Search results for "Oncogenes"

showing 10 items of 40 documents

Mutant p53 induces Golgi tubulo-vesiculation driving a prometastatic secretome

2020

TP53 missense mutations leading to the expression of mutant p53 oncoproteins are frequent driver events during tumorigenesis. p53 mutants promote tumor growth, metastasis and chemoresistance by affecting fundamental cellular pathways and functions. Here, we demonstrate that p53 mutants modify structure and function of the Golgi apparatus, culminating in the increased release of a pro-malignant secretome by tumor cells and primary fibroblasts from patients with Li-Fraumeni cancer predisposition syndrome. Mechanistically, interacting with the hypoxia responsive factor HIF1α, mutant p53 induces the expression of miR-30d, which in turn causes tubulo-vesiculation of the Golgi apparatus, leading …

0301 basic medicineBiopsyGeneral Physics and AstronomyGolgi ApparatusAnimals Biopsy Breast Neoplasms Cell Line Tumor Cell Transformation Neoplastic Female Fibroblasts Gene Expression Regulation Neoplastic Golgi Apparatus Humans Hypoxia-Inducible Factor 1 alpha Subunit Li-Fraumeni Syndrome Mice MicroRNAs Microtubules Mutation Primary Cell Culture Secretory Vesicles Signal TransductionSkin Tumor Microenvironment Tumor Suppressor Protein p53 Xenograft Model Antitumor Assays02 engineering and technologymedicine.disease_causeCell TransformationMicrotubulesSettore BIO/09 - FisiologiaMetastasisLi-Fraumeni SyndromeMiceTumor MicroenvironmentGolgisecretory machinerySuper-resolution microscopyAnimals; Biopsy; Breast Neoplasms; Cell Line Tumor; Cell Transformation Neoplastic; Female; Fibroblasts; Gene Expression Regulation Neoplastic; Golgi Apparatus; Humans; Hypoxia-Inducible Factor 1 alpha Subunit; Li-Fraumeni Syndrome; Mice; MicroRNAs; Microtubules; Mutation; Primary Cell Culture; Secretory Vesicles; Signal Transduction; Skin; Tumor Microenvironment; Tumor Suppressor Protein p53; Xenograft Model Antitumor Assayslcsh:ScienceSkinMultidisciplinaryTumorChemistrymutant p53QCell migrationMicroRNASecretomics021001 nanoscience & nanotechnologyCell biologyGene Expression Regulation NeoplasticCell Transformation NeoplasticsymbolsFibroblastmiR-30dFemaleHypoxia-Inducible Factor 10210 nano-technologyBreast NeoplasmHumanSignal TransductionCancer microenvironmentStromal cellSecretory VesicleSciencePrimary Cell CultureBreast NeoplasmsMicrotubuleGolgi ApparatuSettore MED/08 - Anatomia Patologicaalpha SubunitGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencessymbols.namesakeCell Line TumormedicineAnimalsHumansSettore MED/05 - Patologia ClinicaSecretionTumor microenvironmentNeoplasticAnimalSecretory VesiclesGeneral ChemistryOncogenesGolgi apparatusHDAC6FibroblastsMicroreviewHypoxia-Inducible Factor 1 alpha SubunitmicroenvironmentXenograft Model Antitumor AssaysMicroRNAs030104 developmental biologyGene Expression RegulationMutationlcsh:QTumor Suppressor Protein p53Carcinogenesis
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Normal vs cancer thyroid stem cells: the road to transformation

2015

Recent investigations in thyroid carcinogenesis have led to the isolation and characterisation of a subpopulation of stem-like cells, responsible for tumour initiation, progression and metastasis. Nevertheless, the cellular origin of thyroid cancer stem cells (SCs) remains unknown and it is still necessary to define the process and the target population that sustain malignant transformation of tissue-resident SCs or the reprogramming of a more differentiated cell. Here, we will critically discuss new insights into thyroid SCs as a potential source of cancer formation in light of the available information on the oncogenic role of genetic modifications that occur during thyroid cancer develop…

