Search results for "Cance"

showing 10 items of 12092 documents

Cytosine methylation patterns suggest a role of methylation in plastic and adaptive responses to temperature in European grayling (Thymallus thymallu…

2020

Temperature is a key environmental parameter affecting both the phenotypes and distributions of organisms, particularly ectotherms. Rapid organismal responses to thermal environmental changes have been described for several ectotherms; however, the underlying molecular mechanisms often remain unclear. Here, we studied whole genome cytosine methylation patterns of European grayling (Thymallus thymallus) embryos from five populations with contemporary adaptations of early life history traits at either 'colder' or 'warmer' spawning grounds. We reared fish embryos in a common garden experiment using two temperatures that resembled the 'colder' and 'warmer' conditions of the natal natural enviro…

0301 basic medicineCancer ResearchDATABASEsalmonidPopulationCytosine methylationSNPepigenetic variationCytosine03 medical and health sciences0302 clinical medicineINTRAGENIC DNA METHYLATIONthermal adaptationPHENOTYPIC PLASTICITYAnimalsADAPTATIONeducationMolecular BiologyGENE-EXPRESSIONLocal adaptationeducation.field_of_studyPhenotypic plasticitypromoterCLIMATE-CHANGEbiologyTemperatureGenetic VariationDNA Methylationbiology.organism_classificationThymallusEVOLUTIONEuropean graylingINSIGHTS030104 developmental biologyCpG siteEvolutionary biologydevelopmental plasticity030220 oncology & carcinogenesisEctotherm1181 Ecology evolutionary biologyDNA methylationTHERMAL PLASTICITYtranscriptionSalmonidaeResearch PaperEpigenetics
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Knockdown of hnRNPK leads to increased DNA damage after irradiation and reduces survival of tumor cells.

2017

Radiotherapy is an important treatment option in the therapy of multiple tumor entities among them head and neck squamous cell carcinoma (HNSCC). However, the success of radiotherapy is limited by the development of radiation resistances. Heterogeneous nuclear ribonucleoprotein K (hnRNPK) is a cofactor of p53 and represents a potential target for radio sensitization of tumor cells. In this study, we analyzed the impact of hnRNPK on the DNA damage response after gamma irradiation. By yH2AX foci analysis, we found that hnRNPK knockdown increases DNA damage levels in irradiated cells. Tumor cells bearing a p53 mutation showed increased damage levels and delayed repair. Knockdown of hnRNPK appl…

0301 basic medicineCancer ResearchDNA damageCell Survivalmedicine.medical_treatmentmedicine.disease_causeRadiation ToleranceHeterogeneous-Nuclear Ribonucleoprotein KHistones03 medical and health sciences0302 clinical medicineCell Line TumormedicineCarcinomaGene Knockdown TechniquesHumansMutationGene knockdownChemistrySquamous Cell Carcinoma of Head and NeckStem CellsGeneral Medicinemedicine.diseaseHead and neck squamous-cell carcinomaRadiation therapy030104 developmental biologyCell cultureHead and Neck Neoplasms030220 oncology & carcinogenesisGene Knockdown TechniquesCancer researchCarcinoma Squamous CellTumor Suppressor Protein p53DNA DamageCarcinogenesis
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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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Cancer therapy and treatments during COVID-19 era

2020

The COVID-19 pandemic has put a serious strain on health treatments as well at the economies of many nations. Unfortunately, there is not currently available vaccine for SARS-Cov-2/COVID-19. Various types of patients have delayed treatment or even routine check-ups and we are adapting to a virtual world. In many cases, surgeries are delayed unless they are essential. This is also true with regards to cancer treatments and screening. Interestingly, some existing drugs and nutraceuticals have been screened for their effects on COVID-19. Certain FDA approved drugs, vitamin, natural products and trace minerals may be repurposed to treat or improve the prevention of COVID-19 infections and disea…

