Search results for "Drug resistance"

showing 10 items of 953 documents

Dual targeting of HER3 and MEK may overcome HER3-dependent drug-resistance of colon cancers

2016

// Giulia Bon 1, * , Rossella Loria 1, * , Carla Azzurra Amoreo 2 , Alessandra Verdina 1 , Isabella Sperduti 2 , Arianna Mastrofrancesco 3 , Silvia Soddu 1 , Maria Grazia Diodoro 2 , Marcella Mottolese 2 , Matilde Todaro 4 , Giorgio Stassi 4 , Michele Milella 5 , Ruggero De Maria 6 , Rita Falcioni 1 1 Department of Research, Advanced Diagnostic, and Technological Innovation, IRCCS Regina Elena National Cancer Institute, Rome, Italy 2 Department of Research, Advanced Diagnostic, and Technological Innovation, IRCCS Regina Elena National Cancer Institute, Rome, Italy 3 Physiopathology Laboratory of Skin, IRCCS San Gallicano Dermatological Institute, Rome, Italy 4 Surgical and Oncological Scien…

0301 basic medicineOncologyMAPK/ERK pathwaymedicine.medical_specialtyPatritumabColorectal cancerHER3; MAPK; PI3K; colon cancers; drug resistanceDrug resistancePI3K03 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALEcolon cancersHER3Internal medicinemedicineColon cancers; Drug resistance; HER3; MAPK; PI3K; Oncologyskin and connective tissue diseasesPI3K/AKT/mTOR pathwayTrametinibSettore MED/06 - ONCOLOGIA MEDICAdrug resistancebusiness.industryCancermedicine.diseaseMAPKbody regionsClinical trial030104 developmental biologyOncologycolon cancerbusinessResearch Paper
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Detection of MET Alterations Using Cell Free DNA and Circulating Tumor Cells from Cancer Patients

2020

MET alterations may provide a potential biomarker to evaluate patients who will benefit from treatment with MET inhibitors. Therefore, the purpose of the present study is to investigate the utility of a liquid biopsy-based strategy to assess MET alterations in cancer patients. We analyzed MET amplification in circulating free DNA (cfDNA) from 174 patients with cancer and 49 healthy controls and demonstrated the accuracy of the analysis to detect its alteration in patients. Importantly, a significant correlation between cfDNA concentration and MET copy number (CN) in cancer patients (r = 0.57, p &lt

0301 basic medicineOncologyMale<i>MET</i> copy numbermedicine.medical_treatmentproteínas protooncogénicas c-metdosificación génicahumanosresistencia a medicamentosDrug ResistanceGene Dosagecirculating free DNA (cfDNA)<i>MET</i> amplificationTargeted therapyTargeted therapy0302 clinical medicineCirculating tumor cellestudios prospectivosNeoplasmsantineoplásicosProspective Studieslcsh:QH301-705.5Circulating tumor cells (CTCs)neoplasiasGeneral MedicineProto-Oncogene Proteins c-mettargeted therapyNeoplastic Cells CirculatingErbB ReceptorsCell-free fetal DNA030220 oncology & carcinogenesisinhibidores de proteína cinasasBiomarker (medicine)FemaleMET protein expressionCell-Free Nucleic AcidsMET amplificationmedicine.medical_specialtycirculating tumor cells (CTCs)estudios de casos y controlesMet amplificationCirculating free DNA (cfDNA)Antineoplastic AgentsArticle03 medical and health sciencesInternal medicinemedicineBiomarkers TumorHumansLiquid biopsyProtein Kinase InhibitorsRetrospective Studiesbusiness.industryHead and neck cancerestudios retrospectivosLiquid BiopsyCancermedicine.disease030104 developmental biologylcsh:Biology (General)Drug Resistance NeoplasmCase-Control StudiesMET copy numberbusinessCells
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Daratumumab, Bortezomib, and Dexamethasone for Multiple Myeloma.

