Search results for "EPA"

showing 10 items of 8995 documents

ER+ Breast Cancers Resistant to Prolonged Neoadjuvant Letrozole Exhibit an E2F4 Transcriptional Program Sensitive to CDK4/6 Inhibitors

2018

AbstractPurpose: This study aimed to identify biomarkers of resistance to endocrine therapy in estrogen receptor–positive (ER+) breast cancers treated with prolonged neoadjuvant letrozole.Experimental Design: We performed targeted DNA and RNA sequencing in 68 ER+ breast cancers from patients treated with preoperative letrozole (median, 7 months).Results: Twenty-four tumors (35%) exhibited a PEPI score ≥4 and/or recurred after a median of 58 months and were considered endocrine resistant. Integration of the 47 most upregulated genes (log FC > 1, FDR < 0.03) in letrozole-resistant tumors with transcription-binding data showed significant overlap with 20 E2F4-regulated genes (P =…

0301 basic medicineCancer ResearchBreast NeoplasmsE2F4 Transcription FactorArticle03 medical and health sciences0302 clinical medicineText miningDownregulation and upregulationCell Line TumorBiomarkers TumormedicineHumansEndocrine systemProtein Kinase InhibitorsE2F4GeneAgedCell ProliferationAged 80 and overAromatase Inhibitorsbusiness.industryGene Expression ProfilingLetrozoleEndocrine therapyComputational BiologyMiddle AgedEMTREE drug terms: aromatase inhibitorcyclin dependent kinase 4cyclin dependent kinase 6cyclin dependent kinase inhibitorfulvestrantletrozolepaclitaxelpalbociclibtranscription factor E2F4estrogen receptorletrozoleprotein kinase inhibitortranscription factor E2F4transcriptometumor marker030104 developmental biologyReceptors EstrogenOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisLetrozoleMutationRetreatmentCancer researchFemaleTranscriptomebusinessmedicine.drug
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Colorectal Carcinogenesis: Role of Oxidative Stress and Antioxidants

2017

One of the contributory causes of colon cancer is the negative effect of reactive oxygen species on DNA repair mechanisms. Currently, there is a growing support for the concept that oxidative stress may be an important etiological factor for carcinogenesis. The purpose of this review is to elucidate the role of oxidative stress in promoting colorectal carcinogenesis and to highlight the potential protective role of antioxidants. Several studies have documented the importance of antioxidants in countering oxidative stress and preventing colorectal carcinogenesis. However, there are conflicting data in the literature concerning its proper use in humans, since these studies did not yield defin…

0301 basic medicineCancer ResearchCarcinogenesisSettore MED/06 - Oncologia MedicaColorectal cancerDNA repairCellReviewColorectal Neoplasmmedicine.disease_causeAntioxidants03 medical and health sciences0302 clinical medicineAntioxidants; Colorectal cancer; Dysbiosis; Oxidative stress; Review; Animals; Antioxidants; Carcinogenesis; Colorectal Neoplasms; Humans; Reactive Oxygen Species; Oxidative Stress; Oncology; Cancer ResearchAnimalsHumansMedicinecolorectal cancer dysbiosis microbioma oxodative stress carcinogenesiCarcinogenesichemistry.chemical_classificationReactive oxygen speciesAnimalbusiness.industryOxidative StreGeneral MedicineColorectal carcinogenesismedicine.diseaseColorectal cancerDysbiosiOxidative StressSettore MED/18 - Chirurgia Generalecolorectal cancer dysbiosis microbioma oxodative stress carcinogenesis030104 developmental biologymedicine.anatomical_structureOncologyBiochemistrychemistry030220 oncology & carcinogenesisCancer researchAntioxidantColorectal NeoplasmsReactive Oxygen SpeciesReactive Oxygen SpeciebusinessCarcinogenesisDysbiosisOxidative stressHumanAnticancer Research
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Oleocanthal exerts antitumor effects on human liver and colon cancer cells through ROS generation

