Search results for " Antineoplastic Agents"

showing 10 items of 91 documents

Everolimus as first line therapy for pancreatic neuroendocrine tumours: current knowledge and future perspectives

2017

urpose Everolimus has been shown to be effective for advanced pancreatic neuroendocrine tumours (pNETs), but its positioning in the therapeutic algorithm for pNETs is matter of debate. Methods With the aim to shed light on this point, we performed an up-to-date critical review taking into account the results of both retrospective and prospective published studies, and the recommendations of international guidelines. In addition, we performed an extensive search on the Clinical Trial Registries databases worldwide, to gather information on the ongoing clinical trials related to this specific topic. Results We identified eight retrospective published studies, two prospective published studies…

0301 basic medicinemTOR inhibitorsCancer Researchmedicine.medical_specialtyPathologymTOR inhibitorEverolimus; mTOR inhibitors; Neuroendocrine tumours; Therapy; Antineoplastic Agents; Everolimus; Humans; Neuroendocrine Tumors; Pancreatic Neoplasms; Oncology; Cancer ResearchTherapeutic algorithmEverolimus; mTOR inhibitors; neuroendocrine tumours; therapy; antineoplastic agents; everolimus; humans; neuroendocrine tumours; pancreatic neoplasms; oncology; cancer researchEndocrine SyndromeNeuroendocrine tumorsAntineoplastic Agent03 medical and health sciences0302 clinical medicineFirst line therapyNeuroendocrine tumourantineoplastic agentsmedicinehumansIntensive care medicinetherapyEverolimusbusiness.industryPancreatic Neoplasmpancreatic neoplasmsGeneral Medicineeverolimusmedicine.diseaseDiscovery and development of mTOR inhibitorsClinical trialEverolimuNeuroendocrine Tumors030104 developmental biologyOncology030220 oncology & carcinogenesisneuroendocrine tumoursNeuroendocrine TumorbusinessEverolimus; mTOR inhibitors; Neuroendocrine tumours; Therapy; Antineoplastic Agents; Everolimus; Humans; Neuroendocrine Tumors; Pancreatic NeoplasmsHumanmedicine.drugJournal of Cancer Research and Clinical Oncology
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Cytotoxicity of cucurbitacin E from Citrullus colocynthis against multidrug-resistant cancer cells

2019

Abstract Background Cucurbitacin E (CuE) is an oxygenated tetracyclic triterpenoid isolated from the fruits of Citrullus colocynthis (L.) Schrad. Purpose This study outlines CuE's cytotoxic activity against drug-resistant tumor cell lines. Three members of ABC transporters superfamily, P-glycoprotein (P-gp), breast cancer resistance protein (BCRP) and ABCB5 were investigated, whose overexpression in tumors is tightly linked to multidrug resistance. Further factors of drug resistance studied were the tumor suppressor TP53 and the epidermal growth factor receptor (EGFR). Methods Cytotoxicity assays (resazurin assays) were used to investigate the activity of Citrullus colocynthis and CuE towar…

Abcg2Drug ResistancePharmaceutical ScienceATP-binding cassette transporterMicroarraySubfamily Gchemistry.chemical_compoundGene Knockout Techniques0302 clinical medicineEpidermal growth factorPhytogenicDrug DiscoveryATP Binding Cassette Transporter Subfamily G Member 2Cancer0303 health sciencesTumorLeukemiabiologyChemistryABCB5TransfectionCell cycleNeoplasm ProteinsGene Expression Regulation NeoplasticErbB ReceptorsMolecular Docking SimulationSubfamily B030220 oncology & carcinogenesisMolecular MedicineCitrullus colocynthiMember 2Member 1ATP Binding Cassette Transporter Subfamily BATP Binding Cassette TransporterAntineoplastic AgentsCell Line03 medical and health sciencesCell Line TumorHumansATP Binding Cassette Transporter Subfamily B Member 1030304 developmental biologyCucurbitacin EPharmacologyNeoplasticTraditional herbal medicineCancer; Citrullus colocynthis; Drug resistance; Microarray; Traditional herbal medicine; ATP Binding Cassette Transporter Subfamily B; ATP Binding Cassette Transporter Subfamily B Member 1; ATP Binding Cassette Transporter Subfamily G Member 2; Antineoplastic Agents Phytogenic; Cell Line Tumor; Citrullus colocynthis; Doxorubicin; Drug Resistance Neoplasm; ErbB Receptors; Gene Expression Regulation Neoplastic; Gene Knockout Techniques; Humans; Leukemia; Molecular Docking Simulation; Neoplasm Proteins; Triterpenes; Tumor Suppressor Protein p53Antineoplastic Agents PhytogenicTriterpenesComplementary and alternative medicineGene Expression RegulationDrug Resistance NeoplasmDoxorubicinCancer cellbiology.proteinCancer researchNeoplasmCitrullus colocynthisTumor Suppressor Protein p53
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An in-depth evaluation of acalabrutinib for the treatment of mantle-cell lymphoma