0301 basic medicineCancer ResearchDiseaseComorbidityAntineoplastic Agent0302 clinical medicineRepurposing approved drugNeoplasmsPandemicMedicineViralCancerNatural productsVitaminsSpike GlycoproteinHost-Pathogen InteractionDrug repositioning030220 oncology & carcinogenesisHost-Pathogen InteractionsSpike Glycoprotein CoronavirusMolecular MedicineNutraceuticalAngiotensin-Converting Enzyme 2NutraceuticalsCoronavirus InfectionsHumanHydroxychloroquineSignal Transductionmedicine.medical_specialtyCoronavirus disease 2019 (COVID-19)Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)Pneumonia ViralAntineoplastic AgentsPeptidyl-Dipeptidase AAntiviral AgentsNatural productVitaminArticle03 medical and health sciencesBetacoronavirusGeneticsHumansIntensive care medicineMolecular BiologyPandemicsTrace ElementAntiviral AgentBetacoronaviruCoronavirus Infectionbusiness.industrySARS-CoV-2CanceRepurposing approved drugsDrug RepositioningrNatural productsCancerCOVID-19Pneumoniamedicine.diseaseComorbidityReview articleTrace ElementsCoronavirus030104 developmental biologyGene Expression RegulationSettore BIO/14 - FarmacologiaNeoplasmbusinessSpike Glycoprotein Coronaviru
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Targeting prohibitins with chemical ligands inhibits KRAS-mediated lung tumours.

2017

KRAS is one of the most frequently mutated oncogenes in human non-small cell lung cancers (NSCLCs). RAS proteins trigger multiple effector signalling pathways including the highly conserved RAF-MAPK pathway. CRAF, a direct RAS effector protein, is required for KRAS-mediated tumourigenesis. Thus, the molecular mechanisms driving the activation of CRAF are intensively studied. Prohibitin 1 (PHB1) is an evolutionarily conserved adaptor protein and interaction of CRAF with PHB1 at the plasma membrane is essential for CRAF activation. Here, we demonstrate that PHB1 is highly expressed in NSCLC patients and correlates with poor survival. Targeting of PHB1 with two chemical ligands (rocaglamide an…

0301 basic medicineCancer ResearchEGF Family of ProteinsLung NeoplasmsBiologyLigandsProto-Oncogene Proteins p21(ras)03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineGrowth factor receptorRocaglamideEpidermal growth factorCarcinoma Non-Small-Cell LungCell Line TumorProhibitinsGeneticsAnimalsHumansMolecular Targeted TherapyProhibitinMolecular BiologyBenzofuransCell ProliferationRas InhibitorMice KnockoutTNF Receptor-Associated Factor 3EffectorXenograft Model Antitumor Assaysrespiratory tract diseasesCell biologyProto-Oncogene Proteins p21(ras)Gene Expression Regulation NeoplasticRepressor Proteins030104 developmental biologychemistry030220 oncology & carcinogenesisras Proteinsraf KinasesSignal transductionSignal TransductionOncogene
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Comment on “Endothelial Protein C Receptor (EPCR), Protease Activated Receptor-1 (PAR-1) and Their Interplay in Cancer Growth and Metastatic Dissemin…

2019

Although the interplay between tumor progression and blood coagulation has been recognized [...]

0301 basic medicineCancer ResearchEndothelial protein C receptorChemistryCancermedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenslcsh:RC254-28203 medical and health sciences030104 developmental biology0302 clinical medicineProtease-Activated Receptor 1n/aOncologyCoagulationTumor progression030220 oncology & carcinogenesisCancer researchmedicineCancers
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Melanoma in the liver: Oxidative stress and the mechanisms of metastatic cell survival.

2020

Abstract Metastatic melanoma is a fatal disease with a rapid systemic dissemination. The most frequent target sites are the liver, bone, and brain. Melanoma metastases represent a heterogeneous cell population, which associates with genomic instability and resistance to therapy. Interaction of melanoma cells with the hepatic sinusoidal endothelium initiates a signaling cascade involving cytokines, growth factors, bioactive lipids, and reactive oxygen and nitrogen species produced by the cancer cell, the endothelium, and also by different immune cells. Endothelial cell-derived NO and H2O2 and the action of immune cells cause the death of most melanoma cells that reach the hepatic microvascul…

0301 basic medicineCancer ResearchEndotheliumCell SurvivalPopulationCellmedicine.disease_cause03 medical and health sciences0302 clinical medicineImmune systemDownregulation and upregulationTumor MicroenvironmentMedicineAnimalsHumansEndotheliumeducationMelanomaeducation.field_of_studybusiness.industryMelanomaLiver Neoplasmsmedicine.diseaseCarcinoma NeuroendocrineOxidative Stress030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisCancer cellCancer researchbusinessOxidation-ReductionOxidative stressSeminars in cancer biology
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PHD3 Controls Lung Cancer Metastasis and Resistance to EGFR Inhibitors through TGFα.