2016

Daratumumab, a human IgGκ monoclonal antibody that targets CD38, induces direct and indirect antimyeloma activity and has shown substantial efficacy as monotherapy in heavily pretreated patients with multiple myeloma, as well as in combination with bortezomib in patients with newly diagnosed multiple myeloma.In this phase 3 trial, we randomly assigned 498 patients with relapsed or relapsed and refractory multiple myeloma to receive bortezomib (1.3 mg per square meter of body-surface area) and dexamethasone (20 mg) alone (control group) or in combination with daratumumab (16 mg per kilogram of body weight) (daratumumab group). The primary end point was progression-free survival.A prespecifie…

0301 basic medicineOncologyMaleAntigens CD38Drug ResistanceDexamethasoneIxazomibBortezomibchemistry.chemical_compound0302 clinical medicineRecurrenceMonoclonalAntineoplastic Combined Chemotherapy ProtocolsMedicineInfusions IntravenouElotuzumabInfusions IntravenousMultiple myelomaIsatuximabBortezomibMedicine (all)SLAMF7Antibodies MonoclonalGeneral MedicineMiddle Aged030220 oncology & carcinogenesisFemaleIntravenousMultiple MyelomaHumanmedicine.drugAdult; Aged; Antibodies Monoclonal; Antigens CD38; Antineoplastic Combined Chemotherapy Protocols; Bortezomib; Dexamethasone; Disease-Free Survival; Drug Resistance Neoplasm; Female; Humans; Infusions Intravenous; Male; Middle Aged; Multiple Myeloma; Recurrence; Medicine (all)AdultInfusionsmedicine.medical_specialtyAntibodiesDisease-Free Survival03 medical and health sciencesInternal medicineHumansAntigensAgedAntineoplastic Combined Chemotherapy Protocolbusiness.industryDaratumumabInterim analysismedicine.diseaseADP-ribosyl Cyclase 1Surgery030104 developmental biologychemistryDrug Resistance NeoplasmNeoplasmbusinessCD38The New England journal of medicine
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Clinical utility of plasma-based digital next-generation sequencing in oncogene-driven non-small-cell lung cancer patients with tyrosine kinase inhib…

2019

[Objectives] Resistance to tyrosine-kinase inhibitors (TKIs) is a clinical challenge in patients with oncogene-driven non-small-cell lung cancers (NSCLC). We have analyzed the utility of next-generation sequencing (NGS) of cell-free circulating tumor DNA (ctDNA) to impact the clinical care of patients with TKI resistance.

0301 basic medicineOncologyMaleCancer ResearchLung NeoplasmsTyrosine-kinase inhibitorCirculating Tumor DNAchemistry.chemical_compound0302 clinical medicineCarcinoma Non-Small-Cell LungMedicineOsimertinibNeoplasm MetastasisProspective cohort studyAged 80 and overDisease ManagementHigh-Throughput Nucleotide SequencingMiddle AgedOncology030220 oncology & carcinogenesisFemalemedicine.drugPulmonary and Respiratory MedicineAdultmedicine.medical_specialtyCabozantinibmedicine.drug_class03 medical and health sciencesInternal medicineROS1Biomarkers TumorHumansLung cancerProtein Kinase InhibitorsAgedNeoplasm StagingDigital next-generation sequencingTKI resistanceCrizotinibbusiness.industryOncogene-driven NSCLCOncogenesctDNAmedicine.diseaseLorlatinibrespiratory tract diseases030104 developmental biologychemistryDrug Resistance NeoplasmMutationbusinessOsimertinib
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Progression patterns under BRAF inhibitor treatment and treatment beyond progression in patients with metastatic melanoma

2017

Despite markedly improved treatment options for metastatic melanoma, resistance to targeted therapies such as BRAF inhibitors (BRAFi) or BRAFi plus MEK inhibitors (MEKi) remains a major problem. Our aim was to characterize progression on BRAFi therapy and outcome of subsequent treatment. One hundred and eighty patients with BRAF-mutant metastatic melanoma who had progressed on treatment with single-agent BRAFi from February 2010 to April 2015 were included in a retrospective data analysis focused on patterns of progression, treatment beyond progression (TBP) and subsequent treatments after BRAFi therapy. Analysis revealed that 51.1% of patients progressed with both new and existing metastas…

0301 basic medicineOncologyMaleCancer ResearchSkin NeoplasmsBRAF inhibitorProgrammed Cell Death 1 ReceptorMedizinKaplan-Meier Estimate0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsVemurafenibMelanomaOriginal ResearchAged 80 and overTreatment optionsMiddle AgedMAP Kinase Kinase KinasesPrognosisProgression-Free SurvivalOncology030220 oncology & carcinogenesisDisease ProgressionvemurafenibFemalemedicine.drugmetastatic melanomaBRAF inhibitorAdultProto-Oncogene Proteins B-rafmedicine.medical_specialtyMetastatic melanomaRetrospective data03 medical and health sciencesYoung AdultInternal medicinetreatment beyond progressionmedicineOverall survivalHumansRadiology Nuclear Medicine and imagingIn patientdabrafenibProtein Kinase InhibitorsResponse Evaluation Criteria in Solid TumorsAgedRetrospective Studiesbusiness.industryClinical Cancer ResearchDabrafenib030104 developmental biologyBRAF mutationDrug Resistance NeoplasmMutationprogressionbusinessFollow-Up StudiesCancer Medicine
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Identification of fatal outcome in a childhood nasopharyngeal carcinoma patient by protein expression profiling.

