Search results for "neoplasm"

showing 10 items of 8607 documents

In silico RNA-seq and experimental analyses reveal the differential expression and splicing of EPDR1 and ZNF518B genes in relation to KRAS mutations …

2016

Several drugs used for the treatment of colorectal cancer (CRC) are targeted at the epidermal growth factor receptor, but mutations in genes of the RAS family cause resistance to these drugs. Thus, extensive research is being carried out to counterbalance this resistance. The G13D mutation of KRAS is common in humans, and we previously reported that this mutation results in the epigenetic modification of hnRNP proteins, involved in RNA splicing. As aberrant splicing often results in oncogenicity, the present study aimed to identify the genes which show altered splicing patterns in connection with the G13D KRAS mutation. To accomplish this, we first carried out an in silico analysis of RNA-s…

0301 basic medicineCancer ResearchIn silicoMutation MissenseGene ExpressionNerve Tissue ProteinsBiologymedicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health sciences0302 clinical medicinemedicineHumansProtein IsoformsComputer SimulationEpigeneticsGeneGeneticsMutationBase SequenceModels GeneticSequence Analysis RNAAlternative splicingGeneral Medicinedigestive system diseasesNeoplasm ProteinsDNA-Binding ProteinsAlternative Splicing030104 developmental biologyOncology030220 oncology & carcinogenesisRNA splicingCancer researchKRASCarcinogenesisColorectal NeoplasmsOncology reports
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An Algorithm Combining Patient Performance Status, Second Hit Analysis, PROVEAN and Dann Prediction Tools Could Foretell Sensitization to PARP Inhibi…

2021

Simple Summary PARP inhibitors, a family of targeted cancer therapeutics, have been shown to be efficient in patients with some deficiencies in the homologous recombination machinery. However, a quick and reliable identification of patients who would benefit from such therapies remains a challenge. In particular, patients with tumors carrying variants of unknown significance (VUS) in homologous recombination genes do not currently benefit from PARP inhibitor treatments. In this study, we present an algorithm that may allow classification of these variants with regard to their impact on tumor responsiveness to PARP inhibitors. If validated on a larger patient sample, our algorithm would allo…

0301 basic medicineCancer ResearchIn silicohomologous recombinationArticleOlaparib03 medical and health scienceschemistry.chemical_compound0302 clinical medicineHomologous chromosomeMedicineProgression-free survivalAllele frequencyPARP inhibitorsSensitizationRC254-282responsePerformance statusbusiness.industryNeoplasms. Tumors. Oncology. Including cancer and carcinogensVUS030104 developmental biologymedicine.anatomical_structureOncologychemistry030220 oncology & carcinogenesisPARP inhibitorbusinessAlgorithmprogression-free survivalCancers
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Prospective Image Quality and Lesion Assessment in the Setting of MR-Guided Radiation Therapy of Prostate Cancer on an MR-Linac at 1.5 T: A Compariso…

2021

The objective of this study is to conduct a qualitative and a quantitative image quality and lesion evaluation in patients undergoing MR-guided radiation therapy (MRgRT) for prostate cancer on a hybrid magnetic resonance imaging and linear accelerator system (MR-Linac or MRL) at 1.5 Tesla. This prospective study was approved by the institutional review board. A total of 13 consecutive patients with biopsy-confirmed prostate cancer and an indication for MRgRT were included. Prior to radiation therapy, each patient underwent an MR-examination on an MRL and on a standard MRI scanner at 3 Tesla (MRI3T). Three readers (two radiologists and a radiation oncologist) conducted an independent qualita…

0301 basic medicineCancer ResearchIntraclass correlationImage qualityPIRADSFleiss' kappalcsh:RC254-282ArticleLesion03 medical and health sciences0302 clinical medicineimage qualityMedicineEffective diffusion coefficientimage guidanceRadiation oncologistMR-Linacmedicine.diagnostic_testbusiness.industryMagnetic resonance imaginglcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenslesion detection030104 developmental biologyadaptive radiotherapyOncologyprostate carcinoma030220 oncology & carcinogenesismpMRImedicine.symptombusinessNuclear medicineKappaCancers
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Targeting the MET oncogene by concomitant inhibition of receptor and ligand via an antibody-"decoy" strategy

2018

MET, a master gene sustaining "invasive growth," is a relevant target for cancer precision therapy. In the vast majority of tumors, wild-type MET behaves as a "stress-response" gene and relies on the ligand (HGF) to sustain cell "scattering," invasive growth and apoptosis protection (oncogene "expedience"). In this context, concomitant targeting of MET and HGF could be crucial to reach effective inhibition. To test this hypothesis, we combined an anti-MET antibody (MvDN30) inducing "shedding" (i.e., removal of MET from the cell surface), with a "decoy" (i.e., the soluble extracellular domain of the MET receptor) endowed with HGF-sequestering ability. To avoid antibody/decoy interaction-and …

0301 basic medicineCancer ResearchLung NeoplasmsCellContext (language use)ApoptosisMice SCIDLigands03 medical and health sciencesMice0302 clinical medicineMice Inbred NODanti-HGF therapy; antibodies; decoy; MET oncogene; MET target therapyMET oncogeneExtracellularmedicineTumor Cells CulturedantibodiesAnimalsHumansdecoyCell ProliferationOncogenebiologyMET target therapyChemistryAntibodies MonoclonalProto-Oncogene Proteins c-metXenograft Model Antitumor AssaysIn vitro030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer cellColonic NeoplasmsCancer researchbiology.proteinanti-HGF therapyFemaleAntibodyDecoyGlioblastoma
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Doxorubicin anti-tumor mechanisms include Hsp60 post-translational modifications leading to the Hsp60/p53 complex dissociation and instauration of re…

