Search results for "Tos"

showing 10 items of 12217 documents

M-TRAP: Safety and performance of metastatic tumor cell trap device in advanced ovarian cancer patients

2021

Objective. Despite radical surgery and chemotherapy, most patients with ovarian cancer die due to disease progression. M-Trap is an implantable medical device designed to capture peritoneal disseminated tumor cells with the aim to focalize the disease. This trial analyzed the safety and performance of the device. Methods. This first-in-human prospective, multi-center, non-blinded, single-arm study enrolled 23 women with high-grade serous advanced ovarian cancer. After primary or interval debulking surgery, 3 M-Trap devices were placed in the peritoneum of the abdominal cavity. 18-months post-implantation or at disease progression, devices were initially removed by laparoscopy. The primary s…

0301 basic medicineOncologyAdultmedicine.medical_specialtymedicine.medical_treatmentPerformanceDiseaseCarcinoma Ovarian Epithelial03 medical and health sciences0302 clinical medicineInternal medicinemedicineHumansCytoreductive surgeryProspective StudiesRadical surgeryNeoplasm MetastasisAdverse effectLaparoscopyPeritoneal NeoplasmsAgedOvarian NeoplasmsChemotherapymedicine.diagnostic_testbusiness.industryM-Trap deviceObstetrics and GynecologyCytoreduction Surgical ProceduresMiddle AgedDebulkingmedicine.diseaseSerous fluid030104 developmental biologyTreatment OutcomeOncologySpain030220 oncology & carcinogenesisAdvanced ovarian cancerFemaleNeoplasm Recurrence LocalRecurrent ovarian cancerSafetyOvarian cancerbusinessPeritoneal carcinomatosis
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TEM8/ANTXR1-Specific CAR T Cells as a Targeted Therapy for Triple-Negative Breast Cancer.

2018

Abstract Triple-negative breast cancer (TNBC) is an aggressive disease lacking targeted therapy. In this study, we developed a CAR T cell–based immunotherapeutic strategy to target TEM8, a marker initially defined on endothelial cells in colon tumors that was discovered recently to be upregulated in TNBC. CAR T cells were developed that upon specific recognition of TEM8 secreted immunostimulatory cytokines and killed tumor endothelial cells as well as TEM8-positive TNBC cells. Notably, the TEM8 CAR T cells targeted breast cancer stem–like cells, offsetting the formation of mammospheres relative to nontransduced T cells. Adoptive transfer of TEM8 CAR T cells induced regression of established…

0301 basic medicineOncologyCancer ResearchAdoptive cell transfermedicine.medical_specialtyLung Neoplasmsmedicine.medical_treatmentT-LymphocytesCell- and Tissue-Based TherapyReceptors Antigen T-CellApoptosisReceptors Cell SurfaceTriple Negative Breast NeoplasmsTargeted therapy03 medical and health sciencesMice0302 clinical medicineBreast cancerAntigenInternal medicineBiomarkers TumorTumor Cells CulturedMedicineAnimalsHumansTriple-negative breast cancerCell Proliferationbusiness.industryMicrofilament ProteinsCancerImmunotherapyTriple Negative Breast Neoplasmsmedicine.diseasePrognosisXenograft Model Antitumor AssaysNeoplasm ProteinsSurvival Rate030104 developmental biologyOncology030220 oncology & carcinogenesisCase-Control StudiesFemaleImmunotherapybusinessFollow-Up StudiesCancer research
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Hereditary Leiomyomatosis and Renal Cell Cancer Syndrome in Spain: Clinical and Genetic Characterization

2020

Simple Summary Hereditary leiomyomatosis and renal cell cancer (HLRCC) syndrome is a very rare hereditary disorder characterized by cutaneous leiomyomas (CLMs), uterine leiomyomas (ULMs), renal cysts (RCys) and renal cell cancer (RCC), with no data on its prevalence worldwide. No genotype-phenotype associations have been described. The aim of our study was to describe the genotypic and phenotypic features of the largest series of patients with HLRCC from Spain reported to date. Of 27 FH germline pathogenic variants, 12 were not previously reported in databases. Patients with missense pathogenic variants showed higher frequencies of CLMs, ULMs and RCys, than those with loss-of-function varia…

