Search results for "Neoplastic"

showing 10 items of 2901 documents

From ancient herb to modern drug: Artemisia annua and artemisinin for cancer therapy.

2017

Artemisia annua L. is used throughout Asia and Africa as tea and press juice to treat malaria and related symptomes (fever, chills). Its active ingredient, artemisinin (ARS), has been developed as antimalarial drug and is used worldwide. Interestingly, the bioactivity is not restricted to malaria treatment. We and others found that ARS-type drugs also reveal anticancer in vitro and in vivo. In this review, we give a systematic overview of the literature published over the past two decades until the end of 2016. Like other natural products, ARS acts in a multi-specific manner against tumors. The cellular response of ARS and its derivatives (dihydroartemisinin, artesunate, artemether, arteeth…

0301 basic medicineCancer ResearchNecroptosismedicine.medical_treatmentArtemisia annuaDihydroartemisininPharmacologyArtemisia annua03 medical and health scienceschemistry.chemical_compound0302 clinical medicineNeoplasmsmedicineHumansArtemetherArtemisininPI3K/AKT/mTOR pathwaybiologybiology.organism_classificationArtemisininsNeoplasm ProteinsGene Expression Regulation NeoplasticDrug repositioningOxidative Stress030104 developmental biologychemistryArtesunate030220 oncology & carcinogenesismedicine.drugSeminars in cancer biology
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Parthenolide and DMAPT exert cytotoxic effects on breast cancer stem-like cells by inducing oxidative stress, mitochondrial dysfunction and necrosis

2016

Triple-negative breast cancers (TNBCs) are aggressive forms of breast carcinoma associated with a high rate of recidivism. In this paper, we report the production of mammospheres from three lines of TNBC cells and demonstrate that both parthenolide (PN) and its soluble analog dimethylaminoparthenolide (DMAPT) suppressed this production and induced cytotoxic effects in breast cancer stem-like cells, derived from dissociation of mammospheres. In particular, the drugs exerted a remarkable inhibitory effect on viability of stem-like cells. Such an effect was suppressed by N-acetylcysteine, suggesting a role of reactive oxygen species (ROS) generation in the cytotoxic effect. Instead z-VAD, a ge…

0301 basic medicineCancer ResearchNecrosismedicine.disease_causeCancer -- Treatmentchemistry.chemical_compoundOnium CompoundsMedicineCytotoxic T cellBreast -- CancerMembrane Potential Mitochondrialchemistry.chemical_classificationSuperoxideMitochondrial DNAMitochondriaNeoplastic Stem CellsFemaleOriginal Articlemedicine.symptomOligopeptidesSesquiterpenesCell SurvivalNF-E2-Related Factor 2ImmunologyBreast NeoplasmsReal-Time Polymerase Chain Reaction03 medical and health sciencesCellular and Molecular NeuroscienceDownregulation and upregulationCell Line TumorHumansParthenolideparthenolide cancer stem cell triple-negative breast cancer reactive oxygen species nuclear factor erythroid 2-related factor 2Fluorescent DyesReactive oxygen speciesbusiness.industryAcetophenonesNADPH OxidasesCell BiologyCell nuclei -- AbnormalitiesOxidative Stress030104 developmental biologychemistryApocyninImmunologyCancer researchReactive Oxygen SpeciesbusinessOxidative stressTranscription FactorsCell Death & Disease
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Effects of the MDM-2 inhibitor Nutlin-3a on PDAC cells containing and lacking WT-TP53 on sensitivity to chemotherapy, signal transduction inhibitors …

2019

Abstract Mutations at the TP53 gene are readily detected (approximately 50–75%) in pancreatic ductal adenocarcinoma (PDAC) patients. TP53 was previously thought to be a difficult target as it is often mutated, deleted or inactivated on both chromosomes in certain cancers. In the following study, the effects of restoration of wild-type (WT) TP53 activity on the sensitivities of MIA-PaCa-2 pancreatic cancer cells to the MDM2 inhibitor nutlin-3a in combination with chemotherapy, targeted therapy, as well as, nutraceuticals were examined. Upon introduction of the WT-TP53 gene into MIA-PaCa-2 cells, which contain a TP53 gain of function (GOF) mutation, the sensitivity to the MDM2 inhibitor incre…

0301 basic medicineCancer ResearchNutlin-3aSettore MED/09 - Medicina Internaendocrine system diseasesmedicine.medical_treatmentmedicine.disease_causePiperazinesTargeted therapy0302 clinical medicineTP53MutationbiologyChemistryImidazolesProto-Oncogene Proteins c-mdm2OxaliplatinTargeted TherapeuticsDrug sensitivity; Nutlin-3a; Nutraceuticals; Targeted therapeutics; TP53030220 oncology & carcinogenesisMolecular MedicineMdm2NutraceuticalNutraceuticalsSignal transductionCarcinoma Pancreatic DuctalSignal Transductionmedicine.drugDrug sensitivityAntineoplastic AgentsIrinotecan03 medical and health sciencesCell Line TumorPancreatic cancerGeneticsmedicineHumansMolecular BiologyneoplasmsChemotherapymedicine.diseasedigestive system diseasesOxaliplatinPancreatic Neoplasms030104 developmental biologyCell cultureDietary Supplementsbiology.proteinCancer researchTERAPÊUTICA MÉDICATumor Suppressor Protein p53
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Repurposing of plant alkaloids for cancer therapy: Pharmacology and toxicology.