2020

Introduction: Regimens involving intensive immuno-chemotherapy, followed by high-dose therapy and autologous stem cell transplant represent the standard treatment for younger fit patients with mantle cell lymphoma (MCL). Targeted approaches (i.e. ibrutinib, bortezomib, and lenalidomide) represent the backbone of therapy for relapsed cases. Areas covered: Acalabrutinib is a novel small molecule with a butynamide moiety specifically designed to irreversibly inhibit Bruton tyrosine kinase (BTK), which is more potent and selective than ibrutinib. Relevant publications have been identified through literature searches using the terms 'mantle cell lymphoma' and 'acalabrutinib'. Expert opinion: Aca…

Acalabrutinib; BTK; MCL; therapy; Agammaglobulinaemia Tyrosine Kinase; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Humans; Lymphoma Mantle-Cell; Protein Kinase Inhibitors; PyrazinesOncologymedicine.medical_specialtyLymphomaAntineoplastic AgentsLymphoma Mantle-Cell03 medical and health scienceschemistry.chemical_compound0302 clinical medicineimmune system diseaseshemic and lymphatic diseasesInternal medicineAntineoplastic Combined Chemotherapy ProtocolsAgammaglobulinaemia Tyrosine KinaseHumansMedicineBruton's tyrosine kinasePharmacology (medical)Protein Kinase InhibitorsLenalidomidePharmacologytherapy.therapybiologyAcalabrutinibbusiness.industryBortezomibStandard treatmentMCLGeneral MedicineMantle-Cellmedicine.diseaseClinical trialchemistryBTKPyrazines030220 oncology & carcinogenesisIbrutinibBenzamidesbiology.proteinAcalabrutinibMantle cell lymphomabusiness030217 neurology & neurosurgerymedicine.drugExpert Opinion on Pharmacotherapy
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Biology and management of therapy-related acute promyelocytic leukemia.

2013

Therapy-related acute promyelocytic leukemia (t-APL) has been increasingly reported after exposure to cytotoxic and/or immunosuppressive agents given for prior malignancies or autoimmune diseases. t-APL represents both a model for better understanding human leukemogenesis and an interesting therapeutic subset which requires specific adaptations for optimal management.We discuss here potential risk factors for t-APL development and the main biologic and clinical characteristics of t-APL as compared to de-novo APL.In addition, we review therapeutic results obtained in patients with t-APL receiving conventional retinoic acid and chemotherapy and discuss new treatment opportunities with minimal…

Acute promyelocytic leukemiaAdultMaleCancer ResearchRetinoic acidAntineoplastic AgentsTretinoinAcuteArsenicalschemistry.chemical_compoundArsenic TrioxideLeukemia Promyelocytic Acuteimmune system diseasesRisk FactorsNeoplasmsCytotoxic T cellMedicineHumansArsenic trioxideneoplasmsAdult; Antineoplastic Agents; Arsenicals; Early Diagnosis; Female; Humans; Leukemia Promyelocytic Acute; Male; Middle Aged; Neoplasms Second Primary; Oxides; Retrospective Studies; Risk Factors; TretinoinRetrospective StudiesPromyelocyticTherapy relatedLeukemiabusiness.industryNeoplasms Second PrimaryOxidesMiddle Agedmedicine.diseaseSecond PrimaryEarly DiagnosisOncologychemistryCancer researchFemalebusinessSettore MED/15 - Malattie del SangueCurrent opinion in oncology
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CD73-generated extracellular adenosine in chronic lymphocytic leukemia creates local conditions counteracting drug-induced cell death

