Search results for "Neoplastic"

showing 10 items of 2901 documents

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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In vivo effects of tumor necrosis factor-α or flavone acetic acid in combination with doxorubicin on multidrug-resistant B16 melanoma

1996

Having observed that tumor necrosis factor (TNF)-alpha and doxorubicin (DXR) produce a synergistic inhibition of melanoma B16 and also of its multidrug resistant (MDR) variant in vitro, we tested whether this interaction would occur in vivo as well. C57BL/6 mice with s.c. tumors were treated with TNF or flavone acetic acid (FAA), a biological response modifier, in simultaneous or sequential combination with DXR. The agents were administered systemically. Overall, the results were negative, apart from a trend towards slight synergy, found in the chemosensitive melanoma, when TNF was given 1 or 2 days before DXR. The effects of FAA and DXR were found to be subadditive or antagonistic. However…

Cancer ResearchSkin NeoplasmsMelanoma ExperimentalMiceIn vivoAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsPharmacology (medical)DoxorubicinFlavonoidsPharmacologyAntibiotics AntineoplasticFlavone acetic acidDose-Response Relationship DrugTumor Necrosis Factor-alphaChemistryMelanomamedicine.diseaseDrug Resistance MultipleIn vitroMultiple drug resistanceOncologyBiochemistryDoxorubicinDrug Resistance NeoplasmCancer researchFemaleTumor necrosis factor alphaB16 melanomamedicine.drugAnti-Cancer Drugs
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Second St. Gallen European Organisation for Research and Treatment of Cancer Gastrointestinal Cancer Conference: consensus recommendations on controv…

2016

Contains fulltext : 171468pub.pdf (Publisher’s version ) (Open Access) Primary treatment of rectal cancer was the focus of the second St. Gallen European Organisation for Research and Treatment of Cancer (EORTC) Gastrointestinal Cancer Conference. In the context of the conference, a multidisciplinary international expert panel discussed and voted on controversial issues which could not be easily answered using published evidence. Main topics included optimal pretherapeutic imaging, indication and type of neoadjuvant treatment, and the treatment strategies in advanced tumours. Here we report the key recommendations and summarise the related evidence. The treatment strategy for localised rect…

Cancer ResearchStagingColorectal cancermedicine.medical_treatmentNeoplasias Gastrointestinais030230 surgerySYNCHRONOUS LIVER METASTASESImagingCOLORECTAL-CANCER0302 clinical medicineADJUVANT CHEMOTHERAPYTumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14]SHORT-COURSE RADIOTHERAPYRectal cancerNeoadjuvant therapyGastrointestinal NeoplasmsRectal Neoplasms/drug therapyCombination chemotherapyChemoradiotherapyCombined Modality TherapyTotal mesorectal excisionNeoadjuvant TherapyEuropeNeoplasias do Recto/quimioterapiaOncology030220 oncology & carcinogenesisMEDIAN FOLLOW-UPLife Sciences & BiomedicineDiagnostic Imagingmedicine.medical_specialtyAntineoplastic AgentsLOCAL RECURRENCERisk AssessmentCOURSE PREOPERATIVE RADIOTHERAPY03 medical and health sciencesmedicineHumansGastrointestinal cancerOncology & CarcinogenesisRadiochemotherapyNeoplasm StagingScience & TechnologyRadiotherapyRectal Neoplasmsbusiness.industryGeneral surgeryTOTAL MESORECTAL EXCISIONCancerRANDOMIZED PHASE-IIImedicine.diseaseSurgeryRadiation therapySurgerybusiness1112 Oncology And CarcinogenesisChemoradiotherapyPOSTOPERATIVE CHEMORADIOTHERAPY
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Molecular principles of cancer invasion and metastasis (Review)

2009

The main threat and the reason for most cancer deaths are not the primary neoplasias, but secondary tumors, the metastases. Drastic phenotypic and biochemical changes occur during the metamorphosis of a normal tissue cell into an invasive cancer cell. These alterations concern various areas such as growth factor signaling, cell-cell adhesion, gene expression, motility or cell shape. Cancer cells of epithelial origin can even shed their typical qualities and characteristics and adopt a mesenchymal-like phenotype. This is often referred to as an epithelial-mesenchymal transition. Various oncogenes, tumor suppressor genes and metastasis suppressor genes are known to affect the invasiveness and…

Cancer ResearchStromal cellBiologyModels BiologicalMetastasisCell MovementCancer stem cellNeoplasmsCell AdhesionmedicineHumansGenes Tumor SuppressorNeoplasm InvasivenessNeoplasm MetastasisCell ShapeCell ProliferationCancerSuicide geneAcquired immune systemmedicine.diseaseGene Expression Regulation NeoplasticMetastasis Suppressor GeneCell Transformation NeoplasticOncologyImmunologyCancer cellCancer researchCytokinesSignal TransductionInternational Journal of 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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Preclinical and Clinical Characterization of Fibroblast-derived Neuregulin-1 on Trastuzumab and Pertuzumab Activity in HER2-positive Breast Cancer.

2021

[Purpose]: To characterize expression of neuregulin-1 (NRG1), an HER3 ligand, in HER2-positive breast cancer and its relation with the efficacy of trastuzumab with or without pertuzumab.

