Search results for "cancer cell"

showing 10 items of 756 documents

Cancer-cell traffic in the liver. I. Growth kinetics of cancer cells after portal-vein delivery

1992

Following the intrasplenic injection of B16F10 melanoma cells into mice, at first single cells, and later multicellular tumor foci were observed at different times in the liver. Cell numbers and tumor volumes were determined over the next 12 days, by confocal microscopy of thick liver sections. Fifteen minutes after injection, approximately 20% of the melanoma cells were identified in the liver microvasculature; after 48 hr, only 0.68% of these retained morphologic integrity; by 5 days only 0.13% of the originally detected cells incorporated BUdR; and, by 12 days, these subsequently grew into tumor nodules. Tumor volume changes with time were not exponential and, following a non-replicative…

Cancer ResearchPathologymedicine.medical_specialtyTime FactorsPopulationMelanoma ExperimentalMetastasisMiceMesenteric VeinsParenchymaAnimalsMedicineeducationeducation.field_of_studyPortal Veinbusiness.industryCell growthMelanomaLiver Neoplasmsmedicine.diseaseExtravasationMice Inbred C57BLTransplantationOncologySplenic VeinInjections IntravenousCancer cellFemalebusinessCell DivisionNeoplasm TransplantationInternational Journal of Cancer
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Aurora-A Transcriptional Silencing and Vincristine Treatment Show a Synergistic Effect in Human Tumor Cells

2008

Aurora-A is a centrosome-associated serine/threonine kinase that is overexpressed in multiple types of human tumors. Primarily, Aurora-A functions in centrosome maturation and mitotic spindle assembly. Overexpression of Aurora-A induces centrosome amplification and G 2 /M cell cycle progression. Recently, it was observed that overexpression of Aurora-A renders cells resistant to cisplatin (CDDP)-, etoposide-, and paclitaxel-induced apoptosis.Our results indicate that already in initial stages of cancer progression Aurora-A overexpression could have a major role in inducing supernumerary centrosomes and aneuploidy, as shown by immunohistochemistry on tissue sections from various stages of hu…

Cancer ResearchPathologymedicine.medical_specialtyTranscription GeneticApoptosismacromolecular substancesProtein Serine-Threonine KinasesBiologyTransfectionPLK1Aurora KinasesRNA interferenceCell Line TumormedicineHumansGene silencingGene SilencingRNA Small InterferingMitotic catastropheCentrosomeCisplatinCarcinomaCell CycleDrug SynergismAuroraA/stk15centrosome amplificationAneuploidy CINGeneral MedicineCell cycleAneuploidyAntineoplastic Agents PhytogenicGene Expression Regulation NeoplasticSettore BIO/18 - Geneticaenzymes and coenzymes (carbohydrates)OncologyVincristineCentrosomeColonic Neoplasmsembryonic structuresCancer cellCancer researchbiological phenomena cell phenomena and immunityHeLa Cellsmedicine.drugOncology Research Featuring Preclinical and Clinical Cancer Therapeutics
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Claudin-18 splice variant 2 is a pan-cancer target suitable for therapeutic antibody development

2008

Abstract Purpose: Antibody-based cancer therapies have emerged as the most promising therapeutics in oncology. The purpose of this study was to discover novel targets for therapeutic antibodies in solid cancer. Experimental Design: We combined data mining and wet-bench experiments to identify strictly gastrocyte lineage–specific cell surface molecules and to validate them as therapeutic antibody targets. Results: We identified isoform 2 of the tight junction molecule claudin-18 (CLDN18.2) as a highly selective cell lineage marker. Its expression in normal tissues is strictly confined to differentiated epithelial cells of the gastric mucosa, but it is absent from the gastric stem cell zone. …

Cancer ResearchPathologymedicine.medical_specialtymicemedicine.drug_classMolecular Sequence DataGene ExpressionBiologyMonoclonal antibodyMalignant transformationAntigenmedicineProtein IsoformsAnimalsHumansNeoplasms Glandular and EpithelialMembrane Proteins/geneticsAntibodies Monoclonal/immunologyProtein Isoforms/immunologyBase SequenceReverse Transcriptase Polymerase Chain ReactionNeoplasms Glandular and Epithelial/drug therapyAntibodies MonoclonalImmunotherapy ActiveMembrane ProteinsCancermedicine.diseaseFlow CytometryImmunohistochemistryImmunotherapy Active/methodsOncologyCancer cellClaudinsbiology.proteinCancer researchImmunohistochemistryAntibodyStem cell
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Development of resistance towards artesunate in MDA-MB-231 human breast cancer cells.