2011

Abstract Extracellular adenosine (ADO), generated from ATP or ADP through the concerted action of the ectoenzymes CD39 and CD73, elicits autocrine and paracrine effects mediated by type 1 purinergic receptors. We have tested whether the expression of CD39 and CD73 by chronic lymphocytic leukemia (CLL) cells activates an adenosinergic axis affecting growth and survival. By immunohistochemistry, CD39 is widely expressed in CLL lymph nodes, whereas CD73 is restricted to proliferation centers. CD73 expression is highest on Ki-67+ CLL cells, adjacent to T lymphocytes, and is further localized to perivascular areas. CD39+/CD73+ CLL cells generate ADO from ADP in a time- and concentration-dependen…

AdenosineCellular differentiationChronic lymphocytic leukemia5'-Nucleotidase; Adenosine; Adenosine Diphosphate; Adenosine Triphosphate; Antigens CD; Antineoplastic Agents Phytogenic; Apyrase; Autocrine Communication; Cell Death; Cell Differentiation; Cell Movement; Cell Survival; Etoposide; Extracellular Space; GPI-Linked Proteins; Humans; Leukemia Lymphocytic Chronic B-Cell; Paracrine Communication; Receptor Adenosine A2A; Tumor Cells Cultured; Biochemistry; Immunology; Hematology; Cell BiologyMICROENVIRONMENTCD38BiochemistryACTIVATIONAdenosine TriphosphateCell MovementPhytogenichemic and lymphatic diseasesTumor Cells CulturedChronic5'-NucleotidaseEtoposideLeukemiaCulturedCell DeathTUMOR-GROWTHApyrasePurinergic receptorCell DifferentiationHematologyLymphocyticCDTumor CellsCell biologyAdenosine DiphosphateAutocrine CommunicationLeukemiaReceptorIMMUNE SUPPRESSIONReceptor Adenosine A2ACell SurvivalImmunologyAntineoplastic AgentsAdenosinergicBiologyGPI-Linked ProteinsDAMAGE-INDUCED APOPTOSISAdenosine A2AParacrine signallingAntigens CDParacrine CommunicationmedicineHumansAntigensAutocrine signallingImmunobiologyB-CellCell BiologyDAMAGE-INDUCED APOPTOSIS; T-CELLS; IMMUNE SUPPRESSION; ZAP-70 EXPRESSION; TUMOR-GROWTH; RECEPTOR; CD73; ACTIVATION; CD38; MICROENVIRONMENTmedicine.diseaseAntineoplastic Agents PhytogenicLeukemia Lymphocytic Chronic B-CellSettore MED/15 - MALATTIE DEL SANGUET-CELLSCD73Extracellular SpaceZAP-70 EXPRESSIONCD38Blood
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[Appropriate cytotoxic drug usages in solid tumors: conformity to official labelling and level of scientific evidence]

2006

International audience; The definition of appropriate use of drugs is questioned in oncology. Daily therapeutic practices were compared to official labelling and to published scientific data in this retrospective study. It was carried out in two respective specialised centers, from January to September 2004. All chemotherapies administered for adult solid tumours and including one of the eleven studied drugs were evaluated. The analysis of use was performed by drug : conformity to the validated labelling and level of scientific evidence (at the period study). The study included 1,561 drug uses in 1,211 patients. The overall rate of conformity to official labelling was 81.7 % (67.1 % of stri…

AdultMaleAdolescentMESH : Retrospective StudiesMESH : MaleMESH: Drug LabelingMESH : AgedAntineoplastic Agents[SDV.CAN]Life Sciences [q-bio]/Cancer[ SDV.CAN ] Life Sciences [q-bio]/CancerMESH : BenchmarkingMESH : Drug LabelingMESH: Aged 80 and overMESH: Practice Guidelines as TopicMESH: Benchmarking[SDV.CAN] Life Sciences [q-bio]/CancerNeoplasmsMESH : AdolescentHumansMESH: NeoplasmsMESH : Middle AgedMESH : FemaleMESH : Aged 80 and overAgedDrug LabelingRetrospective StudiesAged 80 and overMESH: AdolescentMESH: AgedMESH: HumansMESH: Middle AgedMESH : HumansMESH: AdultMESH: Retrospective StudiesMiddle AgedMESH : AdultMESH : NeoplasmsMESH: MaleBenchmarkingMESH : Practice Guidelines as TopicMESH : Antineoplastic AgentsPractice Guidelines as TopicMESH: Antineoplastic AgentsFemaleMESH: Female
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Evaluation of erlotinib treatment response in non-small cell lung cancer using metabolic and anatomic criteria