2017

Hsp60 is a pro-carcinogenic chaperonin in certain tumor types by interfering with apoptosis and with tumor cell death. In these tumors, it is not known whether or not doxorubicin anti-tumor effects include a blockage of the pro-carcinogenic action of this protein. We used the human lung mucoepidermoid cell line NCI-H292 and different doses of doxorubicin to measure cell viability, cell cycle progression, cell senescence indicators, Hsp60 levels and its post-translational modifications as well as the release of the chaperonin into the extracellular environment. Cell viability was reduced in relation to doxorubicin dose and this was paralleled by the appearance of cell senescence markers. Con…

0301 basic medicineCancer ResearchLung NeoplasmsChaperoninsCellApoptosismedicine.disease_causeHistones0302 clinical medicineCellular SenescenceAntibiotics AntineoplasticAcetylationG2 Phase Cell Cycle Checkpointsmedicine.anatomical_structureOncology030220 oncology & carcinogenesisCell agingIntracellularProtein BindingSignal TransductionSenescenceCyclin-Dependent Kinase Inhibitor p21animal structuresCell Survivalchemical and pharmacologic phenomenaBiologycomplex mixturesMitochondrial ProteinsDoxorubicin Hsp60 Acetylation Ubiquitination p53 Replicative senescence03 medical and health sciencesDoxorubicin; Hsp60; p53; replicative senescence; post-translational modificationsCell Line TumormedicineHumansCell Proliferationdoxorubicin p53 Hsp60Dose-Response Relationship DrugCell growthfungiUbiquitinationChaperonin 60Molecular biology030104 developmental biologyAcetylationApoptosisDoxorubicinProteolysisCancer researchCarcinoma MucoepidermoidTumor Suppressor Protein p53CarcinogenesisProtein Processing Post-Translational
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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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Immunotherapy in non-small-cell lung cancer: a bridge between research and clinical practice

2018

Lung cancer has been historically considered a poorly immunogenic disease because of the few evidence of immune responses in affected patients and the limited efficacy of immunomodulating strategies. Recent understanding of the molecular mechanisms leading to cancer immune evasion has allowed the development of a new class of drugs called immune checkpoint inhibitors, which reactivate host responses with outstanding clinical benefits in a portion of patients with non-small-cell lung cancer. In this review, we briefly summarize the basis of immunogenicity and immune escape of cancer, with specific focus on non-small-cell lung cancer, mechanisms underlying immune checkpoint inhibitors effica…

0301 basic medicineCancer ResearchLung NeoplasmsSettore MED/06 - Oncologia Medicamedicine.medical_treatmentProgrammed Cell Death 1 Receptorimmune checkpoint inhibitorDiseaseNSCLCBioinformaticsB7-H1 Antigenimmune checkpoint inhibitorsTranslational Research Biomedical0302 clinical medicineCarcinoma Non-Small-Cell LungPD-1clinical studiesNSCLC; PD-1; PD-L1; biomarkers; cancer immunogenicity; clinical studies; immune checkpoint inhibitors; translational researchMolecular Targeted TherapybiologyImmunogenicityGeneral Medicinecancer immunogenicityOncology030220 oncology & carcinogenesisbiomarkerCytokinesImmunotherapyPD-L1chemical and pharmacologic phenomena03 medical and health sciencesLymphocytes Tumor-InfiltratingImmune systemPD-L1Biomarkers TumormedicineHumansLung cancerbusiness.industryImmunitybiomarkersCancerImmunotherapymedicine.disease030104 developmental biologytranslational researchTumor EscapeMutationbiology.proteinTumor Escapebusinessclinical studieFuture Oncology
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Trabectedin Overrides Osteosarcoma Differentiative Block and Reprograms the Tumor Immune Environment Enabling Effective Combination with Immune Check…

2016

Abstract Purpose: Osteosarcoma, the most common primary bone tumor, is characterized by an aggressive behavior with high tendency to develop lung metastases as well as by multiple genetic aberrations that have hindered the development of targeted therapies. New therapeutic approaches are urgently needed; however, novel combinations with immunotherapies and checkpoint inhibitors require suitable preclinical models with intact immune systems to be properly tested. Experimental Design: We have developed immunocompetent osteosarcoma models that grow orthotopically in the bone and spontaneously metastasize to the lungs, mimicking human osteosarcoma. These models have been used to test the effica…

0301 basic medicineCancer ResearchLung Neoplasmsmedicine.medical_treatmentCellular differentiationT-LymphocytesProgrammed Cell Death 1 ReceptorBone NeoplasmsCore Binding Factor Alpha 1 SubunitDioxolesBiology03 medical and health sciences0302 clinical medicineImmune systemCell Line TumorTetrahydroisoquinolinesmedicineTumor MicroenvironmentHumansTrabectedinTumor microenvironmentOsteosarcomaCancerCell DifferentiationImmunotherapymedicine.diseaseCellular ReprogrammingPrimary tumor030104 developmental biologyOncology030220 oncology & carcinogenesisImmunologyCancer researchOsteosarcomaImmunotherapyOsteosarcoma Trabectedin tumor mouse models immune cells immune checkpoint inhibitors.Tumor Suppressor Protein p53medicine.drugTrabectedinClinical cancer research : an official journal of the American Association for Cancer Research
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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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