Search results for "Antineoplastic"

showing 10 items of 2217 documents

COMPliance and Arthralgia in Clinical Therapy: the COMPACT trial, assessing the incidence of arthralgia, and compliance within the first year of adju…

2014

5 Office-based Professional Association Gynecologic Oncologists e.V. in Germany (BNGO e.V.), Berlin; 6 Background: This prospective study evaluated the relationship between arthralgia and compliance during the first year of adjuvant anastrozole therapy in postmenopausal women with hormone receptor-positive early breast cancer. Patients and methods: COMPliance and Arthralgia in Clinical Therapy (COMPACT) was an open-label, multicenter, noninterventional study conducted in Germany. Patients had started adjuvant anastrozole 3-6 months before the study start. The primary end points were arthralgia, compliance, and the relationship between compliance and arthralgia, assessed at specific time poi…

musculoskeletal diseasesmedicine.medical_specialtyAntineoplastic Agents Hormonalmedicine.medical_treatmentSpecific timeAnastrozoleBreast NeoplasmsAnastrozoleMedication AdherenceBreast cancerInternal medicineNitrilesmedicineHumansProspective Studiesskin and connective tissue diseasesProspective cohort studyAgedbusiness.industryDrug SubstitutionIncidence (epidemiology)IncidenceHematologyMiddle AgedTriazolesmedicine.diseaseArthralgiaSurgeryCompliance (physiology)Clinical therapyTreatment OutcomeOncologyChemotherapy AdjuvantFemalebusinessAdjuvantmedicine.drugAnnals of oncology : official journal of the European Society for Medical Oncology
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In vitro effects of AGNPs exopolysaccharide from Klebsiella Oxytoca DSM29614 on breast cancer cells

2015

nanoparticles antineoplastic molecules breast cancer proteomicSettore BIO/06 - Anatomia Comparata E Citologia
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The Major Heat Shock Proteins, Hsp70 and Hsp90, in 2-Methoxyestradiol-Mediated Osteosarcoma Cell Death Model

2020

2-Methoxyestradiol is one of the natural 17&beta

neuronal nitric oxide synthaseProgrammed cell death2-methoxyestradiolLactams MacrocyclicAntineoplastic AgentsBone NeoplasmsModels BiologicalArticleCatalysisHsp90 inhibitorNitric oxidelcsh:ChemistryInorganic Chemistrychemistry.chemical_compoundDownregulation and upregulationosteosarcomaHeat shock proteinBenzoquinonesAnimalsHumansDrug InteractionsHSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsPhysical and Theoretical Chemistrygeldanamycinlcsh:QH301-705.5Molecular BiologySpectroscopyAntibiotics AntineoplasticbiologyOrganic ChemistryGeneral MedicineGeldanamycinHsp90Computer Science ApplicationsHsp70lcsh:Biology (General)lcsh:QD1-999chemistryCancer researchbiology.proteinInternational Journal of Molecular Sciences
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Antineoplastic dosing in overweight and obese cancer patients: an Associazione Italiana Oncologia Medica (AIOM)/Associazione Medici Diabetologi (AMD)…

2021

Most anticancer molecules are administered in body-size-based dosing schedules, bringing up unsolved issues regarding pharmacokinetic data in heavy patients. The worldwide spread of obesity has not been matched by improved methods and strategies for tailored drug dosage in this population. The weight or body surface area (BSA)-based approaches may fail to fully reflect the complexity of the anthropometric features besides obesity in cancer patients suffering from sarcopenia. Likewise, there is a lack of pharmacokinetic data on obese patients for the majority of chemotherapeutic agents as well as for new target drugs and immunotherapy. Therefore, although the available findings point to the …