2016

BACKGROUND: In this paper the clinical value of PET for early prediction of tumor response to erlotinib in patients with advanced or metastatic non-small cell lung cancer (NSCLC) after failure of at least one prior chemotherapy regimen is evaluated. The aim was to compare the early metabolic treatment response using European Organization for Research and Treatment of Cancer (EORTC) 1999 recommendations and PET Response Criteria in Solid Tumors (PERCIST), and the standard treatment response using Response Evaluation Criteria in Solid Tumors (RECIST). METHODS: Twenty patients with stage IV NSCLCwere enrolled prospectively. PET/CT studies were performed before, then 48 hours, and 45 days after…

AdultMaleLung NeoplasmsTime FactorsAntineoplastic AgentsKaplan-Meier EstimateAdult; Aged; Antineoplastic Agents; Carcinoma Non-Small-Cell Lung; Disease-Free Survival; Erlotinib Hydrochloride; Female; Humans; Kaplan-Meier Estimate; Lung Neoplasms; Male; Middle Aged; Positron Emission Tomography Computed Tomography; Prospective Studies; Time Factors; Treatment OutcomeResponse evaluation criteria in solid tumorDisease-Free SurvivalErlotinib Hydrochloridenon–small cell lung cancerPositron Emission Tomography Computed TomographyHumansProspective StudiesNon-Small-Cell LungAgedCarcinomaMiddle AgedCarcinoma non-small-cell lungEORTCTreatment OutcomeRECISTResponse evaluation criteria in solid tumorsFemalePositron-emission tomographyPERCISTDiagnosi18F-FDG PET
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A recommended practical approach to the management of target therapy and angiogenesis inhibitors cardiotoxicity: an opinion paper of the working grou…

2016

The US National Cancer Institute estimates that cardiotoxicity (CTX) from target therapy refers mostly to four groups of drugs: epidermal growth factor receptor 2 inhibitors, angiogenic inhibitors, directed Abelson murine leukemia viral oncogene homolog inhibitors, and proteasome inhibitors. The main cardiotoxic side-effects related to antiepidermal growth factor receptor 2 therapy are left ventricular systolic dysfunction and heart failure. Angiogenesis inhibitors are associated with hypertension, left ventricular dysfunction/heart failure, myocardial ischemia, QT prolongation, and thrombosis. Moreover, other agents may be related to CTX induced by treatment. In this study, we review the g…

AngiogenesisLeftAngiogenesis Inhibitors030204 cardiovascular system & hematologyVentricular Dysfunction Left0302 clinical medicinetyrosine kinase inhibitorNeoplasmstyrosine kinase inhibitorsVentricular DysfunctionMolecular Targeted TherapyEpidermal growth factor receptorSocieties Medicalangiogenesis inhibitors; HER2/epidermal growth factor receptor 2; tyrosine kinase inhibitorABLbiologyDisease ManagementGeneral MedicineItalyCardiovascular DiseasesSupplement Submission030220 oncology & carcinogenesisangiogenesis inhibitors; HER2/epidermal growth factor receptor 2; tyrosine kinase inhibitors; Angiogenesis Inhibitors; Antineoplastic Agents; Cardiology; Cardiomyopathies; Cardiotoxicity; Heart Failure; Humans; Italy; Neoplasms; Practice Guidelines as Topic; Societies Medical; Ventricular Dysfunction Left; Disease ManagementPractice Guidelines as TopicCardiologyCardiology and Cardiovascular MedicineCardiomyopathiesmedicine.medical_specialtyCardiologyAntineoplastic AgentsRisk AssessmentQT interval03 medical and health sciencesGrowth factor receptorInternal medicineMedicalmedicineHumansMonitoring PhysiologicHeart FailureCardiotoxicitybusiness.industryCancerHER2/epidermal growth factor receptor 2medicine.diseaseangiogenesis inhibitors; HER2/epidermal growth factor receptor 2; tyrosine kinase inhibitors; Cardiology and Cardiovascular MedicineCardiotoxicityangiogenesis inhibitorHeart failurebiology.proteinbusinessSocietiesJournal of cardiovascular medicine (Hagerstown, Md.)
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Bax-derived membrane-active peptides act as potent and direct inducers of apoptosis in cancer cells.

