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showing 10 items of 10618 documents

Weight loss programmes using low carbohydrate diets to control the cardiovascular risk in adolescents (Review).

2020

Cardiovascular risk (CVR) is a broad term that includes traditional factors like hypertension, hyper lipidemia, abdominal obesity, hyperinsulinemia or overt type 2 diabetes mellitus (T2DM), and emerging ones such as hypothyroidism or inflammatory diseases. In epidemiologic studies, all of these factors are associated with atherogenesis and have complex interactions between them. They have in common an increased prevalence in the general population beginning in childhood, and are correlated with endothelial damage as demonstrated by echocardiographic modifications of the left ventricle or carotid intima-media thickness. Adolescence is a transition period where behavioural eating patterns dev…

0301 basic medicineCancer ResearchPediatricsmedicine.medical_specialtyPopulationType 2 diabetesReviewOverweight03 medical and health sciences0302 clinical medicineImmunology and Microbiology (miscellaneous)Weight lossmedicineHyperinsulinemiaeducationAbdominal obesityeducation.field_of_studybusiness.industryType 2 Diabetes MellitusGeneral Medicinemedicine.disease030104 developmental biology030220 oncology & carcinogenesismedicine.symptombusinessDyslipidemiaExperimental and therapeutic medicine
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Stem-cell derived hepatocyte-like cells for the assessment of drug-induced liver injury.

2019

Drug-induced liver injury is a major cause of drug discovery failure in clinical trials and a leading cause of liver disease. Current preclinical drug testing does not predict hepatotoxicity which highlights the importance of developing highly predictive cell-based models. The use of stem cell technology and differentiation into hepatocyte-like cells (HLCs) could provide a stable source of hepatocytes for multiple applications, including drug screening. HLCs derived from both embryonic and induced pluripotent stem cells have been used to accurately predict hepatotoxicity as well as to test individual-specific toxicity. Although there are still many limitations, mainly related to the lack of…

0301 basic medicineCancer ResearchPopulationCellInduced Pluripotent Stem CellsDrug Evaluation PreclinicalBiology03 medical and health sciencesLiver disease0302 clinical medicinemedicineAnimalsHumansInduced pluripotent stem celleducationMolecular BiologyEmbryonic Stem Cellseducation.field_of_studyDrug discoveryCell DifferentiationCell Biologymedicine.diseaseEmbryonic stem cell030104 developmental biologymedicine.anatomical_structurePhenotypeHepatocyteCancer researchHepatocytesStem cellChemical and Drug Induced Liver Injury030217 neurology & neurosurgeryDevelopmental BiologyDifferentiation; research in biological diversity
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HDAC1 and HDAC2 integrate the expression of p53 mutants in pancreatic cancer.

2015

Mutation of p53 is a frequent genetic lesion in pancreatic cancer being an unmet clinical challenge. Mutants of p53 have lost the tumour-suppressive functions of wild type p53. In addition, p53 mutants exert tumour-promoting functions, qualifying them as important therapeutic targets. Here, we show that the class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of p53 mutants in human and genetically defined murine pancreatic cancer cells. Our data reveal that the inhibition of these HDACs with small molecule HDAC inhibitors (HDACi), as well as the specific genetic elimination of HDAC1 and HDAC2, reduce the expression of mutant p53 mRNA and protein levels. We fur…

0301 basic medicineCancer ResearchProteasome Endopeptidase ComplexMutantHistone Deacetylase 2Histone Deacetylase 1Biologymedicine.disease_causeMolecular oncologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicePancreatic cancerGeneticsmedicineAnimalsHumansRNA MessengerPromoter Regions GeneticMolecular BiologyRegulation of gene expressionMice KnockoutMutationWild typeCancerProto-Oncogene Proteins c-mdm2medicine.diseaseGenes p53HDAC13. Good healthGene Expression Regulation NeoplasticHistone Deacetylase InhibitorsPancreatic NeoplasmsDisease Models Animal030104 developmental biologyMutationCancer researchOncogene
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Tumor-Associated Fibroblasts Promote HER2-Targeted Therapy Resistance through FGFR2 Activation

2020

AbstractPurpose:Despite the therapeutic success of existing HER2-targeted therapies, tumors invariably relapse. This study aimed at identifying new mechanisms responsible for HER2-targeted therapy resistance.Experimental Design:We have used a platform of HER2-targeted therapy–resistant cell lines and primary cultures of healthy and tumor-associated fibroblasts (TAF) to identify new potential targets related to tumor escape from anti-HER2 therapies.Results:We have shown that TAFs promote resistance to HER2-targeted therapies. TAFs produce and secrete high levels of FGF5, which induces FGFR2 activation in the surrounding breast cancer cells. FGFR2 transactivates HER2 via c-Src, leading to res…