Cancer ResearchStromal cellReceptor ErbB-2medicine.medical_treatmentNeuregulin-1Drug Evaluation PreclinicalBreast NeoplasmsAntibodies Monoclonal HumanizedBreast cancerAntineoplastic Agents ImmunologicalTrastuzumabAntineoplastic Combined Chemotherapy Protocolsmental disordersmedicineTumor Cells CulturedHumansNeuregulin 1skin and connective tissue diseasesneoplasmsNeoadjuvant therapyRetrospective Studiesbiologybusiness.industryFibroblastsTrastuzumabmedicine.diseasebody regionsTreatment OutcomeOncologyCancer cellbiology.proteinCancer researchImmunohistochemistryFemalePertuzumabbusinessmedicine.drug
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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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MYCN and survivin cooperatively contribute to malignant transformation of fibroblasts

2013

The oncogenes MYCN and survivin (BIRC5) maintain aggressiveness of diverse cancers including sarcomas. To investigate whether these oncogenes cooperate in initial malignant transformation, we transduced them into Rat-1 fibroblasts. Indeed, survivin enhanced MYCN-driven contact-uninhibited and anchorage-independent growth in vitro. Importantly, upon subcutaneous transplantation into mice, cells overexpressing both instead of either one of the oncogenes generated tumors with shortened latency, marked anaplasia and an increased proliferation-to-apoptosis ratio resulting in accelerated growth. Mechanistically, the increased tumorigenicity was associated with an enhanced Warburg effect and a hyp…

Cancer ResearchSurvivinBlotting WesternApoptosisBiologyReal-Time Polymerase Chain ReactionN-Myc Proto-Oncogene ProteinInhibitor of Apoptosis ProteinsMalignant transformationImmunoenzyme TechniquesMiceAdenosine TriphosphateSurvivinmedicineAnimalsHumansLactic AcidRNA MessengerneoplasmsAnaplasiaCells CulturedCell ProliferationHomeodomain ProteinsOncogene ProteinsN-Myc Proto-Oncogene ProteinReverse Transcriptase Polymerase Chain ReactionCell growthNuclear ProteinsGeneral MedicineFibroblastsWarburg effectCell HypoxiaRatsTransplantationCell Transformation NeoplasticGlucoseHypoxia-inducible factorsCancer researchmedicine.symptomGlycolysisCarcinogenesis
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Regulation of CD1d expression by murine tumor cells: escape from immunosurveillance or alternate target molecules?

2002

alpha beta+ TCR T cells recognize peptide fragments displayed by MHC-class I or -class II molecules. Recently, additional mechanisms of antigen recognition by T cells have been identified, including CD1-mediated presentation of nonpeptide antigens. Only a limited number of CD1 antigens is retained in the mouse, i.e., the group II CD1 antigens, which are split into CD1D1 and CD1d2. Several T cell subsets have been shown to interact with murine CD1 antigens, including NK cells or "natural T cells" with the invariant V alpha 14 J alpha 281 TCR chain. Even if TAP defects may prevent classical endogenous antigen presentation in tumor cell lines, antigen presentation via CD1 is still functional. …

Cancer ResearchT cellAntigen presentationCD1chemical and pharmacologic phenomenaBiologyNatural killer cellAntigens CD1Immunoenzyme TechniquesInterferon-gammaMiceNK-92Monitoring ImmunologicmedicineCytotoxic T cellAnimalsRNA MessengerAntigen-presenting cellCells CulturedDNA PrimersMice Inbred BALB CReverse Transcriptase Polymerase Chain ReactionAntibodies MonoclonalGranulocyte-Macrophage Colony-Stimulating Factorhemic and immune systemsNeoplasms ExperimentalCytotoxicity Tests ImmunologicFlow CytometryCell biologyGene Expression Regulation NeoplasticKiller Cells NaturalMice Inbred C57BLmedicine.anatomical_structureOncologyCD1DImmunologybiology.proteinCytokinesAntigens CD1dInternational journal of cancer
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Blockade of PD-L1 (B7-H1) augments human tumor-specific T cell responsesin vitro

2006

Human tumors frequently escape immune destruction, despite the presence of cytotoxic T cells (CTL) recognizing tumor-associated antigens (TAA). We have previously shown that programmed death ligand-1 (PD-L1), a recently identified ligand of the B7 superfamily, is expressed on murine tumors and can inhibit antitumor immune responses. To evaluate the clinical relevance of our animal model findings, we examined human tumors and tumor-specific T cells. We found PD-L1 to be constitutively expressed on human renal cell carcinoma (RCC) cell lines and upregulated on human melanoma cell lines upon exposure to interferon-gamma. Similarly, we found binding of anti-PD-L1 monoclonal antibody (mAb) on fr…

Cancer ResearchT cellAntineoplastic AgentsB7-H1 AntigenInterleukin 21Immune systemAntigenAntigens CDTumor Cells CulturedmedicineHumansCytotoxic T cellCTLA-4 AntigenIL-2 receptorAntigen-presenting cellCarcinoma Renal CellMelanomabusiness.industryAntibodies MonoclonalFlow CytometryAntigens DifferentiationImmunohistochemistryKidney NeoplasmsUp-RegulationGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyImmunologyB7-1 AntigenCancer researchbusinessB7-H1 AntigenT-Lymphocytes CytotoxicInternational Journal of Cancer
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