2017

The beneficial health properties of the Mediterranean diet are well recognized. The principle source of fat in Mediterranean diet is extra-virgin olive oil (EVOO). Oleocanthal (OC) is a naturally occurring minor phenolic compound isolated from EVOO, which has shown a potent anti-inflammatory activity, by means of its ability to inhibit the cyclooxygenase (COX) enzymes COX-1 and COX-2. A large body of evidence indicates that phenols exhibit anticancer activities. The aim of the present study was to evaluate the potential anticancer effects of OC in hepatocellular carcinoma (HCC) and colorectal carcinoma (CRC) models. A panel of human HCC (HepG2, Huh7, Hep3B and PLC/PRF/5) and CRC (HT29, SW48…

0301 basic medicineCancer ResearchCarcinoma HepatocellularHepatocellular carcinomaOleocanthalExtra-virgin olive oilCellApoptosisCyclopentane Monoterpenes03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhenolsOleocanthalmedicineHumansCyclooxygenase InhibitorsViability assayOlive OilCaspaseCell ProliferationAldehydesbiologyCell growthLiver NeoplasmsApoptosiHep G2 CellsCell cycledigestive system diseasesColorectal carcinoma030104 developmental biologymedicine.anatomical_structureOncologychemistryApoptosisCell culture030220 oncology & carcinogenesisImmunologybiology.proteinCancer researchReactive oxygen specieColorectal NeoplasmsReactive Oxygen SpeciesDNA DamageInternational Journal of Oncology
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Trabectedin triggers direct and NK-mediated cytotoxicity in multiple myeloma

2019

Background Genomic instability is a feature of multiple myeloma (MM), and impairment in DNA damaging response (DDR) has an established role in disease pathobiology. Indeed, a deregulation of DNA repair pathways may contribute to genomic instability, to the establishment of drug resistance to genotoxic agents, and to the escape from immune surveillance. On these bases, we evaluated the role of different DDR pathways in MM and investigated, for the first time, the direct and immune-mediated anti-MM activity of the nucleotide excision repair (NER)-dependent agent trabectedin. Methods Gene-expression profiling (GEP) was carried out with HTA2.0 Affymetrix array. Evaluation of apoptosis, cell cyc…

0301 basic medicineCancer ResearchCell cycle checkpointNatural killerDNA repairmedicine.medical_treatmentMyelomalcsh:RC254-28203 medical and health sciences0302 clinical medicineMicro-RNAmedicineHumansMolecular BiologyAntineoplastic Agents AlkylatingTrabectedin3D-modelChemistrylcsh:RC633-647.5ResearchMicro-RNAsHematologylcsh:Diseases of the blood and blood-forming organsCell cycleNKG2Dlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensKiller Cells Natural030104 developmental biologyCytokineOncologyApoptosis3D-models030220 oncology & carcinogenesis3D-models; Micro-RNAs; Myeloma; Natural killer; TrabectedinCancer researchDNA fragmentationMultiple Myelomamedicine.drugTrabectedinJournal of Hematology & Oncology
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Context-Dependent Role of NF-κB Signaling in Primary Liver Cancer—from Tumor Development to Therapeutic Implications

2019

Chronic inflammatory cell death is a major risk factor for the development of diverse cancers including liver cancer. Herein, disruption of the hepatic microenvironment as well as the immune cell composition are major determinants of malignant transformation and progression in hepatocellular carcinomas (HCC). Considerable research efforts have focused on the identification of predisposing factors that promote induction of an oncogenic field effect within the inflammatory liver microenvironment. Among the most prominent factors involved in this so-called inflammation-fibrosis-cancer axis is the NF-κB pathway. The dominant role of this pathway for malignant transformation and progression…

0301 basic medicineCancer ResearchCell typechronic inflammationContext (language use)Reviewlcsh:RC254-282Malignant transformation03 medical and health sciences0302 clinical medicineImmune systemMedicinebusiness.industryhepatocarcinogenesishepatocellular carcinomalcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseNf κb signaling030104 developmental biologyOncology030220 oncology & carcinogenesisHepatocellular carcinomaNF-κB signalingCancer researchbusinessLiver cancerPrimary liver cancerCancers
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A PDCD1 Role in the Genetic Predisposition to NAFLD-HCC?