0301 basic medicineCancer ResearchReceptor ErbB-2medicine.medical_treatmentMice NudeBreast NeoplasmsDrug resistanceTargeted therapy03 medical and health sciencesMice0302 clinical medicineBreast cancerCancer-Associated FibroblastsTrastuzumabCell Line TumorAntineoplastic Combined Chemotherapy ProtocolsmedicineNeoplasmAnimalsHumansReceptor Fibroblast Growth Factor Type 2skin and connective tissue diseasesneoplasmsbusiness.industryLapatinibTrastuzumabmedicine.diseaseXenograft Model Antitumor AssaysSurvival Rate030104 developmental biologyOncologyTumor EscapeApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchFemaleSignal transductionNeoplasm Recurrence Localbusinessmedicine.drugSignal Transduction
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A g316a polymorphism in the ornithine decarboxylase gene promoter modulates mycn‐driven childhood neuroblastoma

2021

Simple Summary Neuroblastoma is a devasting childhood cancer in which multiple copies (amplification) of the cancer-causing gene MYCN strongly predict poor outcome. Neuroblastomas are reliant on high levels of cellular components called polyamines for their growth and malignant behavior, and the gene regulating polyamine synthesis is called ODC1. ODC1 is often coamplified with MYCN, and in fact is regulated by MYCN, and like MYCN is prognostic of poor outcome. Here we studied a naturally occurring genetic variant or polymorphism that occurs in the ODC1 gene, and used gene editing to demonstrate the functional importance of this variant in terms of ODC1 levels and growth of neuroblastoma cel…

0301 basic medicineCancer ResearchSNPSingle-nucleotide polymorphismBiologylcsh:RC254-282ArticleOrnithine decarboxylase03 medical and health sciencesneuroblastomaNeuroblastoma0302 clinical medicineNeuroblastomaGenotypeMYCNMedicine and Health SciencesTranscriptional regulationmedicineODC1neoplasmsWild typePromotermedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMolecular biology030104 developmental biologyOncology030220 oncology & carcinogenesisChildhood Neuroblastoma
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Melanoma Lesions Independently Acquire T-cell Resistance during Metastatic Latency

2016

Abstract Melanoma often recurs after a latency period of several years, presenting a T cell–edited phenotype that reflects a role for CD8+ T cells in maintaining metastatic latency. Here, we report an investigation of a patient with multiple recurrent lesions, where poorly immunogenic melanoma phenotypes were found to evolve in the presence of autologous tumor antigen–specific CD8+ T cells. Melanoma cells from two of three late recurrent metastases, developing within a 6-year latency period, lacked HLA class I expression. CD8+ T cell–resistant, HLA class I–negative tumor cells became clinically apparent 1.5 and 6 years into stage IV disease. Genome profiling by SNP arrays revealed that HLA …

0301 basic medicineCancer ResearchT cellmedicine.medical_treatmentMedizinHuman leukocyte antigenCD8-Positive T-LymphocytesBiology03 medical and health sciencesAntigens NeoplasmmedicineHumansNeoplasm MetastasisMelanomaMelanomaCancerImmunosuppressionmedicine.diseasePhenotypeNeoplasm Proteins030104 developmental biologymedicine.anatomical_structureOncologyLatency stageImmunologyCD8Cancer Research
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Cadmium-Associated Molecular Signatures in Cancer Cell Models

2021

Simple Summary The exposure of cancer cells to cadmium compounds may be associated with the acceleration of tumor progression. It is known that cadmium is a transcriptional regulator, and the study of differentially expressed genes has enabled the identification and classification of cadmium-associated molecular signatures as useful biomarkers that are potentially transferable to clinical research. This review recapitulates the studies that report the detection of such signatures in breast, gastric, colon, liver, lung, and nasopharyngeal tumor cell models, as specifically demonstrated by individual gene or whole genome expression profiling. Abstract The exposure of cancer cells to cadmium a…

