Search results for "C25"

showing 10 items of 566 documents

NGS‐based liquid biopsy profiling identifies mechanisms of resistance to ALK inhibitors: a step toward personalized NSCLC treatment

2021

Despite impressive and durable responses, nonsmall cell lung cancer (NSCLC) patients treated with anaplastic lymphoma kinase (ALK) inhibitors (ALK‐Is) ultimately progress due to development of resistance. Here, we have evaluated the clinical utility of circulating tumor DNA (ctDNA) profiling by next‐generation sequencing (NGS) upon disease progression. We collected 26 plasma and two cerebrospinal fluid samples from 24 advanced ALK‐positive NSCLC patients at disease progression to an ALK‐I. These samples were analyzed by NGS and digital PCR. A tool to retrieve variants at the ALK locus was developed (VALK tool). We identified at least one resistance mutation in the ALK locus in ten (38.5%) p…

0301 basic medicineCancer ResearchLung NeoplasmsEML4-ALKAntineoplastic AgentsEML4‐ALKmedicine.disease_causeNSCLCIDH2Circulating Tumor DNA03 medical and health sciencesALK-TKI0302 clinical medicineCarcinoma Non-Small-Cell LungMAP2K1hemic and lymphatic diseasesALK‐TKIGeneticsmedicineHumansAnaplastic lymphoma kinaseAnaplastic Lymphoma KinaseDigital polymerase chain reactionPrecision MedicineLiquid biopsyProtein Kinase InhibitorsneoplasmsResearch ArticlesRC254-282MutationCrizotinibliquid biopsybusiness.industryHigh-Throughput Nucleotide SequencingNeoplasms. Tumors. Oncology. Including cancer and carcinogensGeneral MedicineResistance mutation3. Good health030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisNGSMutationCancer researchMolecular MedicinebusinessResearch Articlemedicine.drugMolecular Oncology
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The PDGFRβ/ERK1/2 pathway regulates CDCP1 expression in triple-negative breast cancer

2018

Background CDCP1, a transmembrane protein with tumor pro-metastatic activity, was recently identified as a prognostic marker in TNBC, the most aggressive breast cancer subtype still lacking an effective molecular targeted therapy. The mechanisms driving CDCP1 over-expression are not fully understood, although several stimuli derived from tumor microenvironment, such as factors present in Wound Healing Fluids (WHFs), reportedly increase CDCP1 levels. Methods The expression of CDCP1, PDGFRβ and ERK1/2cell was tested by Western blot after stimulation of MDA-MB-231 cells with PDGF-BB and, similarly, in presence or not of ERK1/2 inhibitor in a panel of TNBC cell lines. Knock-down of PDGFRβ was e…

0301 basic medicineCancer ResearchMAP Kinase Signaling SystemCDCP1medicine.medical_treatmentPDGFRβPDGF-BBBecaplerminTriple Negative Breast NeoplasmsBiologylcsh:RC254-282Targeted therapyReceptor Platelet-Derived Growth Factor beta03 medical and health sciences0302 clinical medicineFISHDownregulation and upregulationWestern blotAntigens CDAntigens NeoplasmCell Line TumorGeneticsmedicineHumansRNA Small InterferingReceptorTriple-negative breast cancerMitogen-Activated Protein Kinase 1Tumor microenvironmentMitogen-Activated Protein Kinase 3ERK1/2medicine.diagnostic_testMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensNeoplasm ProteinsUp-RegulationGene Expression Regulation Neoplastic030104 developmental biologyOncologyGene Knockdown Techniques030220 oncology & carcinogenesisCDCP1Cancer researchImmunohistochemistryFemaleCell Adhesion MoleculesTNBCResearch ArticleIHCBMC Cancer
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Breast Cancer Organoids Model Patient-Specific Response to Drug Treatment

2020

Tumor organoids are tridimensional cell culture systems that are generated in vitro from surgically resected patients&rsquo

0301 basic medicineCancer ResearchMechanotransductionBreast cancer; Dasatinib; Drug testing; Heterogeneity; Mechanotransduction; Patient‐derived tumor organoids; Statin; YAPPatient‐derived tumor organoidCellDasatinibDrug resistanceSettore MED/08 - Anatomia PatologicaBiologylcsh:RC254-282Article03 medical and health sciencesBreast cancer0302 clinical medicineBreast cancerbreast cancermedicineOrganoidSettore MED/05 - Patologia Clinicadasatinibdrug testingmechanotransductionpatient-derived tumor organoidsGenetic heterogeneitystatinStatinDrug testingBreast cancerDasatinib Drug testing Drug testing Heterogeneity Patient‐derived tumor organoids Statin YAPmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensIn vitroDasatinib030104 developmental biologymedicine.anatomical_structureOncologyCell culture030220 oncology & carcinogenesisCancer researchPatient‐derived tumor organoidsYAPHeterogeneityheterogeneitymedicine.drugCancers
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Integrating the Tumor Microenvironment into Cancer Therapy

2020

© 2020 by the authors.