2011

SUMMARYAlthough many cancer cells are primed for apoptosis, they usually develop resistance to cell death at multiple levels. Permeabilization of the outer mitochondrial membrane, which is mediated by proapoptotic Bcl-2 family members like Bax, is considered as a point-of-no-return for initiating apoptotic cell death. This crucial role has placed Bcl-2 family proteins as recurrent targets for anticancer drug development. Here, we propose and demonstrate a new concept based on using minimal active version of Bax to induce cell death independently of endogenous Bcl-2 proteins. We show that membrane-active segments of Bax can directly induce the release of mitochondria-residing apoptogenic fac…

ApoptosisMitochondrionMiceMESH: Protein Structure Tertiary0302 clinical medicineNeoplasmsgeneticsMESH: AnimalsMESH: Neoplasmsbcl-2-Associated X Protein0303 health sciencesbiologyMESH: PeptidesCytochrome capoptosisCytochromes cMESH: Cytochromes cproapoptotic BaxCell biologyMitochondriadrug therapymitochondria030220 oncology & carcinogenesisBacterial outer membraneProgrammed cell deathMESH: Cell Line TumorMESH: MitochondriaAntineoplastic Agents[SDV.CAN]Life Sciences [q-bio]/Cancerpore-forming peptideschemistryArticle03 medical and health sciencesBcl-2-associated X proteinBcl-2 familyCell Line TumorAnimalsHumansMESH: bcl-2-Associated X ProteinMESH: Mice030304 developmental biologyMESH: HumansMESH: ApoptosisBcl-2 familyCell BiologyProtein Structure Tertiaryanticancer agentantivascular therapyApoptosisdrug effectsCancer cellbiology.proteinMESH: Antineoplastic AgentspharmacologyphysiopathologyPeptidesmetabolism
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Arterial hypertension in cancer: The elephant in the room

2019

The great therapeutical success achieved by oncology is counterbalanced by growing evidences of cardiovascular (CV) toxicity due to many antineoplastic treatments. Cardiac adverse events may cause premature discontinuation of effective oncologic treatments or occur as late events undermining the oncologic success. Arterial hypertension is both the most common comorbidity in cancer patients and a frequent adverse effect of anticancer therapies. A pre-existing hypertension is known to increase the risk of other cardiac adverse events due to oncologic treatments, in particular heart failure. Moreover, as a strict association between cancer and CV diseases has emerged over the recent years, var…

Arterial hypertensionVascular Endothelial Growth Factor AAnthracyclines Anti VEGF agents Anti-hypertensive therapy Arterial hypertension Cancer Cardiotoxicitymedicine.medical_specialtyAnti VEGF agentmedicine.medical_treatmentAntineoplastic AgentsBlood PressureAnthracycline030204 cardiovascular system & hematologyAnthracyclines; Anti VEGF agents; Anti-hypertensive therapy; Arterial hypertension; Cancer; Cardiotoxicity; Antihypertensive Agents; Antineoplastic Agents; Blood Pressure; Humans; Hypertension; Neoplasms; Vascular Endothelial Growth Factor A03 medical and health sciences0302 clinical medicineNeoplasmsmedicineHumansAnthracyclines030212 general & internal medicineAnti-hypertensive therapyAdverse effectIntensive care medicineAntihypertensive AgentsCancerChemotherapyCardiotoxicitybusiness.industryAnti VEGF agentsCancermedicine.diseaseComorbidityCardiotoxicityDiscontinuationBlood pressureHeart failureHypertensionCardiology and Cardiovascular MedicinebusinessInternational Journal of Cardiology
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