2017

Nasopharyngeal carcinoma (NPC) is a rare disease in children with good prognosis and high cure rate. Nevertheless, certain patients have an unfavorable prognosis due to development of refractory NPC that is unresponsive to any therapeutic strategies. The current study studies a case of a 17 years-old female with non-keratinizing NPC type IIb (T2N0M0), who passed away as a consequence of resistance to chemo-, radio- and β-interferon therapy, and to an allogenic stem cell transplantation. In order to identify factors that lead to treatment failure and fatal outcome, immunohistochemical analyses of different tumor biomarkers and hierarchical cluster analysis were performed and compared with th…

0301 basic medicineOncologyMaleCancer Researchmedicine.medical_specialtyHerpesvirus 4 HumanAdolescentBiologymedicine.disease_causeVirusViral Matrix Proteins03 medical and health sciencesImmunocompromised Host0302 clinical medicineLymphocytes Tumor-InfiltratingInternal medicineotorhinolaryngologic diseasesmedicineBiomarkers TumorHumansProspective StudiesChildImmunodeficiencyNasopharyngeal CarcinomaTumor-infiltrating lymphocytesGene Expression ProfilingVaricella zoster virusCancermedicine.diseasePrognosisImmunohistochemistryTransplantationstomatognathic diseases030104 developmental biologyHerpes simplex virusOncologyNasopharyngeal carcinomaDrug Resistance Neoplasm030220 oncology & carcinogenesisFemaleNeoplasm Recurrence LocalStem Cell TransplantationInternational journal of oncology
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Decreased Time to Treatment Initiation for Multidrug-Resistant Tuberculosis Patients after Use of Xpert MTB/RIF Test, Latvia

2016

This test decreased time to treatment initiation by 66%–84%.

0301 basic medicineOncologyMaleEpidemiologylcsh:Medicine0302 clinical medicine1108 Medical MicrobiologyTuberculosis Multidrug-Resistant030212 general & internal medicinebacteriaDecreased Time to Treatment Initiation for Multidrug-Resistant Tuberculosis Patients after Use of Xpert MTB/RIF Test Latviabiologytime to treatment initiationDrug Resistance MicrobialMiddle Agedmultidrug-resistant tuberculosisRifampin resistanceInfectious Diseases1117 Public Health And Health ServicesTuberculosis Multidrug-Resistant/diagnosisFemaleRifampinLife Sciences & BiomedicineMicrobiology (medical)Adultmedicine.medical_specialtyTuberculosisAdolescentpulmonary030106 microbiologyXpert MTB/RIFImmunologyTime to treatmentMicrobiologylcsh:Infectious and parasitic diseasesTime-to-TreatmentMycobacterium tuberculosismolecular diagnostics03 medical and health sciencesYoung AdultAntibiotic resistancemultidrug resistanceInternal medicinemedicineHumanslcsh:RC109-216Multivariable modelantimicrobial resistanceTuberculin testAntibiotics AntitubercularScience & Technologybusiness.industryTuberculin TestResearchlcsh:RMycobacterium tuberculosis/drug effects1103 Clinical SciencesMycobacterium tuberculosisbiology.organism_classificationmedicine.diseaseAntibiotics Antitubercular/pharmacologyLatviatuberculosis and other mycobacteriaMultiple drug resistanceMODELTuberculin Test/methodsbusinessRifampin/pharmacologyMDR TB
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The role of miR-26a and miR-30b in HER2+ breast cancer trastuzumab resistance and regulation of the CCNE2 gene

2016

AbstractA subset of HER2+ breast cancer patients manifest clinical resistance to trastuzumab. Recently, miR-26a and miR-30b have been identified as trastuzumab response regulators, and their target gene CCNE2 seems to play an important role in resistance to trastuzumab therapy. Cell viability was evaluated in trastuzumab treated HER2+ BT474 wt (sensitive), BT474r (acquired resistance), HCC1954 (innate resistance), and MDA-MB-231 (HER2−) cell lines, and the expression of miR-26a, miR-30b, and their target genes was measured. BT474 wt cell viability decreased by 60% and miR-26a and miR-30b were significantly overexpressed (~3-fold, p = 0.003 and p = 0.002, respectively) after trastuzumab trea…