2021

Obesity and non-alcoholic fatty liver disease (NAFLD) are contributing to the global rise in deaths from hepatocellular carcinoma (HCC). The pathogenesis of NAFLD-HCC is not well understood. The severity of hepatic steatosis, steatohepatitis and fibrosis are key pathogenic mechanisms, but animal studies suggest altered immune responses are also involved. Genetic studies have so far highlighted a major role of gene variants promoting fat deposition in the liver (PNPLA3 rs738409

0301 basic medicineCancer ResearchCirrhosisprimary liver cancer<i>PDCD1</i>610 Medicine & healthDiseaseBioinformaticslcsh:RC254-282digestive systemArticleTM6SF2metabolic syndrome03 medical and health sciences0302 clinical medicinePD-1medicineGenetic predispositionPNPLA3business.industry<i>TM6SF2</i>PDCD1Fatty livernutritional and metabolic diseaseshepatocellular carcinomasingle-nucleotide polymorphismlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasedigestive system diseases3. Good health<i>PNPLA3</i>030104 developmental biologyOncology030211 gastroenterology & hepatologyMetabolic syndromeSteatohepatitisSteatosisbusinessgenetic predispositionTM6SF2Cancers
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Spontaneous and Radiation-Induced Chromosome Aberrations in Primary Fibroblasts of Patients With Pediatric First and Second Neoplasms

2020

Frontiers in oncology 10, 1338 (2020). doi:10.3389/fonc.2020.01338

0301 basic medicineCancer ResearchDNA repairSomatic cell610Chromosomal translocationlcsh:RC254-28203 medical and health sciences0302 clinical medicineRadiation sensitivityChromosome instabilitymedicinechildhood cancerddc:610spontaneous chromosomal instabilityOriginal Researchmedicine.diagnostic_testbusiness.industryChromosomeradiation sensitivitysecond primary malignancieslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrimary Neoplasm030104 developmental biologychromosome aberrationsOncology030220 oncology & carcinogenesisCancer researchbusinessionizing radiationSecond primary malignancies ; Radiation sensitivity ; Chromosome aberrations ; Childhood cancer ; Spontaneous chromosomal instability ; Ionizing radiationFluorescence in situ hybridization
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A receptor-antibody hybrid hampering MET-driven metastatic spread

2021

AbstractBackgroundThe receptor encoded by the MET oncogene and its ligand Hepatocyte Growth Factor (HGF) are at the core of the invasive-metastatic behavior. In a number of instances genetic alterations result in ligand-independent onset of malignancy (METaddiction). More frequently, ligand stimulation of wild-type MET contributes to progression toward metastasis (METexpedience). Thus, while MET inhibitors alone are effective in the first case, combination therapy with ligand inhibitors is required in the second condition.MethodsIn this paper, we generated hybrid molecules gathering HGF and MET inhibitory properties. This has been achieved by ‘head-to-tail’ or ‘tail-to-head’ fusion of a sin…