2018

Abstract Lung cancer is the leading cause of cancer-related death worldwide, in large part due to its high propensity to metastasize and to develop therapy resistance. Adaptive responses to hypoxia and epithelial–mesenchymal transition (EMT) are linked to tumor metastasis and drug resistance, but little is known about how oxygen sensing and EMT intersect to control these hallmarks of cancer. Here, we show that the oxygen sensor PHD3 links hypoxic signaling and EMT regulation in the lung tumor microenvironment. PHD3 was repressed by signals that induce EMT and acted as a negative regulator of EMT, metastasis, and therapeutic resistance. PHD3 depletion in tumors, which can be caused by the EM…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionLung NeoplasmsMice NudeAntineoplastic AgentsSMADDrug resistanceMetastasisHypoxia-Inducible Factor-Proline DioxygenasesMitochondrial Proteins03 medical and health sciencesErlotinib HydrochlorideMice0302 clinical medicineDownregulation and upregulationCell Line TumorTumor MicroenvironmentMedicineAnimalsHumansNeoplasm MetastasisLung cancerProtein Kinase InhibitorsEGFR inhibitorsbusiness.industryIntracellular Signaling Peptides and ProteinsCancerTransforming Growth Factor alphamedicine.diseaseHCT116 CellsXenograft Model Antitumor AssaysCell HypoxiaErbB Receptors030104 developmental biologyOncologyA549 CellsDrug Resistance Neoplasm030220 oncology & carcinogenesisembryonic structuresCancer researchFemaleErlotinibbusinessApoptosis Regulatory Proteinsmedicine.drugCancer research
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Transcriptional profiling of circulating tumor cells in multiple myeloma: a new model to understand disease dissemination

2020

The reason why a few myeloma cells egress from the bone marrow (BM) into peripheral blood (PB) remains unknown. Here, we investigated molecular hallmarks of circulating tumor cells (CTCs) to identify the events leading to myeloma trafficking into the bloodstream. After using next-generation flow to isolate matched CTCs and BM tumor cells from 32 patients, we found high correlation in gene expression at single-cell and bulk levels (r ≥ 0.94, P = 10−16), with only 55 genes differentially expressed between CTCs and BM tumor cells. CTCs overexpressed genes involved in inflammation, hypoxia, or epithelial–mesenchymal transition, whereas genes related with proliferation were downregulated in CTCs…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionTranscription GeneticGene ExpressionBiologycirculating tumor cell03 medical and health sciences0302 clinical medicineCirculating tumor cellBone MarrowCell MovementCancer stem cellCell Line TumorTumor MicroenvironmentmedicineHumansHypoxiaMultiple myelomaCell ProliferationInflammationGene knockdownliquid biopsyCD44CENPFHematologyNeoplastic Cells CirculatingPrognosismedicine.disease3. Good healthmultiple myeloma030104 developmental biologymedicine.anatomical_structureOncologyCell culture030220 oncology & carcinogenesisNeoplastic Stem CellsCancer researchbiology.proteinBone marrow
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MiR-205-5p inhibition by locked nucleic acids impairs metastatic potential of breast cancer cells.

2018

AbstractMir-205 plays an important role in epithelial biogenesis and in mammary gland development but its role in cancer still remains controversial depending on the specific cellular context and target genes. We have previously reported that miR-205-5p is upregulated in breast cancer stem cells targeting ERBB pathway and leading to targeted therapy resistance. Here we show that miR-205-5p regulates tumorigenic properties of breast cancer cells, as well as epithelial to mesenchymal transition. Silencing this miRNA in breast cancer results in reduced tumor growth and metastatic spreading in mouse models. Moreover, we show that miR-205-5p knock-down can be obtained with the use of specific lo…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal Transitionmedicine.medical_treatmentAntagomirSettore MED/50 - Scienze Tecniche Mediche ApplicateImmunologyTransplantation HeterologousOligonucleotidesBreast NeoplasmsBiologyArticleTargeted therapy03 medical and health sciencesCellular and Molecular NeuroscienceMiceBreast cancerErbBCell MovementMice Inbred NODOligonucleotideCell Line TumormicroRNAmedicineGene silencingAnimalsHumansEpithelial–mesenchymal transitionlcsh:QH573-671Neoplasm MetastasisCell ProliferationAnimallcsh:CytologyCancerAntagomirsMicroRNACell Biologymedicine.diseaseNeoplasm MetastasiMicroRNAs030104 developmental biologyCancer researchFemaleStem cellBreast NeoplasmHumanCell deathdisease
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