obesityCancer Researchmedicine.medical_specialtypharmacokinetic parametersConsensusBSAcancer drug dosingPopulationchemotherapy doseAntineoplastic AgentsReviewOverweightNODosing schedulesNeoplasmsPhysiciansInternal medicineHumansMedicineDosingLS4_3educationBody surface areaeducation.field_of_studybusiness.industryCancerCytotoxic chemotherapymedicine.diseaseOncologyBSA; cancer drug dosing; chemotherapy dose; obesity; pharmacokinetic parametersPosition paperBSA; cancer drug dosing; chemotherapy dose; obesity; pharmacokinetic parameters; Consensus; Humans; Obesity; Antineoplastic Agents; Neoplasms; Physiciansmedicine.symptombusinessESMO Open
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Nanosistemi polimerici con un core di oro colloidale per la veicolazione di farmaci antineoplastici ed imaging di tumori solidi

oro colloidale acido folico polimeri biocompatibili farmaci antineoplastici teranostica
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Targeting HSP90 with the small molecule inhibitor AUY922 (luminespib) as a treatment strategy against hepatocellular carcinoma

2018

Hepatocellular carcinoma (HCC) is a highly malignant tumor that responds very poorly to existing therapies, most probably due to its extraordinary inter- and intra-tumor molecular heterogeneity. The modest therapeutic response to molecular targeted agents underlines the need for new therapeutic approaches for HCC. In our study, we took advantage of well-characterized human HCC cell lines, differing in transcriptomic subtypes, DNA mutation and amplification alterations, reflecting the heterogeneity of primary HCCs, to provide a preclinical evaluation of the specific heat shock protein 90 (HSP90) inhibitor AUY922 (luminespib). Indeed, HSP90 is highly expressed in different tumor types, but it…

p53MaleCancer ResearchCellTranscriptome0302 clinical medicineHCCbeta CateninAged 80 and overLuminespibAUY922Liver NeoplasmsHep G2 CellsSorafenibMiddle AgedUp-RegulationGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyCaspases030220 oncology & carcinogenesisHepatocellular carcinomaFemaleNUPR1medicine.drugAdultSorafenibCarcinoma Hepatocellularβ-CateninMice NudeAntineoplastic AgentsSmall Molecule Libraries03 medical and health sciencesDownregulation and upregulationIn vivoCell Line TumormedicineHSP90AnimalsHumansHSP90 Heat-Shock ProteinsAgedCell growthbusiness.industryMcl-1IsoxazolesResorcinolsHCCSmedicine.diseasedigestive system diseasesMutationCancer researchTranscriptomebusinessInternational Journal of Cancer
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Plant Specialized Metabolites in Hazelnut (Corylus avellana) Kernel and Byproducts: An Update on Chemistry, Biological Activity, and Analytical Aspec…

2019

Abstract Corylus avellana (hazelnut) is one of the most popular tree nuts on a worldwide basis. The main products of C. avellana are kernels, a nutritious food, with a high content of healthy lipids, contained in a hard shell. In recent years, along with the ongoing research carried out on hazelnut kernels, a growing interest has been addressed to the hazelnut byproducts including hazelnut skin, hazelnut hard shell, and hazelnut green leafy cover as well as hazelnut tree leaf. These byproducts deriving from the roasting, cracking, shelling/hulling, and harvesting processes have been found as a source of “phytochemicals” with biological activity. The aim of this review is to provide a compre…

phenolicsPharmaceutical ScienceAntineoplastic Agents01 natural sciencesNutritious foodAnalytical ChemistryHuman healthCorylusAnti-Infective AgentsBetulaceaeDrug Discoveryanalytical tools; Betulaceae; biological activities; Corylus avellana; diarylheptanoids; phenolics; taxanes; Animals; Anti-Infective Agents; Antineoplastic Agents; Antipain; Corylus; Humans; Nuts; Plant ExtractsAnimalsAntipainHumansNutsFood scienceHazelnut treeBeneficial effectsRoastingPharmacology010405 organic chemistryChemistryPlant ExtractsOrganic Chemistrybiological activitiestaxanes0104 chemical sciences010404 medicinal & biomolecular chemistrydiarylheptanoidsComplementary and alternative medicineMolecular Medicineanalytical toolsCorylus avellana
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Photochemotherapeutic heterocyclic agents having antiproliferative and antineoplastic activity

