Search results for "Protocol"

showing 10 items of 1808 documents

Challenges and new prospects in hepatosplenic γδ T-cell lymphoma.

2014

Peripheral T-cell lymphomas (PTCLs) are a heterogeneous group of lymphoid neoplasms characterized by aggressive clinical behavior and dismal prognosis. Hepatosplenic γδ T-cell lymphoma (γδ-HSTL) is a particular form of PTCL that arises from a small subset of γ/δ T-cell receptor-expressing lymphocytes. γδ-HSTL has a rapidly progressive course and poor outcome due also to its refractoriness to conventional chemotherapy regimens. The very low incidence of γδ-HSTL, along with its propensity to mimic different pathological entities, makes this lymphoma a true diagnostic challenge. In this review, we highlight the biological and clinical features of γδ-HSTL that contribute to making this lymphoma…

Cancer ResearchHepatosplenic T-cell lymphomaSpleenDiseaseBiologyT cell lymphomaAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansT-cell lymphomaPathologicalgamma delta T cell lymphomahepatosplenic T cell lymphomaSplenic NeoplasmsLiver NeoplasmsLymphoma T-Cell PeripheralReceptors Antigen T-Cell gamma-deltaHematologymedicine.diseaseCombined Modality Therapyperipheral T cell lymphomasLymphomaT cell lymphoma; gamma delta T cell lymphomas; hepatosplenic T cell lymphoma; peripheral T cell lymphomasTreatment Outcomemedicine.anatomical_structureOncologyImmunologyConventional chemotherapyBone marrowStem Cell Transplantation
researchProduct

Temporal molecular and biological assessment of an erlotinib-resistant lung adenocarcinoma model reveals markers of tumor progression and treatment r…

2012

Abstract Patients with lung cancer with activating mutations in the EGF receptor (EGFR) kinase, who are treated long-term with tyrosine kinase inhibitors (TKI), often develop secondary mutations in EGFR associated with resistance. Mice engineered to develop lung adenocarcinomas driven by the human EGFR T790M resistance mutation are similarly resistant to the EGFR TKI erlotinib. By tumor volume endpoint analysis, these mouse tumors respond to BIBW 2992 (an irreversible EGFR/HER2 TKI) and rapamycin combination therapy. To correlate EGFR-driven changes in the lung with response to drug treatment, we conducted an integrative analysis of global transcriptome and metabolite profiling compared wit…

Cancer ResearchLung NeoplasmsCombination therapyAfatinibGene ExpressionAdenocarcinoma of LungCell Growth ProcessesAdenocarcinomaAfatinibArticleErlotinib HydrochlorideMiceAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsEpidermal growth factor receptorLung cancerErlotinib HydrochlorideProtein Kinase InhibitorsSirolimusbiologymedicine.diseaserespiratory tract diseasesErbB ReceptorsOncologyTumor progressionDrug Resistance NeoplasmCancer researchbiology.proteinDisease ProgressionQuinazolinesErlotinibTyrosine kinasemedicine.drugTranscription FactorsCancer research
researchProduct

Uncommon Synchronous Association between Ovarian Carcinoma and Gastrointestinal Stromal Tumor: A Case Study and Literature Review

2013

Background The association of gastrointestinal stromal tumors (GIST) and other cancers is well known, but its synchronous occurrence with gynecological malignancies is very uncommon. Usually, the diagnosis is accidentally established. We describe a patient with GIST and concurrent ovarian cancer and discuss the clinical implications of this finding. Case report A 64-year-old woman with a prior diagnosis of ovarian cancer developed a second recurrence after having undergone two operations and adjuvant chemotherapy. While tumor debulking was performed, a small, nonsuspicious lesion was removed from the greater curvature of the stomach. Histology revealed a GIST. Conclusion The association of …

Cancer ResearchPaclitaxelGastrointestinal Stromal TumorsOvariectomyAntigens CD34Carcinoma Ovarian EpithelialCystectomyHysterectomyCarboplatin030218 nuclear medicine & medical imagingNeoplasms Multiple PrimarySalpingectomy03 medical and health sciencesPancreatectomy0302 clinical medicineOvarian cancerSynchronous occurrenceStomach NeoplasmGastrectomyStomach NeoplasmsAntineoplastic Combined Chemotherapy ProtocolsGastrointestinal Stromal TumorBiomarkers TumorHumansNeoplasms Glandular and EpithelialColectomyOvarian NeoplasmsAntineoplastic Combined Chemotherapy ProtocolOvarian NeoplasmGeneral MedicineMiddle AgedImmunohistochemistryProto-Oncogene Proteins c-kitTreatment OutcomeOncologyChemotherapy AdjuvantCA-125 Antigen030220 oncology & carcinogenesisSplenectomyLymph Node ExcisionFemaleHumanTumori Journal
researchProduct