2011

Breast cancer is the most common cancer and the second leading cause of cancer death in industrialized countries. Systemic treatment of breast cancer is effective at the beginning of therapy. However, after a variable period of time, progression occurs due to therapy resistance. Artesunate, clinically used as anti-malarial agent, has recently revealed remarkable anti-tumor activity offering a role as novel candidate for cancer chemotherapy. We analyzed the anti-tumor effects of artesunate in metastasizing breast carcinoma in vitro and in vivo. Unlike as expected, artesunate induced resistance in highly metastatic human breast cancer cells MDA-MB-231. Likewise acquired resistance led to abol…

Cancer ResearchPhytochemistryPhytopharmacologyCancer TreatmentArtesunateApoptosisElectrophoretic Mobility Shift AssayDrug resistanceNude MiceMetastasischemistry.chemical_compoundMiceMolecular Cell BiologyDrug DiscoveryBreast TumorsBasic Cancer ResearchMedicinebcl-2-Associated X ProteinMultidisciplinaryQRNF-kappa BArtemisininsChemistryOncologyMedicineFemaleMatrix Metalloproteinase 1Breast carcinomamedicine.drugResearch Article570Drugs and DevicesDrug Research and DevelopmentCell SurvivalScienceMice Nude570 Life SciencesBreast NeoplasmsTumor Cell Line610 Medical Sciences MedicineBreast cancerComplementary and Alternative MedicineCell Line TumorAnimalsHumansDoxorubicinBiologyNeoplasm Drug Resistancebusiness.industryCancers and NeoplasmsChemotherapy and Drug Treatmentmedicine.diseaseXenograft Model Antitumor AssaysTranscription Factor AP-1chemistryTumor progressionArtesunateDrug Resistance NeoplasmCancer cellImmunologyEthnopharmacologyCancer researchbusinessPloS one
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Cannabinoid-associated cell death mechanisms in tumor models

2012

In recent years, cannabinoids (the active compo- nents of Cannabis sativa) and their derivatives have received considerable interest due to findings that they can affect the viability and invasiveness of a variety of different cancer cells. Moreover, in addition to their inhibitory effects on tumor growth and migration, angiogenesis and metastasis, the ability of these compounds to induce different pathways of cell death has been highlighted. Here, we review the most recent results generating interest in the field of death mechanisms induced by cannabinoids in cancer cells. In particular, we analyze the pathways triggered by cannabinoids to induce apoptosis or autophagy and investigate the …

Cancer ResearchProgrammed cell deathAngiogenesismedicine.medical_treatmentAutophagyCancerBiologyCell cyclemedicine.diseaseMetastasisCell biologyOncologyCancer cellmedicineCancer researchCannabinoidInternational Journal of Oncology
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Mcl-1 is an anti-apoptotic factor for human hepatocellular carcinoma

2005

Defects in apoptosis signaling in hepatocytes contribute to tumorigenesis in hepatocellular carcinoma (HCC). In addition, treatment with chemotherapeutic drugs is often ineffective in HCC patients due to the apoptosis resistance of cancer cells. Anti-apoptotic members of the Bcl-2 family, including myeloid cell leukemia-1 (Mcl-1), which regulate intrinsic apoptosis induction at the mito-chondrial level, are often overexpressed in human cancer, and are implicated with disease grade and prognosis. Yet, little is known about the role of Mcl-1 in HCC. In this study, we analyzed the relevance of Mcl-1 expression for the apop-tosis resistance of human HCC. Mcl-1 protein expression was considerabl…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularApoptosisBiologyPhosphatidylinositol 3-KinasesEpidermal growth factorhemic and lymphatic diseasesTumor Cells CulturedmedicineHumansneoplasmsProtein kinase BPI3K/AKT/mTOR pathwayAkt/PKB signaling pathwayGene Expression ProfilingLiver NeoplasmsIntrinsic apoptosisPrognosisdigestive system diseasesNeoplasm ProteinsProto-Oncogene Proteins c-bcl-2OncologyImmunologyCancer cellCancer researchMyeloid Cell Leukemia Sequence 1 ProteinHepatocyte growth factorProto-Oncogene Proteins c-aktmedicine.drugInternational Journal of Oncology
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Artesunate induces oxidative DNA damage, sustained DNA double-strand breaks, and the ATM/ATR damage response in cancer cells.

2011

Abstract Artesunate, the active agent from Artemisia annua L. used in the traditional Chinese medicine, is being applied as a first-line drug for malaria treatment, and trials are ongoing that include this drug in cancer therapy. Despite increasing interest in its therapeutic application, the mode of cell killing provoked by artesunate in human cells is unknown. Here, we show that artesunate is a powerful inducer of oxidative DNA damage, giving rise to formamidopyrimidine DNA glycosylase–sensitive sites and the formation of 8-oxoguanine and 1,N6-ethenoadenine. Oxidative DNA damage was induced in LN-229 human glioblastoma cells dose dependently and was paralleled by cell death executed by ap…

