Search results for "INHIBITOR"

showing 10 items of 3742 documents

A Pan-Cancer Approach to Predict Responsiveness to Immune Checkpoint Inhibitors by Machine Learning

2019

Immunotherapy by using immune checkpoint inhibitors (ICI) has dramatically improved the treatment options in various cancers, increasing survival rates for treated patients. Nevertheless, there are heterogeneous response rates to ICI among different cancer types, and even in the context of patients affected by a specific cancer. Thus, it becomes crucial to identify factors that predict the response to immunotherapeutic approaches. A comprehensive investigation of the mutational and immunological aspects of the tumor can be useful to obtain a robust prediction. By performing a pan-cancer analysis on gene expression data from the Cancer Genome Atlas (TCGA, 8055 cases and 29 cancer types), we …

0301 basic medicineCancer ResearchImmune checkpoint inhibitorsmedicine.medical_treatmentimmunology-pancancerimmune checkpoint inhibitorContext (language use)Machine learningcomputer.software_genrelcsh:RC254-282Article03 medical and health sciences0302 clinical medicinemedicineExtreme gradient boostingPan cancerbusiness.industryCancerImmunotherapylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMatthews correlation coefficientmedicine.diseaseSupport vector machine030104 developmental biologymachine learningOncology030220 oncology & carcinogenesisArtificial intelligencebusinesscomputerCancers
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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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9-ING-41, a small-molecule glycogen synthase kinase-3 inhibitor, is active in neuroblastoma.

2018

Advanced stage neuroblastoma is a very aggressive pediatric cancer with limited treatment options and a high mortality rate. Glycogen Synthase Kinase-3β (GSK-3β) is a potential therapeutic target in neuroblastoma. Using immunohistochemical staining, we observed positive GSK-3β expression in 67% of human neuroblastomas (34 out of 51 cases). Chemically distinct GSK-3 inhibitors (AR-A014418, TDZD8 and 9-ING-41), suppressed the growth of neuroblastoma cells whereas 9-ING-41, a clinically relevant small molecule GSK-3β inhibitor with broad spectrum pre-clinical antitumor activity, being the most potent. Inhibition of GSK-3 resulted in a decreased expression of the antiapoptotic molecule XIAP and…

0301 basic medicineCancer ResearchIndolesMice NudeCell Growth ProcessesIrinotecanArticleMaleimides03 medical and health sciencesMiceNeuroblastoma0302 clinical medicineGSK-3NeuroblastomaCell Line TumorAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsHumansPharmacology (medical)Enzyme InhibitorsGlycogen synthasePharmacologyGlycogen Synthase Kinase 3 betabiologyChemistryDrug Synergismmedicine.diseasePediatric cancerXenograft Model Antitumor AssaysXIAP030104 developmental biologyOncologyCell cultureApoptosis030220 oncology & carcinogenesisCancer researchbiology.proteinImmunohistochemistryFemaleAnti-cancer drugs
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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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Introduction of WT-TP53 into pancreatic cancer cells alters sensitivity to chemotherapeutic drugs, targeted therapeutics and nutraceuticals

2018

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive, highly metastatic malignancy and accounts for 85% of pancreatic cancers. PDAC patients have poor prognosis with a five-year survival of only 5–10%. Mutations at the TP53 gene are readily detected in pancreatic tumors isolated from PDAC patients. We have investigated the effects of restoration of wild-type (WT) TP53 activity on the sensitivity of pancreatic cancer cells to: chemotherapy, targeted therapy, as well as, nutraceuticals. Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisp…

0301 basic medicineCancer ResearchPaclitaxelendocrine system diseasesmedicine.medical_treatmentTargeted therapeuticIrinotecanDeoxycytidineTargeted therapyGlycogen Synthase Kinase 303 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorPancreatic cancerGeneticsmedicineHumansDoxorubicinTP53Signal transduction inhibitorneoplasmsMolecular BiologyCell ProliferationCisplatinChemotherapybusiness.industryPancreatic Neoplasmmedicine.diseaseGemcitabinedigestive system diseasesGemcitabinePancreatic NeoplasmsOxaliplatin030104 developmental biologyPaclitaxelchemistryFluorouracil030220 oncology & carcinogenesisCancer researchMolecular MedicineFluorouracilCisplatinbusinessDrug sensitivityHumanSignal Transductionmedicine.drug
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Xenograft models for undifferentiated pleomorphic sarcoma not otherwise specified are essential for preclinical testing of therapeutic agents

2016

Undifferentiated pleomorphic sarcoma not otherwise specified belongs to the heterogeneous group of soft tissue tumors. It is preferentially located in the upper and lower extremities of the body, and surgical resection remains the only curative treatment. Preclinical animal models are crucial to improve the development of novel chemotherapeutic agents for the treatment of undifferentiated pleomorphic sarcoma. However, this approach has been hampered by the lack of reproducible animal models. The present study established two xenograft animal models generated from stable non-clonal cell cultures, and investigated the difference in chemotherapeutic effects on tumor growth between undifferenti…

0301 basic medicineCancer ResearchPathologymedicine.medical_specialtymedicine.drug_classHistone deacetylase inhibitorArticlesCell cycleBiologyUndifferentiated Pleomorphic SarcomaTyrosine-kinase inhibitorPazopanib03 medical and health sciences030104 developmental biology0302 clinical medicineOncologyIn vivo030220 oncology & carcinogenesismedicineDoxorubicinVorinostatmedicine.drugOncology Letters
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Concepts to Target MYC in Pancreatic Cancer.

2016

Abstract Current data suggest that MYC is an important signaling hub and driver in pancreatic ductal adenocarcinoma (PDAC), a tumor entity with a strikingly poor prognosis. No targeted therapies with a meaningful clinical impact were successfully developed against PDAC so far. This points to the need to establish novel concepts targeting the relevant drivers of PDAC, like KRAS or MYC. Here, we discuss recent developments of direct or indirect MYC inhibitors and their potential mode of action in PDAC. Mol Cancer Ther; 15(8); 1792–8. ©2016 AACR.

0301 basic medicineCancer ResearchPoor prognosisPancreatic ductal adenocarcinomaendocrine system diseasesGene regulatory networkAntineoplastic AgentsBiologymedicine.disease_causeBioinformaticsProto-Oncogene Proteins c-myc03 medical and health sciencesPancreatic cancerCarcinomamedicineAnimalsHumansGene Regulatory NetworksMolecular Targeted TherapyProtein Kinase InhibitorsCancerGenetic Variationmedicine.diseasedigestive system diseasesGene Expression Regulation NeoplasticPancreatic Neoplasms030104 developmental biologyOncologyCarrier proteinCancer researchKRASCarrier ProteinsCarcinoma Pancreatic DuctalProtein BindingSignal TransductionMolecular cancer therapeutics
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