0301 basic medicineCancer ResearchThyroid GlandBiologymedicine.disease_causeMalignant transformationMetastasis03 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALECancer stem cellGeneticsmedicineHumansThyroid Neoplasmsthyroid stem cellsMolecular BiologyThyroid cancerThyroidCancerThyroid Cancer Stem Cells Cancer Stem Cells Oncogenes Metastasismedicine.diseaseCell Transformation Neoplastic030104 developmental biologymedicine.anatomical_structureImmunologyNeoplastic Stem CellsCancer researchStem cellCarcinogenesisOncogene
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Hormone Involvement in Tissue Development, Physiology and Oncogenesis: A Preface to the Special Issue

2020

Hormones, i.e., the products of specialized endocrine cells which spread throughout the body via the bloodstream, control the normal development and growth of organisms at the embryo-fetal stage and, in adult life, regulate, integrate, and coordinate a range of different physiological processes which concern virtually all body tissues. They exert their biological effects by interacting with either surface or intracellular receptors, thereby activating signalization pathways [1]. For example, steroid hormones, such as those released by the adrenal glands, testes and ovaries, once freely crossed through the plasmalemma, bind to receptors that act as ligand-dependent transcriptional regulators…

0301 basic medicineCancer Researchbusiness.industrylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease_causeBioinformaticslcsh:RC254-282hormones development physiology oncogenesis03 medical and health sciencesEditorialn/a030104 developmental biology0302 clinical medicineOncology030220 oncology & carcinogenesismedicineSettore BIO/06 - Anatomia Comparata E CitologiaCarcinogenesisbusinessHormoneCancers
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The MDS and EVI1 complex locus (MECOM) isoforms regulate their own transcription and have different roles in the transformation of hematopoietic stem…

2016

Transcriptional activation of the EVI1 oncogene (3q26) leads to aggressive forms of human acute myeloid leukemia (AML). However, the mechanism of EVI1-mediated leukemogenesis has not been fully elucidated. Previously, by characterizing the EVI1 promoter, we have shown that RUNX1 and ELK1 directly regulate EVI1 transcription. Intriguingly, bioinformatic analysis of the EVI1 promoter region identified the presence of several EVI1 potential binding sites. Thus, we hypothesized that EVI1 could bind to these sites regulating its own transcription. In this study, we show that there is a functional interaction between EVI1 and its promoter, and that the different EVI1 isoforms (EVI1-145kDa, EVI1-Δ…

0301 basic medicineGene isoformMECOMResponse elementBiophysicsBiologyBiochemistryCell LineMice03 medical and health scienceschemistry.chemical_compoundStructural BiologyTranscription (biology)Proto-OncogenesGeneticsAnimalsHumansProgenitor cellPromoter Regions GeneticMolecular BiologyTranscription factorGeneticsLeukemiaGene Expression Regulation LeukemicPromoterHematopoietic Stem CellsMDS1 and EVI1 Complex Locus ProteinCell biologyDNA-Binding ProteinsCell Transformation Neoplastic030104 developmental biologyRUNX1chemistryTranscription FactorsBiochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms
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Exome-wide somatic mutation characterization of small bowel adenocarcinoma

2018

Small bowel adenocarcinoma (SBA) is an aggressive disease with limited treatment options. Despite previous studies, its molecular genetic background has remained somewhat elusive. To comprehensively characterize the mutational landscape of this tumor type, and to identify possible targets of treatment, we conducted the first large exome sequencing study on a population-based set of SBA samples from all three small bowel segments. Archival tissue from 106 primary tumors with appropriate clinical information were available for exome sequencing from a patient series consisting of a majority of confirmed SBA cases diagnosed in Finland between the years 2003–2011. Paired-end exome sequencing was…