0301 basic medicineCancer Researchcadmiumnasopharyngeal cancerReviewBiologygene signaturedifferential expressionliver cancer03 medical and health sciences0302 clinical medicinebreast cancerGene silencingSettore BIO/06 - Anatomia Comparata E CitologiaRC254-282Regulation of gene expressiongastric cancerNeoplasms. Tumors. Oncology. Including cancer and carcinogensGene signaturein vitro cell modelsPhenotypein vitro cell modelGene expression profilinglung cancer030104 developmental biologyOncologycolon cancerTumor progression030220 oncology & carcinogenesisCancer cellCancer researchReprogrammingCancers
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Genetic variations in the PSMA6 and PSMC6 proteasome genes are associated with multiple sclerosis and response to interferon‑β therapy in Latvians

2021

Several polymorphisms in genes related to the ubiquitin-proteasome system exhibit an association with pathogenesis and prognosis of various human autoimmune diseases. Our previous study reported the association between multiple sclerosis (MS) and the PSMA3-rs2348071 polymorphism in the Latvian population. The current study aimed to evaluate the PSMA6 and PSMC6 genetic variations, their interaction between each other and with the rs2348071, on the susceptibility to MS risk and response to therapy in the Latvian population. PSMA6-rs2277460, -rs1048990 and PSMC6-rs2295826, -rs2295827 were genotyped in the MS case/control study and analysed in terms of genotype-protein correlation network. The …

0301 basic medicineCancer Researcheducation.field_of_studybusiness.industryMultiple sclerosisHaplotypePopulationPSMA6Single-nucleotide polymorphismGeneral MedicineDiseasePSMA3medicine.diseasePSMC603 medical and health sciences030104 developmental biology0302 clinical medicineImmunology and Microbiology (miscellaneous)030220 oncology & carcinogenesisImmunologyMedicinebusinesseducationExperimental and Therapeutic Medicine
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Pattern of Invasion in Human Pancreatic Cancer Organoids Is Associated with Loss of SMAD4 and Clinical Outcome

2020

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy characterized by extensive local invasion and systemic spread. In this study, we employed a three-dimensional organoid model of human pancreatic cancer to characterize the molecular alterations critical for invasion. Time-lapse microscopy was used to observe invasion in organoids from 25 surgically resected human PDAC samples in collagen I. Subsequent lentiviral modification and small-molecule inhibitors were used to investigate the molecular programs underlying invasion in PDAC organoids. When cultured in collagen I, PDAC organoids exhibited two distinct, morphologically defined invasive phenotypes, mesenchymal an…

0301 basic medicineCancer Researchendocrine system diseasesPancreatic ductal adenocarcinoma (PDAC)RAC1CDC42AdenocarcinomaBiologyArticle03 medical and health sciences0302 clinical medicineHuman Pancreatic CancerCell MovementPancreatic cancerBiomarkers TumorTumor Cells CulturedmedicineOrganoidHumansNeoplasm InvasivenessCell ProliferationSmad4 ProteinRegulation of gene expressionCell growthMesenchymal stem cellPrognosismedicine.diseasePhenotypedigestive system diseasesGene Expression Regulation NeoplasticOrganoidsPancreatic NeoplasmsSurvival Rate030104 developmental biologyOncology030220 oncology & carcinogenesisembryonic structuresCancer researchCarcinoma Pancreatic DuctalSignal TransductionCancer Research
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Identification of clinical phenotypes and related survival in patients with large hccs

2021

Background. Hepatocellular carcinoma (HCC) factors, especially maximum tumor diameter (MTD), tumor multifocality, portal vein thrombosis (PVT), and serum alpha-fetoprotein (AFP), influence survival. Aim. To examine patterns of tumor factors in large HCC patients. Methods. A database of large HCC patients was examined. Results. A multiple Cox proportional hazard model on death identified low serum albumin levels and the presence of PVT and multifocality, with each having a hazard ratio ≥2.0. All combinations of these three parameters were examined in relation to survival. Using univariate Cox analysis, the combination of albumin &gt

0301 basic medicineCancer Researchmedicine.medical_specialtyPVTSettore MED/12 - GASTROENTEROLOGIASerum albuminlcsh:RC254-282GastroenterologyArticle03 medical and health sciences0302 clinical medicineInternal medicineMedicinePlateletHCCneoplasmsSurvival ratePVT.biologybusiness.industryProportional hazards modelAlbuminHazard ratioSettore MED/09 - MEDICINA INTERNAAlbuminMultifocalityHCC; large; phenotypes; PVT; multifocality; albuminlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasedigestive system diseasesPortal vein thrombosisAlbumin; HCC; Large; Multifocality; Phenotypes; PVTPhenotypesPhenotype030104 developmental biologyOncology030220 oncology & carcinogenesisHepatocellular carcinomabiology.proteinLargebusiness
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