2012

The present invention concerns the synthesis of new analogs of angelicins, pyrrolo[3,2-h]quinoline, for the treatment of pathologie having hyperproliferative character including those having neoplastic nature. The treatment is based on the combined action of pyrrolo[3,2-h]quinolines and UV-A light, through a clinical approach defined as PUVA (psoralen-UVA light). The most important feature of these compounds is that they exert their remarkable phototoxicity without any DNA damage, which is the main origin of the side effects of the PUVA therapy

phototoxicityantineoplasticangelicinphotochemotherapeutic
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Inhibition of Rac1 signaling by lovastatin protects against anthracycline-induced cardiac toxicity

2011

Normal tissue damage limits the efficacy of anticancer therapy. For anthracyclines, the clinically most relevant adverse effect is cardiotoxicity. The mechanisms involved are poorly understood and putative cardioprotectants are controversially discussed. Here, we show that the lipid-lowering drug lovastatin protects rat H9c2 cardiomyoblasts from doxorubicin in vitro. Protection by lovastatin is related to inhibition of the Ras-homologous GTPase Rac1. It rests on a reduced formation of DNA double-strand breaks, resulting from the inhibition of topoisomerase II by doxorubicin. Doxorubicin transport and reactive oxygen species are not involved. Protection by lovastatin was confirmed in vivo. I…

rac1 GTP-Binding ProteinCancer ResearchAnthracyclineDoxorubicin transportCardiac fibrosismedicine.medical_treatmentImmunologyPharmacologyBiologyDNA damage responsestatinsMiceCellular and Molecular NeuroscienceRho GTPasespolycyclic compoundsmedicineAnimalsDNA Breaks Double-StrandedMyocytes CardiacDoxorubicinLovastatinanthracyclinesCardiotoxicityAntibiotics AntineoplasticTroponin IConnective Tissue Growth FactorCell Biologymedicine.diseaseRatsCTGFDNA Topoisomerases Type IICytokinenormal tissue damageDoxorubicinOriginal Articlelipids (amino acids peptides and proteins)LovastatinAtrial Natriuretic FactorSignal Transductionmedicine.drugCell Death & Disease
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Aplidin® induces JNK-dependent apoptosis in human breast cancer cells via alteration of glutathione homeostasis, Rac1 GTPase activation, and MKP-1 ph…

2006

Aplidin® is an antitumor agent in phase II clinical trials that induces apoptosis through the sustained activation of Jun N-terminal kinase (JNK). We report that Aplidin® alters glutathione homeostasis increasing the ratio of oxidized to reduced forms (GSSG/GSH). Aplidin® generates reactive oxygen species and disrupts the mitochondrial membrane potential. Exogenous GSH inhibits these effects and also JNK activation and cell death. We found two mechanisms by which Aplidin® activates JNK: rapid activation of Rac1 small GTPase and downregulation of MKP-1 phosphatase. Rac1 activation was diminished by GSH and enhanced by L-buthionine (SR)-sulfoximine, which inhibits GSH synthesis. Downregulatio…

rac1 GTP-Binding ProteinProgrammed cell deathSmall interfering RNAGlutathione reductaseDown-RegulationAntineoplastic AgentsApoptosisBreast NeoplasmsCell Cycle ProteinsBiologyPeptides CyclicImmediate-Early ProteinsMembrane Potentialschemistry.chemical_compoundMiceDownregulation and upregulationDepsipeptidesProtein Phosphatase 1Phosphoprotein PhosphatasesAnimalsHomeostasisHumansMolecular Biologychemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidaseGlutathione DisulfideJNK Mitogen-Activated Protein KinasesProtein phosphatase 1Dual Specificity Phosphatase 1Cell BiologyGlutathioneCell biologyEnzyme ActivationOxidative StressGlutathione ReductasechemistryMitochondrial MembranesGlutathione disulfideCalciumProtein Tyrosine PhosphatasesReactive Oxygen SpeciesCopperHeLa CellsCell Death and Differentiation
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