0301 basic medicineMaleCancer ResearchMICROSATELLITE INSTABILITYColorectal canceroncogenesReceptor ErbB-2medicine.disease_causeCOLORECTAL-CANCERACTIVATIONCohort Studies0302 clinical medicineAnimal CellsAdenocarcinomasMedicine and Health SciencesExomeFrameshift MutationExomeGenetics (clinical)Exome sequencingAged 80 and overSMALL-INTESTINEeducation.field_of_study1184 Genetics developmental biology physiologyCELIAC-DISEASENonsense MutationMiddle Aged3. Good healthsyöpägeenitOncology030220 oncology & carcinogenesissyöpätauditFemaleSIGNALING PATHWAYKRASCellular TypesResearch ArticleAdultProto-Oncogene Proteins B-raflcsh:QH426-470SEQUENCING DATAImmune CellsNonsense mutationPopulationImmunologyAntigen-Presenting CellsComputational biologysuolistosyövätBiologyAdenocarcinomata3111CarcinomasFrameshift mutation03 medical and health sciencesGermline mutationQUALITY-CONTROLGenetiikka kehitysbiologia fysiologia - Genetics developmental biology physiologySyöpätaudit - CancersIntestinal NeoplasmsmedicineGeneticsPoint MutationHumanseducationMolecular BiologyEcology Evolution Behavior and SystematicsAgedColorectal CancerBiology and Life SciencesCancers and Neoplasmscancerous diseasesCell Biologymedicine.diseaseta3122mutationsCOMPREHENSIVE MOLECULAR CHARACTERIZATIONlcsh:Genetics030104 developmental biologyMutationSomatic Mutationbowel cancer3111 BiomedicinemutaatiotHIGH-RESOLUTIONPLoS Genetics
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Female-specific association among I, J and K mitochondrial genetic haplogroups and cancer:A longitudinal cohort study

2018

Recent studies highlighted the role of mitochondrial dysregulation in cancer, suggesting that the different mitochondrial haplogroups might play a role in tumorigenesis and risk of cancer development. Our aim is to investigate whether any mitochondrial haplogroups carried a significant higher risk of cancer development in a large prospective cohort of North American people. The haplogroup assignment was performed by a combination of sequencing and PCR-RFLP techniques. Our specific outcome of interest was the incidence of any cancer during follow-up period. Overall, 3222 participants were included in the analysis. Women having I, J, K haplogroup reported a significant higher incidence of can…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtygenetic structuresBiologymedicine.disease_causeDNA MitochondrialHaplogroupHaplogroupArticleCohort Studies03 medical and health sciences0302 clinical medicineInternal medicineNeoplasmsGeneticsmedicineHumansGenetic Predisposition to DiseaseLongitudinal StudiesLongitudinal cohortProspective cohort studyMolecular BiologyOncogenesisCancerCancer Screening Oncogenesis Mitochondrial HaplogroupIncidence (epidemiology)Cancermedicine.diseaseeye diseaseshumanitiesMitochondrial030104 developmental biologyHaplotypes030220 oncology & carcinogenesisScreeningCancer; Haplogroup; Mitochondrial; Oncogenesis; ScreeningFemaleCancer developmentCarcinogenesis
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Clinical utility of plasma-based digital next-generation sequencing in oncogene-driven non-small-cell lung cancer patients with tyrosine kinase inhib…

2019

[Objectives] Resistance to tyrosine-kinase inhibitors (TKIs) is a clinical challenge in patients with oncogene-driven non-small-cell lung cancers (NSCLC). We have analyzed the utility of next-generation sequencing (NGS) of cell-free circulating tumor DNA (ctDNA) to impact the clinical care of patients with TKI resistance.

0301 basic medicineOncologyMaleCancer ResearchLung NeoplasmsTyrosine-kinase inhibitorCirculating Tumor DNAchemistry.chemical_compound0302 clinical medicineCarcinoma Non-Small-Cell LungMedicineOsimertinibNeoplasm MetastasisProspective cohort studyAged 80 and overDisease ManagementHigh-Throughput Nucleotide SequencingMiddle AgedOncology030220 oncology & carcinogenesisFemalemedicine.drugPulmonary and Respiratory MedicineAdultmedicine.medical_specialtyCabozantinibmedicine.drug_class03 medical and health sciencesInternal medicineROS1Biomarkers TumorHumansLung cancerProtein Kinase InhibitorsAgedNeoplasm StagingDigital next-generation sequencingTKI resistanceCrizotinibbusiness.industryOncogene-driven NSCLCOncogenesctDNAmedicine.diseaseLorlatinibrespiratory tract diseases030104 developmental biologychemistryDrug Resistance NeoplasmMutationbusinessOsimertinib
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MassARRAY determination of somatic oncogenic mutations in solid tumors: Moving forward to personalized medicine.