The dual PI3K/mTOR inhibitor PKI-587 enhances sensitivity to cetuximab in EGFR-resistant human head and neck cancer models

2014

Background:Cetuximab is the only targeted agent approved for the treatment of head and neck squamous cell carcinomas (HNSCC), but low response rates and disease progression are frequently reported. As the phosphoinositide 3-kinase (PI3K) and the mammalian target of rapamycin (mTOR) pathways have an important role in the pathogenesis of HNSCC, we investigated their involvement in cetuximab resistance.Methods:Different human squamous cancer cell lines sensitive or resistant to cetuximab were tested for the dual PI3K/mTOR inhibitor PF-05212384 (PKI-587), alone and in combination, both in vitro and in vivo.Results:Treatment with PKI-587 enhances sensitivity to cetuximab in vitro, even in the co…

Cancer ResearchPathologyCetuximabApoptosisHNSCCHNSCCMiceAntineoplastic Combined Chemotherapy ProtocolsNeoplasmPhosphoinositide-3 Kinase InhibitorsMice Inbred BALB CCetuximabCaspase 3TriazinesTOR Serine-Threonine KinasesCetuximab resistanceErbB ReceptorsOncologyHead and Neck NeoplasmsMonoclonalCarcinoma Squamous Cellmedicine.drugmedicine.medical_specialtyMorpholinesPI3K-mTOR inhibitorsMice NudeAntineoplastic AgentsBiologyAntibodies Monoclonal HumanizedCell Line TumorAutophagymedicineCarcinomaAnimalsHumansneoplasmsPI3K/AKT/mTOR pathwayCell Proliferationcetuximab resistanceSquamous Cell Carcinoma of Head and Necktarget therapyCell growthAutophagyCancermedicine.diseaseXenograft Model Antitumor Assaysdigestive system diseasesDrug Resistance NeoplasmPI3K7mTOR inhibitorsCancer researchTranslational TherapeuticsBritish Journal of Cancer
researchProduct

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
researchProduct

Early deaths in acute lymphoblastic leukemia (ALL): results of the Italian Pediatric Cooperative Group for Therapy of Acute Leukemia (AIL-AIEOP).

1984

In this retrospective multicentric study, we report on early deaths (ie, those that occurred during the first month of treatment) in a total of 943 newly diagnosed ALL pediatric patients registered from 1976 to 1981 at 21 centers of the AIL-AIEOP. Objectives of this study were as follows: (1) to verify the incidence and the cause of early death in a wide population of children with ALL and (2) to elucidate factors associated with early death and therefore to identify “high-risk” groups of patients. Out of the 943 ALL patients, 39 (4.1%) early deaths were registered. Main causes were infection, 20 patients (51.3%); hemorrhage, 11 patients (28.3%); uric acid nephropathy, 2 patients (5.1%); ca…

Cancer ResearchPediatricsmedicine.medical_specialtyAdolescentHeart DiseasesLymphoblastic LeukemiaPopulationEarly deathHemorrhageInfectionsMediastinal NeoplasmsNephropathyAntineoplastic Combined Chemotherapy ProtocolsmedicineHumanseducationChildRetrospective Studieseducation.field_of_studyAcute leukemiabusiness.industryIncidence (epidemiology)Age FactorsMediastinumInfantmedicine.diseasePrognosisLeukemia Lymphoidmedicine.anatomical_structureOncologyChild PreschoolPediatrics Perinatology and Child HealthSyndrome of inappropriate antidiuretic hormone secretionKidney DiseasesbusinessMedical and pediatric oncology
researchProduct

Histone deacetylase inhibition by valproic acid down-regulates c-FLIP/CASH and sensitizes hepatoma cells towards CD95-and TRAIL receptor-mediated apo…