Cancer ResearchProgrammed cell deathDNA RepairRAD51Drug Evaluation PreclinicalArtesunateApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiologyProtein Serine-Threonine KinasesModels Biologicalchemistry.chemical_compoundNeoplasmsTumor Cells CulturedHumansDNA Breaks Double-StrandedTumor Suppressor ProteinsMolecular biologyAntineoplastic Agents PhytogenicArtemisininsUp-RegulationNon-homologous end joiningDNA-Binding ProteinsOxidative StressCell killingOncologychemistryArtesunateApoptosisCancer cellHomologous recombinationDNA DamageMolecular cancer therapeutics
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Estrogen receptor α regulates non-canonical autophagy that provides stress resistance to neuroblastoma and breast cancer cells and involves BAG3 func…

2015

AbstractBreast cancer is a heterogeneous disease and approximately 70% of newly diagnosed breast cancers are estrogen receptor (ER) positive. Out of the two ER types, α and β, ERα is the only ER that is detectable by immunohistochemistry in breast cancer biopsies and is the predominant subtype expressed in breast tumor tissue. ER-positive tumors are currently treated with anti-hormone therapy to inhibit ER signaling. It is well known that breast cancer cells can develop endocrine resistance and resistance to anti-hormone therapy and this can be facilitated via the autophagy pathway, but so far the description of a detailed autophagy expression profile of ER-positive cancer cells is missing.…

Cancer ResearchProgrammed cell deathImmunologyEstrogen receptorBreast NeoplasmsBiologyBAG3Cellular and Molecular NeuroscienceNeuroblastomaBreast cancermedicineAutophagyEstrogen Receptor betaHumansPrecision MedicineEstrogen receptor betaPI3K/AKT/mTOR pathwayAdaptor Proteins Signal TransducingEstrogen Replacement TherapyEstrogen Receptor alphaCell Biologymedicine.disease3. Good healthCell biologyGene Expression Regulation NeoplasticCancer cellMCF-7 CellsOriginal ArticleFemaleApoptosis Regulatory ProteinsEstrogen receptor alphaSignal TransductionCell Death & Disease
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Midregion PTHrP regulates Rip1 and caspase expression in MDA-MB231 breast cancer cells.

2007

It was previously reported that the midregion PTHrP domain (38-94)-amide restrains growth and invasion "in vitro", causes striking toxicity and accelerates death of some breast cancer cell lines, the most responsive being MDA-MB231 whose tumorigenesis was also attenuated "in vivo". In addition, we have demonstrated that midregion PTHrP is imported in the nucleoplasm of cultured MDA-MB231 cells, and that "in vitro" it can bind chromatin of metaphase spread preparations and also an isolated 20-mer oligonucleotide, thereby appearing endowed with a putative transcription factor-like DNA-binding ability. Here, we examined whether PTHrP (38-94)-amide was able to modulate the expression of genes e…

Cancer ResearchProgrammed cell deathbcl-X ProteinApoptosisBreast NeoplasmsPTHrP Rip1 caspase breast cancer cellsmedicine.disease_causeTransfectionCell MovementCell Line TumorGene expressionmedicineTranscriptional regulationHumansNeoplasm InvasivenessSettore BIO/06 - Anatomia Comparata E Citologiaskin and connective tissue diseasesCaspaseCell ProliferationNucleoplasmbiologyJNK Mitogen-Activated Protein KinasesParathyroid Hormone-Related ProteinRNA-Binding ProteinsOligonucleotides AntisenseMolecular biologyPeptide FragmentsChromatinCell biologyNuclear Pore Complex ProteinsSettore BIO/12 - Biochimica Clinica E Biologia Molecolare ClinicaOncologyApoptosisCaspasesbiology.proteinFemalebcl-Associated Death ProteinCarcinogenesisSignal TransductionBreast cancer research and treatment
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The Proton-Boron Reaction Increases the Radiobiological Effectiveness of Clinical Low- and High-Energy Proton Beams: Novel Experimental Evidence and …

2021

Protontherapy is a rapidly expanding radiotherapy modality where accelerated proton beams are used to precisely deliver the dose to the tumor target but is generally considered ineffective against radioresistant tumors. Proton-Boron Capture Therapy (PBCT) is a novel approach aimed at enhancing proton biological effectiveness. PBCT exploits a nuclear fusion reaction between low-energy protons and 11B atoms, i.e. p+11B→ 3α (p-B), which is supposed to produce highly-DNA damaging α-particles exclusively across the tumor-conformed Spread-Out Bragg Peak (SOBP), without harming healthy tissues in the beam entrance channel. To confirm previous work on PBCT, here we report new in-vitro data obtained…

Cancer ResearchProtonmedicine.medical_treatmentSobpBragg peakBSH030218 nuclear medicine & medical imaging03 medical and health sciences0302 clinical medicineRadioresistancemedicineIrradiationRC254-282Original Researchprotontherapycancer cell killingChemistryalpha-particleNeoplasms. Tumors. Oncology. Including cancer and carcinogensProton-Boron ReactionRadiation therapyCell killingchromosome aberrationsOncology030220 oncology & carcinogenesisCancer researchproton-boron (B) fusion-enhanced proton therapy (PBFEPT)chromosome aberrationBeam (structure)Frontiers in Oncology
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