2016

This article will review the impact of the recently developed MassARRAY technology on our understanding of cancer biology and treatment. Analysis of somatic mutations is a useful tool in selecting personalized therapy, and for predicting the outcome of many solid tumors. Here, we review the literature on the application of MassARRAY technology (Sequenom Hamburg, Germany) to determine the mutation profile of solid tumors from patients. We summarize the use of commercially available panels of mutations - such as OncoCarta™ or other combinations - and their concordance with results obtained by using other technologies, such as next generation sequencing.

0301 basic medicineSomatic cellConcordanceComputational biologymedicine.disease_causeBioinformatics03 medical and health sciences0302 clinical medicineNeoplasmsMedicineHumansRadiology Nuclear Medicine and imagingCancer biologyPersonalized therapyPrecision MedicineOligonucleotide Array Sequence AnalysisMutationbusiness.industryHigh-Throughput Nucleotide SequencingGeneral MedicineOncogenesPrecision medicine030104 developmental biologyOncology030220 oncology & carcinogenesisMutationPersonalized medicinebusinessCancer treatment reviews
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ROS and Lipid Droplet accumulation induced by high glucose exposure in healthy colon and Colorectal Cancer Stem Cells

2020

Lipid Droplets (LDs) are emerging as crucial players in colon cancer development and maintenance. Their expression has been associated with high tumorigenicity in Cancer Stem Cells (CSCs), so that they have been proposed as a new functional marker in Colorectal Cancer Stem Cells (CR-CSCs). They are also indirectly involved in the modulation of the tumor microenvironment through the production of pro-inflammatory molecules. There is growing evidence that a possible connection between metabolic alterations and malignant transformation exists, although the effects of nutrients, primarily glucose, on the CSC behavior are still mostly unexplored. Glucose is an essential fuel for cancer cells, an…

0301 basic medicinelcsh:QH426-470Colorectal cancerColorectal cancer stem cellsSettore MED/50 - Scienze Tecniche Mediche ApplicateLipid dropletBiochemistryMalignant transformation03 medical and health sciences0302 clinical medicineCancer stem cellLipid dropletFull Length ArticlemedicineCholesterol metabolismMolecular BiologyOncogeneGenetics (clinical)PI3K/AKT/mTOR pathwaySettore MED/04 - Patologia Generalelcsh:R5-920Tumor microenvironmentChemistryPI3K-AKTColorectal cancer stem cellCell BiologyOncogenesmedicine.diseaseLipid droplets3. Good healthlcsh:GeneticsSettore BIO/12 - Biochimica Clinica E Biologia Molecolare Clinica030104 developmental biologyOxidative stress030220 oncology & carcinogenesisFatty acid metabolismCancer cellCancer researchOxidative streSettore MED/46 - Scienze Tecniche Di Medicina Di LaboratorioStem cellHigh glucoselcsh:Medicine (General)Genes & Diseases
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A subset of flavaglines inhibits KRAS nanoclustering and activation.

2020

The RAS oncogenes are frequently mutated in human cancers and among the three isoforms (KRAS, HRAS and NRAS), KRAS is the most frequently mutated oncogene. Here, we demonstrate that a subset of flavaglines, a class of natural anti-tumour drugs and chemical ligands of prohibitins, inhibit RAS GTP loading and oncogene activation in cells at nanomolar concentrations. Treatment with rocaglamide, the first discovered flavagline, inhibited the nanoclustering of KRAS, but not HRAS and NRAS, at specific phospholipid-enriched plasma membrane domains. We further demonstrate that plasma membrane-associated prohibitins directly interact with KRAS, phosphatidylserine and phosphatidic acid, and these int…

:Bioengineering [Engineering]Neuroblastoma RAS viral oncogene homologGene isoformLung NeoplasmsGTP'[SDV]Life Sciences [q-bio]AucunBiology: Biochemistry biophysics & molecular biology [F05] [Life sciences]medicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRocaglamideCarcinoma Non-Small-Cell LungmedicineKRASHumansdrug therapy;geneticsgeneticsHRASProhibitin: Biochimie biophysique & biologie moléculaire [F05] [Sciences du vivant]neoplasmsComputingMilieux_MISCELLANEOUS030304 developmental biology0303 health sciencesOncogeneLipid nanoclusterOncogenesCell Biologydigestive system diseases3. Good healthrespiratory tract diseasesPhospholipidchemistry030220 oncology & carcinogenesisMutationCancer researchKRASFlavaglineRocaglamideProhibitinSignal Transduction
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