2019

Drug repurposing (or repositioning) is an emerging concept to use old drugs for new treatment indications. Phytochemicals isolated from medicinal plants have been largely neglected in this context, although their pharmacological activities have been well investigated in the past, and they may have considerable potentials for repositioning. A grand number of plant alkaloids inhibit syngeneic or xenograft tumor growth in vivo. Molecular modes of action in cancer cells include induction of cell cycle arrest, intrinsic and extrinsic apoptosis, autophagy, inhibition of angiogenesis and glycolysis, stress and anti-inflammatory responses, regulation of immune functions, cellular differentiation, a…

0301 basic medicineCancer ResearchPhytochemicalsContext (language use)Antineoplastic AgentsPharmacologymedicine.disease_causeMetastasis03 medical and health sciences0302 clinical medicineAlkaloidsNeoplasmsDrug DiscoveryToxicity TestsmedicineAnimalsHumansRepurposingCardiotoxicitybusiness.industryDrug Repositioningmedicine.diseaseDrug repositioning030104 developmental biology030220 oncology & carcinogenesisCancer cellbusinessCarcinogenesisGenotoxicitySeminars in cancer biology
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Concepts to Target MYC in Pancreatic Cancer.

2016

Abstract Current data suggest that MYC is an important signaling hub and driver in pancreatic ductal adenocarcinoma (PDAC), a tumor entity with a strikingly poor prognosis. No targeted therapies with a meaningful clinical impact were successfully developed against PDAC so far. This points to the need to establish novel concepts targeting the relevant drivers of PDAC, like KRAS or MYC. Here, we discuss recent developments of direct or indirect MYC inhibitors and their potential mode of action in PDAC. Mol Cancer Ther; 15(8); 1792–8. ©2016 AACR.

0301 basic medicineCancer ResearchPoor prognosisPancreatic ductal adenocarcinomaendocrine system diseasesGene regulatory networkAntineoplastic AgentsBiologymedicine.disease_causeBioinformaticsProto-Oncogene Proteins c-myc03 medical and health sciencesPancreatic cancerCarcinomamedicineAnimalsHumansGene Regulatory NetworksMolecular Targeted TherapyProtein Kinase InhibitorsCancerGenetic Variationmedicine.diseasedigestive system diseasesGene Expression Regulation NeoplasticPancreatic Neoplasms030104 developmental biologyOncologyCarrier proteinCancer researchKRASCarrier ProteinsCarcinoma Pancreatic DuctalProtein BindingSignal TransductionMolecular cancer therapeutics
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Betulinic acid induces a novel cell death pathway that depends on cardiolipin modification

2016

Cancer is associated with strong changes in lipid metabolism. For instance, normal cells take up fatty acids (FAs) from the circulation, while tumour cells generate their own and become dependent on de novo FA synthesis, which could provide a vulnerability to target tumour cells. Betulinic acid (BetA) is a natural compound that selectively kills tumour cells through an ill-defined mechanism that is independent of BAX and BAK, but depends on mitochondrial permeability transition-pore opening. Here we unravel this pathway and show that BetA inhibits the activity of steroyl-CoA-desaturase (SCD-1). This enzyme is overexpressed in tumour cells and critically important for cells that utilize de n…

0301 basic medicineCancer ResearchProgrammed cell deathCardiolipinsMitochondrionCell Line03 medical and health scienceschemistry.chemical_compoundSDG 3 - Good Health and Well-beingBetulinic acidGeneticsCardiolipinHumansBetulinic AcidCytotoxicityMolecular BiologyCell DeathbiologyCytochrome cFatty AcidsCytochromes cLipid metabolismAntineoplastic Agents PhytogenicTriterpenesMitochondriaCell biology030104 developmental biologyBiochemistrychemistryCancer cellbiology.protein/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingPentacyclic TriterpenesStearoyl-CoA Desaturase
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HDAC1 and HDAC2 integrate the expression of p53 mutants in pancreatic cancer.

2015

Mutation of p53 is a frequent genetic lesion in pancreatic cancer being an unmet clinical challenge. Mutants of p53 have lost the tumour-suppressive functions of wild type p53. In addition, p53 mutants exert tumour-promoting functions, qualifying them as important therapeutic targets. Here, we show that the class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of p53 mutants in human and genetically defined murine pancreatic cancer cells. Our data reveal that the inhibition of these HDACs with small molecule HDAC inhibitors (HDACi), as well as the specific genetic elimination of HDAC1 and HDAC2, reduce the expression of mutant p53 mRNA and protein levels. We fur…

0301 basic medicineCancer ResearchProteasome Endopeptidase ComplexMutantHistone Deacetylase 2Histone Deacetylase 1Biologymedicine.disease_causeMolecular oncologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicePancreatic cancerGeneticsmedicineAnimalsHumansRNA MessengerPromoter Regions GeneticMolecular BiologyRegulation of gene expressionMice KnockoutMutationWild typeCancerProto-Oncogene Proteins c-mdm2medicine.diseaseGenes p53HDAC13. Good healthGene Expression Regulation NeoplasticHistone Deacetylase InhibitorsPancreatic NeoplasmsDisease Models Animal030104 developmental biologyMutationCancer researchOncogene
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Comparative analysis of the effects of a sphingosine kinase inhibitor to temozolomide and radiation treatment on glioblastoma cell lines.