0301 basic medicineCancer ResearchImmunoconjugatesmedicine.medical_treatmentMice SCIDEpitopeFusion proteins; HGF; MET; Metastasis; Targeted therapy; A549 Cells; Animals; Binding Sites Antibody; Cell Line Tumor; Cell Proliferation; Female; Hepatocyte Growth Factor; Humans; Immunoconjugates; Immunoglobulin Fab Fragments; Mice; Mice SCID; Neoplasm Metastasis; Neoplasms; Proto-Oncogene Proteins c-met; Rats; Rats Sprague-Dawley; Recombinant Proteins; Xenograft Model Antitumor AssaysMetastasisTargeted therapyMetastasisRats Sprague-DawleyTargeted therapyMice0302 clinical medicineNeoplasmsHGFNeoplasm MetastasisReceptorTumorHepatocyte Growth FactorChemistryProto-Oncogene Proteins c-metlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensRecombinant ProteinsOncology030220 oncology & carcinogenesisMETFemaleHepatocyte growth factormedicine.drugSCIDlcsh:RC254-282Cell LineImmunoglobulin Fab Fragments03 medical and health sciencesCell Line TumorPancreatic cancermedicineAnimalsHumansAntibodyCell ProliferationBinding SitesResearchmedicine.diseaseXenograft Model Antitumor AssaysFusion proteinRatsFusion proteins030104 developmental biologyA549 CellsCancer cellCancer researchBinding Sites AntibodySprague-DawleyJournal of Experimental &amp; Clinical Cancer Research
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Efficacy and epigenetic interactions of novel DNA hypomethylating agent guadecitabine (SGI-110) in preclinical models of hepatocellular carcinoma.

2016

ABSTRACT Hepatocellular carcinoma (HCC) is a deadly malignancy characterized at the epigenetic level by global DNA hypomethylation and focal hypermethylation on the promoter of tumor suppressor genes. In most cases it develops on a background of liver steatohepatitis, fibrosis, and cirrhosis. Guadecitabine (SGI-110) is a second-generation hypomethylating agent, which inhibits DNA methyltransferases. Guadecitabine is formulated as a dinucleotide of decitabine and deoxyguanosine that is resistant to cytidine deaminase (CDA) degradation and results in prolonged in vivo exposure to decitabine following small volume subcutaneous administration of guadecitabine. Here we found that guadecitabine i…

0301 basic medicineCancer ResearchMethyltransferasesteatohepatitisDecitabineBiologyDecitabineDNA methylation Decitabine guadecitabine hepatocellular carcinoma (HCC) histone macroH2A1 steatohepatitishepatocellular carcinoma (HCC)03 medical and health scienceschemistry.chemical_compoundCDKN2AmedicineEpigeneticsMolecular BiologyneoplasmsDNA methylationGuadecitabineguadecitabinehistone macroH2A1steatohepatitidigestive system diseases3. Good healthDemethylating agent030104 developmental biologychemistryHypomethylating agentDNA methylationCancer researchResearch Papermedicine.drug
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Dual Constant Domain-Fab: A novel strategy to improve half-life and potency of a Met therapeutic antibody

2016

The kinase receptor encoded by the Met oncogene is a sensible target for cancer therapy. The chimeric monovalent Fab fragment of the DN30 monoclonal antibody (MvDN30) has an odd mechanism of action, based on cell surface removal of Met via activation of specific plasma membrane proteases. However, the short half-life of the Fab, due to its low molecular weight, is a severe limitation for the deployment in therapy. This issue was addressed by increasing the Fab molecular weight above the glomerular filtration threshold through the duplication of the constant domains, in tandem (DCD-1) or reciprocally swapped (DCD-2). The two newly engineered molecules showed biochemical properties comparable…

0301 basic medicineCancer ResearchMice SCIDCancer targeted therapy0302 clinical medicineMice Inbred NODEpidermal growth factor receptorPhosphorylationbiologyChemistryImmunoglobulin Fab FragmentsAntibodies MonoclonalGeneral MedicineArticlesProto-Oncogene Proteins c-metHalf-lifeCell biologyOncology030220 oncology & carcinogenesisColonic NeoplasmsMetMolecular MedicineFemalemedicine.symptomSignal transductionAntibodySignal Transductionmedicine.drug_classColonAntibody; Cancer targeted therapy; Fab; Half-life; Met; Protein engineering; Cancer Research; Genetics; Molecular MedicineAntineoplastic AgentsMonoclonal antibody03 medical and health sciencesImmunoglobulin Fab FragmentsProtein DomainsCell Line TumormedicineGeneticsAnimalsHumansFabAntibodyCell growthMolecular biology030104 developmental biologyHEK293 CellsMechanism of actionHepatocyte Growth Factor ReceptorA549 Cellsbiology.proteinProtein engineering
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