0301 basic medicineCancer ResearchMechanotransductionReviewGut floralcsh:RC254-28203 medical and health sciences0302 clinical medicineImmune systemStromamedicineMechanotransductionStromal reprogrammingTumor microenvironmentbiologybusiness.industryMicrobiotaCancerlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasebiology.organism_classificationPrognostic toolsMetforminMitochondria030104 developmental biologyMetabolismOncologyImmune therapyTumor progression030220 oncology & carcinogenesisCancer researchBiomarker discoverybusinessReprogrammingVitamin D3
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Bacitracin and Rutin Regulate Tissue Factor Production in Inflammatory Monocytes and Acute Myeloid Leukemia Blasts

2021

Simple Summary Aberrant tissue factor (TF) expression by transformed myeloblasts and inflammatory monocytes contributes to coagulation activation in acute myeloid leukemia (AML). TF procoagulant activity (PCA) is regulated by protein disulfide isomerase (PDI), an oxidoreductase with chaperone activity, but its specific role in AML-associated TF biology is unclear. Here, we provide novel mechanistic insights into this interrelation. We show that bacitracin and rutin, two pan-inhibitors of the PDI family, prevent lipopolysaccharide (LPS)-induced monocyte TF production under inflammatory conditions and constitutive TF expression by THP1 cells and AML blasts, thus exerting promising anticoagula…

0301 basic medicineCancer ResearchMyeloidDaunorubicinacute myeloid leukemia030204 cardiovascular system & hematologyPeripheral blood mononuclear cellArticleFlow cytometry03 medical and health sciencesTissue factor0302 clinical medicineDownregulation and upregulationhemic and lymphatic diseasesmedicinecoagulationProtein disulfide-isomeraseRC254-282medicine.diagnostic_testChemistryrutinNeoplasms. Tumors. Oncology. Including cancer and carcinogensMyeloid leukemiatissue factorprotein disulfide isomeraseMolecular biology030104 developmental biologymedicine.anatomical_structureOncologyinflammationtissue factor; protein disulfide isomerase; acute myeloid leukemia; coagulation; inflammation; rutin; monocytesmonocytesmedicine.drugCancers
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Imiquimod inhibits growth and induces differentiation of myeloid leukemia cell lines

2018

Background: The antitumoral effects of different Toll-like receptor (TLRs) agonists is mediated by activating immune responses to suppress tumors growth, although TLR ligands may also have a direct effect on tumoral cells. Given that TLR signaling induces hematopoietic cell differentiations this may serve as a novel differentiation therapeutic approach for AML. Methods: We investigated the effects of agonists for the ten human TLRs on the proliferation, apoptosis, cell cycle and differentiation of ten different types of myeloid leukemia cell lines (HL-60, U-937, KG-1, KG-1a, K-562, Kasumi-1, EOL-1, NB4, MOLM-13 and HEL). Proliferation was measured using the CellTiter 96 (R) Aqueous One Solu…

0301 basic medicineCancer ResearchMyeloidImiquimodlcsh:RC254-282Flow cytometry03 medical and health sciences0302 clinical medicineToll-like receptorGeneticsmedicineCytotoxic T cellMyeloid leukemia cell lineslcsh:QH573-671Toll-like receptorImiquimodmedicine.diagnostic_testChemistryCell growthlcsh:CytologyMyeloid leukemiaCell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer researchPrimary Researchmedicine.drugCancer Cell International
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Using the r package spatstat to assess inhibitory effects of microregional hypoxia on the infiltration of cancers of the head and neck region by cyto…

2021

Simple Summary Progress in the field of in situ proteomics allows for the simultaneous detection of multiple biomarkers within one cancer tissue specimen. As a result, biological hypotheses previously only assessable ex vivo can now be studied in human cancer tissue. However, methods for objective analysis have so far been lacking behind. In this study, we established a free, objective, and entirely open-source-based method for the analysis of multiplexed immunofluorescence specimens. This will gain further importance with the availability of more advanced multiplexing methods in the future. Abstract (1) Background: The immune system has physiological antitumor activity, which is partially …