0301 basic medicineOncologyMama -- Càncer -- Aspectes genèticsmedicine.medical_specialtyCell SurvivalReceptor ErbB-2Down-RegulationMama -- Càncer -- TractamentBreast NeoplasmsDrug resistanceArticle03 medical and health sciences0302 clinical medicineBreast cancerTrastuzumabInternal medicineCell Line TumorCyclinsmedicineGene silencingHumansViability assayGene SilencingReceptorskin and connective tissue diseasesneoplasmsRegulation of gene expressionMultidisciplinarybusiness.industryCell CycleTrastuzumabmedicine.diseaseNeoplasm ProteinsGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologyCell cultureDrug Resistance Neoplasm030220 oncology & carcinogenesisFemalebusinessmedicine.drugScientific Reports
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Resminostat plus sorafenib as second-line therapy of advanced hepatocellular carcinoma - The SHELTER study

2016

Background & Aims No established therapies for patients with hepatocellular carcinoma (HCC) and progression on first-line sorafenib treatment currently exist. This phase I/II trial investigated safety, pharmacokinetics and potential biomarkers of the histone deacetylase inhibitor resminostat and a combination therapy with resminostat and sorafenib. Methods Patients with HCC and radiologically confirmed progression on sorafenib were treated in an exploratory, multi-center, open-label, uncontrolled, non-randomized, parallel group phase I/II study. In the combination group (n=38) four dose levels ranged from daily 200 to 600mg resminostat plus 400 to 800mg sorafenib. The monotherapy group (n=1…

0301 basic medicineOncologySorafenibmedicine.medical_specialtyCombination therapymedicine.drug_classMedizinCancer epigeneticPharmacology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCancer epigeneticsResminostatInternal medicineClinical endpointmedicineCarcinomaneoplasmsEpigenetic treatmentFirst-in-man studyHistone deacetylase inhibitorHepatologybusiness.industryHistone deacetylase inhibitormedicine.diseasedigestive system diseases030104 developmental biologyZinc finger protein 64chemistryCancer epigenetics; Drug resistance; Epigenetic treatment; Histone deacetylase inhibitor; Zinc finger protein 64030220 oncology & carcinogenesisHepatocellular carcinomaDrug resistancebusinessmedicine.drug
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Suppressive role exerted by microRNA-29b-1-5p in triple negative breast cancer through SPIN1 regulation

2017

MiR-29 family dysregulation occurs in various cancers including breast cancers. We investigated miR-29b-1 functional role in human triple negative breast cancer (TNBC) the most aggressive breast cancer subtype. We found that miR-29b-1-5p was downregulated in human TNBC tissues and cell lines. To assess whether miR- 29b-1-5p correlated with TNBC regenerative potential, we evaluated cancer stem cell enrichment in our TNBC cell lines, and found that only MDA-MB-231 and BT-20 produced primary, secondary and tertiary mammospheres, which were progressively enriched in OCT4, NANOG and SOX2 stemness genes. MiR-29b-1-5p expression inversely correlated with mammosphere stemness potential, and miR-29b…

0301 basic medicineOncologycancer stem cellsCarcinogenesisCell Cycle ProteinsTriple Negative Breast NeoplasmsMicroRNA 29b0302 clinical medicineCell MovementSettore BIO/10 - BiochimicaCancer stem cells; MiR-29b-1; SPIN1; Triple-negative breast cancer; Wnt/β-catenin and Akt signaling pathwaysMedicineBreastBreast -- CancerTriple-negative breast cancerWnt signaling pathwayMicroRNANanog Homeobox ProteinGene Expression Regulation NeoplasticOncologyWnt/β-catenin and Akt signaling pathway030220 oncology & carcinogenesisMiR-29b-1Wnt/β-catenin and Akt signaling pathwaysNeoplastic Stem Cellstriple-negative breast cancerFemaleMicrotubule-Associated ProteinsSignal TransductionResearch Papermedicine.medical_specialtycancer stem cellPaclitaxelDown-Regulation03 medical and health sciencesBreast cancerSOX2Cancer stem cellInternal medicineCell Line TumormicroRNAHumansNeoplasm InvasivenessCell ProliferationSPIN1business.industrySOXB1 Transcription Factorsmedicine.diseasePhosphoproteinsMolecular medicineAntineoplastic Agents PhytogenicMicroRNAs030104 developmental biologyDrug Resistance NeoplasmbusinessOctamer Transcription Factor-3
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