2005

Hepatocellular carcinoma (HCC) is highly resistant to chemotherapy, leading to a poor prognosis of advanced disease. Inhibitors of histone deacetylase (HDACi) induce re-differentiation in tumor cells and thereby re-establish sensitivity towards apoptotic stimuli. HDACi are entering the clinical stage of tumor treatment, and several substances are currently being tested in clinical trials to prove their efficacy in the treatment of leukemias and solid tumors. In this study, we investigated the impact of the HDACi valproic acid (VA) on TRAIL- and CD95-mediated apoptosis in hepatoma cells, as well as its sensitizing effect on a chemotherapeutic agent. Treatment of HepG2 cells with VA increased…

Cancer ResearchProgrammed cell deathCarcinoma Hepatocellularmedicine.medical_treatmentCellCASP8 and FADD-Like Apoptosis Regulating ProteinDown-RegulationCaspase 3ApoptosisBiologyReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansfas ReceptorEpirubicinChemotherapyMembrane GlycoproteinsCaspase 3Tumor Necrosis Factor-alphaValproic AcidLiver NeoplasmsIntracellular Signaling Peptides and ProteinsGeneral MedicineCell cycleFas receptorHistone Deacetylase Inhibitorsmedicine.anatomical_structureOncologyApoptosisDrug Resistance NeoplasmCaspasesCancer researchHistone deacetylaseApoptosis Regulatory Proteins
researchProduct

Temozolomide- and fotemustine-induced apoptosis in human malignant melanoma cells: response related to MGMT, MMR, DSBs, and p53

2009

Malignant melanomas are highly resistant to chemotherapy. First-line chemotherapeutics used in melanoma therapy are the methylating agents dacarbazine (DTIC) and temozolomide (TMZ) and the chloroethylating agents BCNU and fotemustine. Here, we determined the mode of cell death in 11 melanoma cell lines upon exposure to TMZ and fotemustine. We show for the first time that TMZ induces apoptosis in melanoma cells, using therapeutic doses. For both TMZ and fotemustine apoptosis is the dominant mode of cell death. The contribution of necrosis to total cell death varied between 10 and 40%. The O(6)-methylguanine-DNA methyltransferase (MGMT) activity in the cell lines was between 0 and 1100 fmol m…

Cancer ResearchProgrammed cell deathDNA repairDacarbazineBlotting WesternApoptosistemozolomideBiologyCollagen Type XIDNA Mismatch RepairNecrosisGliomaAntineoplastic Combined Chemotherapy ProtocolsTumor Cells CulturedmedicineHumansDNA Breaks Double-StrandedEverolimusPhosphorylationDNA Modification MethylasesMelanomaneoplasmsSirolimusTemozolomideTumor Suppressor ProteinsMelanomafotemustinemelanoma therapymedicine.diseaseDacarbazineEnzyme Activationmismatch repairDNA Repair EnzymesOncologyApoptosisCaspasesCancer researchFotemustineTumor Suppressor Protein p53Translational TherapeuticsMGMTmedicine.drugBritish Journal of Cancer
researchProduct

Galangin increases the cytotoxic activity of imatinib mesylate in imatinib-sensitive and imatinib-resistant Bcr-Abl expressing leukemia cells

2008

Resistance to imatinib mesylate is an emergent problem in the treatment of Bcr-Abl expressing myelogenous leukemias and additional therapeutic strategies are required. We observed that galangin, a non-toxic, naturally occurring flavonoid was effective as anti-proliferative, and apoptotic agent in Bcr-Abl expressing K562 and KCL22 cells and in imatinib mesylate resistant K562-R and KCL22-R cells. Galangin induced an arrest of cells in G0–G1phase of cell cycle and a decrease in pRb, cdk4, cdk1, cycline B levels; moreover, it was able to induce a monocytic differentiation of leukemic Bcr-Abl+ cells. Of note, galangin caused a decrease in Bcl-2 levels and markedly increased the apoptotic activi…

Cancer ResearchSettore MED/17 - Malattie InfettiveSettore MED/06 - Oncologia MedicaApoptosisPharmacologyResting Phase Cell CyclePiperazineschemistry.chemical_compoundCell Line TumorLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansCytotoxic T cellChrysinneoplasmsFlavonoidsLeukemiaG1 PhaseApoptosiCell DifferentiationImatinibmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaGalanginLeukemiaPyrimidinesImatinib mesylateOncologychemistryDrug Resistance NeoplasmImatinibBenzamidesSettore BIO/14 - FarmacologiaImatinib MesylateK562 CellsFisetinBcr-AblK562 cellsmedicine.drugCancer Letters
researchProduct

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
researchProduct