0301 basic medicineCancer ResearchOpen-sourcespatial analysisCellBiologyArticle03 medical and health sciences0302 clinical medicineImmune systemmedicineCytotoxic T cellCancer immune evasionHead and neck cancerHypoxiacancer immune evasionRC254-282open-sourceTumor hypoxiaMultichannel im-munofluorescencehypoxiaHead and neck cancerRSpatial analysisNeoplasms. Tumors. Oncology. Including cancer and carcinogensHypoxia (medical)medicine.diseaseCTL*030104 developmental biologymedicine.anatomical_structureOncologymultichannel immunofluorescence030220 oncology & carcinogenesisCancer researchhead and neck cancermedicine.symptomInfiltration (medical)
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Multiple myeloma-derived exosomes are enriched of amphiregulin (AREG) and activate the epidermal growth factor pathway in the bone microenvironment l…

2019

Background Multiple myeloma (MM) is a clonal plasma cell malignancy associated with osteolytic bone disease. Recently, the role of MM-derived exosomes in the osteoclastogenesis has been demonstrated although the underlying mechanism is still unknown. Since exosomes-derived epidermal growth factor receptor ligands (EGFR) are involved in tumor-associated osteolysis, we hypothesize that the EGFR ligand amphiregulin (AREG) can be delivered by MM-derived exosomes and participate in MM-induced osteoclastogenesis. Methods Exosomes were isolated from the conditioned medium of MM1.S cell line and from bone marrow (BM) plasma samples of MM patients. The murine cell line RAW264.7 and primary human CD1…

0301 basic medicineCancer ResearchOsteoclastsPlasma cellInterleukin 8ExosomesLigandsMice0302 clinical medicineEpidermal growth factorOsteogenesisMultiple myelomaBone diseaseTumor MicroenvironmentEpidermal growth factor receptorbiologyChemistryAntibodies MonoclonalOsteoblastCell DifferentiationHematologylcsh:Diseases of the blood and blood-forming organslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensErbB Receptorsmedicine.anatomical_structureOncology030220 oncology & carcinogenesislcsh:RC254-282Amphiregulin03 medical and health sciencesAmphiregulinOsteoclastCell Line TumormedicineCell AdhesionAnimalsHumansMolecular BiologyOsteoblastsEpidermal Growth Factorlcsh:RC633-647.5Epidermal growth factor receptorResearchMesenchymal stem cellInterleukin-8Mesenchymal Stem CellsMicrovesiclesExosome030104 developmental biologyRAW 264.7 CellsCancer researchbiology.protein
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Constitutive psgl-1 correlates with cd30 and tcr pathways and represents a potential target for immunotherapy in anaplastic large t-cell lymphoma

2021

Simple Summary P-selectin glycoprotein ligand-1 (PSGL-1), coded by the SELPLG gene, is the major ligand of selectins and plays a pivotal role in tethering, rolling and extravasation of immune cells. PSGL-1 involvement in core molecular programs, such as SYK, PLCγ2, PI3Kγ or MAPK pathways, suggests additional functions beyond the modulation of cell trafficking. Recently, several studies identified a novel mechanism responsible for PSGL-1-mediated immune suppression in the tumor microenvironment and proved a novel concept of PSGL-1 as a critical checkpoint molecule for tumor immunotherapy. The immunotherapeutic approach has gained an ever-growing interest in the treatment of several hematolog…

0301 basic medicineCancer ResearchPTCLCD30medicine.medical_treatmentSykLymphoproliferative disordersBiologyALCL; ALK; CD30; Immunotherapy; PSGL-1; PTCL; TCRArticle03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesmedicineT-cell lymphomaPSGL-1RC254-282integumentary systemT-cell receptorNeoplasms. Tumors. Oncology. Including cancer and carcinogensImmunotherapymedicine.diseaseALCLLymphomaGene expression profiling030104 developmental biologyOncologyALK030220 oncology & carcinogenesisCD30Cancer researchImmunotherapyTCR
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Potential of induced metabolic bioluminescence imaging to uncover metabolic effects of antiangiogenic therapy in tumors

2016

Tumor heterogeneity at the genetic level has been illustrated by a multitude of studies on the genomics of cancer, but whether tumors can be heterogeneous at the metabolic level is an issue which has been less systematically investigated so far. A burning related question is whether the metabolic features of tumors can change either following natural tumor progression (i.e. in primary tumors versus metastasis) or therapeutic interventions. In this regard, recent findings by independent teams indicate that anti-angiogenic drugs cause metabolic perturbations in tumors as well as metabolic adaptations associated with increased malignancy. Induced metabolic bioluminescence imaging (imBI) is an …

0301 basic medicineCancer ResearchPathologymedicine.medical_specialtyAngiogenesisMini ReviewBiologyMalignancylcsh:RC254-282MetastasisImaging03 medical and health sciencesAngiogenesis; Cancer mouse models; Glycolysis; Imaging; MetabolismmedicineBioluminescence imagingGlycolysismouse modelsCancerCancerMetabolismlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease030104 developmental biologyMetabolismOncologyTumor progressionCancer researchAngiogenesisGlycolysis
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