as a sensor of early, pre-invasive, epithelial malignancy

2018

Abstract Tumor development and progression is in part dependent on the ability of bystander cells, mostly of bone marrow (BM) origin, to establish a pro-tumorigenic microenvironment. We hypothesized that signs of the cross-talk between elements of the tumor microenvironment and the BM can be identified in the very early phases of cancer development, being finalized to the instruction of a tumor-promoting hematopoiesis. By integrating in situ BM histopathological and immunophenotypical analyses with flow cytometry and gene expression profiling of hematopoietic populations in a spontaneous mouse model of breast carcinogenesis (MMTV/NeuT) we investigated the occurrence and quality of modificat…

Cancer ResearchTumor microenvironmentStromal cellBiologyGene signatureGene expression profilingHaematopoiesisImmunophenotypingmedicine.anatomical_structureOncologyTumor progressionCancer researchmedicineBone marrowCancer Research
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Abstract 2141: Stromal SPARC deficiency skews prostate cancer toward neuroendocrine differentiation

2018

Abstract Tumor progression is a multifaceted process in which, complex interactions between tumor and different types of stromal cells and extracellular matrix components, actively contribute to its phenotypic heterogeneity. Among extracellular matrix proteins, secreted protein acidic and rich in cysteine (SPARC) has been deeply studied since conflicting reports have described its expression to be either increased or decreased in different cancer settings, also depending on whether it is produced by the neoplasm or by the neighboring stroma. Nevertheless, the different contribution of tumor- or stromal-derived SPARC in prostate tumor microenvironment has not been addressed at least for tumo…

Cancer ResearchTumor microenvironmentStromal cellCancerBiologymedicine.diseaseNeuroendocrine differentiationProstate cancerOncologyTumor progressionmedicineCancer researchAdenocarcinomaTrampCancer Research
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Abstract LB-099: Metabolic vulnerabilities of mesenchymal-like EGFR-mutant NSCLC cells with acquired resistance to tyrosine kinase inhibitors

2018

Abstract Despite the availability of the effective targeted therapies in lung cancer, such as EGFR tyrosine kinase inhibitors (TKIs), drug tolerance and acquired resistance are two common problems that negatively impact lung cancer patient survival. Consequently it is important to understand the molecular basis of the drug tolerance and resistance so that we could formulate effective strategies to ameliorate the efficacy of existing drug and to suppress the emergence of drug resistance. A burgeoning body of literature demonstrated that epigenetic changes by the methylation of DNA and histones are critical in acquired drug resistance, especially in those cancer cells with stem cell-like prop…

Cancer Researchbusiness.industryCancerDrug resistanceMethylationmedicine.diseaseOncologyTumor progressionCancer cellDNA methylationCancer researchMedicineEpigeneticsbusinessEpigenomicsCancer Research
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Abstract A22: PanDrugsDB: Identifying druggable genetic dependencies for personalized cancer therapy

2015

Abstract The paradigm of personalized medicine is the identification of the appropriate drug for the right patient, using molecular profiles. In Oncology, it is well established that the anticancer drugs are effective in only a small subset of patients. Moreover, many of the new targeted therapies inhibit specific proteins, and they are only effective in tumors that are genetically altered. Consequently, the success of personalized treatment depends on each individual molecular profile, which a priori can be considered as very heterogeneous. Here, we present a new computational approach (PanDrugsDB) based on the analysis and integration of genomic data (mutations, copy number variations or …

Cancer Researchbusiness.industryGenomic dataDruggabilityCancer therapyCancermedicine.diseaseBioinformaticsOncologyTumor progressionmedicineIdentification (biology)Copy-number variationPersonalized medicinebusinessMolecular Cancer Therapeutics
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