0301 basic medicineOncologyCancer ResearchCancer cellsmedicine.disease_causeurologic and male genital diseases:Male Urogenital Diseases::Urogenital Neoplasms::Urologic Neoplasms::Kidney Neoplasms::Male Urogenital Diseases::Carcinoma Renal Cell [DISEASES]<i>FH</i> gene0302 clinical medicineMalalties hereditàriesMissense mutationFH geneFH gene hereditary leiomyomatosis leiomyomas missense pathogenic variants renal cell cancerRenal cell cancerMutationKidney diseasesHereditary leiomyomatosis:Otros calificadores::Otros calificadores::/genética [Otros calificadores]:enfermedades urogenitales masculinas::neoplasias urogenitales::neoplasias urológicas::neoplasias renales::enfermedades urogenitales masculinas::carcinoma de células renales [ENFERMEDADES]leiomyomasmissense pathogenic variants renal cell cancerlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensRare diseases:Geographic Locations::Europe::Spain [GEOGRAPHICALS]Oncology030220 oncology & carcinogenesisCohortCèl·lules cancerosesMalalties raresRenal Cell CancersGenetic disordersmedicine.medical_specialtyMissense pathogenic variantsBiología Celularlcsh:RC254-282Article03 medical and health sciencesLeiomyomasInternal medicine:Other subheadings::Other subheadings::/genetics [Other subheadings]medicineRonyons - Malalties - Espanya:localizaciones geográficas::Europa (continente)::España [DENOMINACIONES GEOGRÁFICAS]business.industry:neoplasias::neoplasias por tipo histológico::neoplasias de tejido conjuntivo y de tejidos blandos::neoplasias de tejido muscular::leiomioma::leiomiomatosis [ENFERMEDADES]Retrospective cohort studymedicine.diseaseGenética030104 developmental biologyFumaraseClinical diagnosisHereditary leiomyomatosis and renal cell cancer syndromeMalalties del ronyó:Neoplasms::Neoplasms by Histologic Type::Neoplasms Connective and Soft Tissue::Neoplasms Muscle Tissue::Leiomyoma::Leiomyomatosis [DISEASES]hereditary leiomyomatosisbusiness
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Transcriptomic and Genetic Associations between Alzheimer's Disease, Parkinson's Disease, and Cancer.

2021

Simple Summary Epidemiological studies have identified a link between neurodegenerative disorders and a reduced risk of overall cancer. Increases and decreases in the risk of site-specific cancers have also been reported. However, it is still unknown whether these associations arise due to shared genetic and molecular factors or are explained by other phenomena (e.g., biases in epidemiological studies or the use of medication). In this study, we aimed to investigate the potential molecular, genetic, and pharmacological links between Alzheimer’s and Parkinson’s diseases and a large panel of 22 cancer types. To examine the overlapping involvement of genes and pathways, we obtained differentia…

0301 basic medicineOncologyCancer ResearchParkinson's diseaseGenetic correlationsGenome-wide association studyDiseaseComorbidityParkinson Enfermedad de - Aspectos genéticos.chemistry.chemical_compound0302 clinical medicineExemestaneParkinson's disease - Genetic aspects.MedicineParkinsonCáncer - Aspectos genéticos.Càncer -- Aspectes genèticsRC254-282Alzheimer's disease - Genetic aspects.NeurodegenerationNeoplasms. Tumors. Oncology. Including cancer and carcinogensCódigo genético.comorbidityOncology:Informàtica::Aplicacions de la informàtica::Bioinformàtica [Àrees temàtiques de la UPC]medicine.medical_specialtyGenetic code.Alzheimer Enfermedad de - Aspectos genéticos.Article03 medical and health sciencesInternal medicineParkinson Malaltia dePI3K/AKT/mTOR pathwaygenetic correlationsCancer - Genetic aspects.business.industryCancertranscriptomicmedicine.diseaseComorbidityAlzheimer Malaltia d'030104 developmental biologychemistryTranscriptomicmeta-analysesMeta-analysesNeurodegenerative disordersAlzheimerGene expressionbusiness030217 neurology & neurosurgeryCancers
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Loss of HER2 and decreased T-DM1 efficacy in HER2 positive advanced breast cancer treated with dual HER2 blockade: the SePHER Study