2017

ABSTRACT Glioblastoma multiforme (GBM) exhibits high resistance to the standard treatment of temozolomide (TMZ) combined with radiotherapy, due to its remarkable cell heterogeneity. Accordingly, there is a need to target alternative molecules enhancing specific GBM autocrine or paracrine mechanisms and amplifying the effect of standard treatment. Sphingosine 1-phosphate (S1P) is such a lipid target molecule with an important role in cell invasion and proliferation. Sphingosine kinase inhibitors (SKI) prevent S1P formation and induce increased production of reactive oxygen species (ROS), which may potentiate radiation cytotoxicity. We analyzed the effect of SKI singular versus combined treat…

0301 basic medicineCancer ResearchRadiation-Sensitizing AgentsCell SurvivalCellSphingosine kinaseApoptosistemozolomideBiologyRadiation Tolerancesphingosine kinase inhibition03 medical and health scienceschemistry.chemical_compoundCell Line TumorX-raysmedicineHumansGPx1oxidative stressCytotoxicityAutocrine signallingAntineoplastic Agents AlkylatingPharmacologychemistry.chemical_classificationReactive oxygen speciesTemozolomideSphingosineBrain NeoplasmsDrug SynergismChemoradiotherapyMolecular biologyDacarbazinePhosphotransferases (Alcohol Group Acceptor)030104 developmental biologymedicine.anatomical_structureOncologychemistryCell cultureradiosensitivityCancer researchMolecular MedicineDrug Screening Assays AntitumorGlioblastomamedicine.drugResearch PaperCancer biologytherapy
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Monoclonal Antibodies, Bispecific Antibodies and Antibody-Drug Conjugates in Oncohematology

2020

Background: The therapeutic outcomes and the prognosis of patients with various hematologic malignancies are not always ideal with the current standard of care. Objective: The aim of this study is to analyze the results of the use of monoclonal antibodies, bispecific antibodies and antibody-drug conjugates for the therapy of malignant hemopathies. Methods: A mini-review was achieved using the articles published in Web of Science and PubMed between January 2017 and January 2020 and the new patents were made in this field. Results: Naked monoclonal antibodies have improved the therapeutic results obtained with standard of care, but they also have side effects and the use of some of them can …

0301 basic medicineCancer ResearchReceptor complexAntibody-drug conjugateImmunoconjugatesmedicine.drug_classmedicine.medical_treatmentAntineoplastic AgentsOfatumumabMonoclonal antibodyPatents as Topic03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAntigenObinutuzumabAntibodies BispecificDrug DiscoveryAnimalsHumansMedicinePharmacology (medical)Clinical Trials as Topicbusiness.industryAntibodies MonoclonalGeneral MedicineImmunotherapy030104 developmental biologyOncologychemistryHematologic Neoplasms030220 oncology & carcinogenesisMonoclonalCancer researchImmunotherapybusinessRecent Patents on Anti-Cancer Drug Discovery
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Tumor-Associated Fibroblasts Promote HER2-Targeted Therapy Resistance through FGFR2 Activation

2020

AbstractPurpose:Despite the therapeutic success of existing HER2-targeted therapies, tumors invariably relapse. This study aimed at identifying new mechanisms responsible for HER2-targeted therapy resistance.Experimental Design:We have used a platform of HER2-targeted therapy–resistant cell lines and primary cultures of healthy and tumor-associated fibroblasts (TAF) to identify new potential targets related to tumor escape from anti-HER2 therapies.Results:We have shown that TAFs promote resistance to HER2-targeted therapies. TAFs produce and secrete high levels of FGF5, which induces FGFR2 activation in the surrounding breast cancer cells. FGFR2 transactivates HER2 via c-Src, leading to res…

0301 basic medicineCancer ResearchReceptor ErbB-2medicine.medical_treatmentMice NudeBreast NeoplasmsDrug resistanceTargeted therapy03 medical and health sciencesMice0302 clinical medicineBreast cancerCancer-Associated FibroblastsTrastuzumabCell Line TumorAntineoplastic Combined Chemotherapy ProtocolsmedicineNeoplasmAnimalsHumansReceptor Fibroblast Growth Factor Type 2skin and connective tissue diseasesneoplasmsbusiness.industryLapatinibTrastuzumabmedicine.diseaseXenograft Model Antitumor AssaysSurvival Rate030104 developmental biologyOncologyTumor EscapeApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchFemaleSignal transductionNeoplasm Recurrence Localbusinessmedicine.drugSignal Transduction
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