2020

AbstractBackgroundHER2-targeting agents have dramatically changed the therapeutic landscape of HER2+ advanced breast cancer (ABC). Within a short time frame, the rapid introduction of new therapeutics has led to the approval of pertuzumab combined with trastuzumab and a taxane in first-line, and trastuzumab emtansine (T-DM1) in second-line. Thereby, evidence of T-DM1 efficacy following trastuzumab/pertuzumab combination is limited, with data from some retrospective reports suggesting lower activity. The purpose of the present study is to investigate T-DM1 efficacy in pertuzumab-pretreated and pertuzumab naïve HER2 positive ABC patients. We also aimed to provide evidence on the exposure to d…

0301 basic medicineOncologyCancer ResearchReceptor ErbB-2ApoptosisAdo-Trastuzumab EmtansineSettore MED/06chemistry.chemical_compound0302 clinical medicineTrastuzumabAntineoplastic Combined Chemotherapy ProtocolsTumor Cells Culturedskin and connective tissue diseasesAged 80 and overMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisGene Expression Regulation NeoplasticSurvival RateOncology030220 oncology & carcinogenesisFemalePertuzumabmedicine.drugT-DM1 efficacymusculoskeletal diseasesAdultmedicine.medical_specialtyHER2+ breast cancer; Trastuzumab/pertuzumab blockade; T-DM1 efficacyBreast NeoplasmsAntibodies Monoclonal Humanizedlcsh:RC254-28203 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALEInternal medicinemedicineBiomarkers TumorHumansneoplasmsAgedCell ProliferationRetrospective StudiesHER2+ breast cancer; T-DM1 efficacy; Trastuzumab/pertuzumab blockadeTaxanebusiness.industryResearchCancerHER2+ breast cancerTrastuzumabmedicine.diseaseTrastuzumab/pertuzumab blockadeBlockadeLog-rank test030104 developmental biologychemistryTrastuzumab emtansineCancer cellbusiness
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HDAC5 Inhibitors as a Potential Treatment in Breast Cancer Affecting Very Young Women

2020

Background: Breast cancer in very young women (BCVY) defined as &lt

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyDose dependencelcsh:RC254-282ArticleLMK-23503 medical and health sciences0302 clinical medicineBreast cancerbreast cancerOlder patientsInternal medicinemedicineskin and connective tissue diseasesPathologicalHDAC5 inhibitorsHistone deacetylase 5young womenbusiness.industrylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease030104 developmental biologyOncologyApoptosisCell culture030220 oncology & carcinogenesishistone deacetylaseHistone deacetylasebusiness
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Recent Advances in Desmoid Tumor Therapy

2020

The desmoid tumor is a locally aggressive proliferative disease within the family of soft-tissue sarcomas. Despite its relatively good prognosis, the clinical management of desmoid tumors requires constant multidisciplinary evaluation due to its highly variable clinical behavior. Recently, active surveillance has being regarded as the appropriate strategy at diagnosis, as indolent persistence or spontaneous regressions are not uncommon. Here, we review the most recent advances in desmoid tumor therapy, including low-dose chemotherapy and treatment with tyrosine kinase inhibitors. We also explore the recent improvements in our knowledge of the molecular biology of this disease, which are lea…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtymedicine.medical_treatmentProliferative diseasedesmoid tumorDiseaseReviewchemotherapylcsh:RC254-282aggressive fibromatosis03 medical and health sciences0302 clinical medicineInternal medicinedesmoid tumor; aggressive fibromatosis; active surveillance; chemotherapy; tyrosine kinase inhibitorstyrosine kinase inhibitorsmedicineChemotherapybusiness.industryactive surveillanceTumor therapyaggressive fibromatosimedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensClinical trialbody regions030104 developmental biologyOncology030220 oncology & carcinogenesisAggressive fibromatosisGood prognosisbusinessCancers
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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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Phospho-Akt overexpression is prognostic and can be used to tailor the synergistic interaction of Akt inhibitors with gemcitabine in pancreatic cancer

2017

Background There is increasing evidence of a constitutive activation of Akt in pancreatic ductal adenocarcinoma (PDAC), associated with poor prognosis and chemoresistance. Therefore, we evaluated the expression of phospho-Akt in PDAC tissues and cells, and investigated molecular mechanisms influencing the therapeutic potential of Akt inhibition in combination with gemcitabine. Methods Phospho-Akt expression was evaluated by immunohistochemistry in tissue microarrays (TMAs) with specimens tissue from radically-resected patients (n = 100). Data were analyzed by Fisher and log-rank test. In vitro studies were performed in 14 PDAC cells, including seven primary cultures, characterized for their…

0301 basic medicineOncologyMaleCancer ResearchBiopsyAKT1ApoptosisAkt; Gemcitabine; Pancreatic ductal adenocarcinoma; Synergism; Hematology; Molecular Biology; Oncology; Cancer ResearchDeoxycytidinePancreatic ductal adenocarcinoma0302 clinical medicineCell MovementTumor Cells CulturedGlucose Transporter Type 1medicine.diagnostic_testChemistryCell CyclePancreatic NeoplasmDrug Synergismlcsh:Diseases of the blood and blood-forming organsHematologyCell cycleMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisOncologyAkt; Gemcitabine; Pancreatic ductal adenocarcinoma; Synergism; Aged; Apoptosis; Biopsy; Carcinoma Pancreatic Ductal; Cell Cycle; Cell Movement; Deoxycytidine; Drug Synergism; Female; Glucose Transporter Type 1; Humans; Male; Middle Aged; Pancreatic Neoplasms; Phosphoproteins; Prognosis; Proto-Oncogene Proteins c-akt; RNA Messenger; Spheroids Cellular; Tumor Cells Cultured; Hematology; Molecular Biology; Oncology; Cancer Research030220 oncology & carcinogenesisPhosphoproteinFemalemedicine.drugHumanCarcinoma Pancreatic Ductalmedicine.medical_specialtyPrognosilcsh:RC254-282Flow cytometry03 medical and health sciencesInternal medicinePancreatic cancerSpheroids CellularmedicineHumansRNA MessengerProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayAgedlcsh:RC633-647.5ResearchAktSynergismApoptosimedicine.diseasePhosphoproteinsGemcitabineGemcitabinePancreatic Neoplasms030104 developmental biologyCancer cellCancer researchProto-Oncogene Proteins c-akt
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Bladder cancer recurrence surveillance by urine metabolomics analysis.

2018

AbstractNon Muscle Invasive Bladder Cancer (NMIBC) is among the most frequent malignant cancers worldwide. NMIBC is treated by transurethral resection of the bladder tumor (TURBT) and intravesical therapies, and has the highest recurrence rate among solid tumors. It requires a lifelong patient monitoring based on repeated cystoscopy and urinary cytology, both having drawbacks that include lack of sensitivity and specificity, invasiveness and care costs. We conducted an investigative clinical study to examine changes in the urinary metabolome of NMBIC patients before and after TURBT, as well during the subsequent surveillance period. Adjusting by prior probability of recurrence per risk, dis…

0301 basic medicineOncologyMalemedicine.medical_specialtyUrinary systemlcsh:MedicineUrineArticlelaw.invention03 medical and health sciences0302 clinical medicineMetabolomicsRandomized controlled triallawCytologyInternal medicinemedicineMetabolomeBiomarkers TumorHumansMetabolomicslcsh:ScienceAgedAged 80 and overMultidisciplinaryBladder cancermedicine.diagnostic_testbusiness.industrylcsh:RCystoscopyMiddle Agedmedicine.disease030104 developmental biologyUrinary Bladder Neoplasms030220 oncology & carcinogenesisMetabolomelcsh:QFemalebusinessScientific reports
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