Search results for "GENETICS"

showing 10 items of 12494 documents

Abilities of berberine and chemically modified berberines to interact with metformin and inhibit proliferation of pancreatic cancer cells.

2019

Abstract Pancreatic cancer is devastating cancer worldwide with few if any truly effective therapies. Pancreatic cancer has an increasing incidence and may become the second leading cause of death from cancer. Novel, more effective therapeutic approaches are needed as pancreatic cancer patients usually survive for less than a year after being diagnosed. Control of blood sugar levels by the prescription drug metformin in diseases such as diabetes mellitus has been examined in association with pancreatic cancer. While the clinical trials remain inconclusive, there is hope that certain diets and medications may affect positively the outcomes of patients with pancreatic and other cancers. Other…

0301 basic medicineCancer ResearchSettore MED/09 - Medicina Internaendocrine system diseasesBerberineSignal transduction inhibitorsBlood sugarPharmacologyAMP-Activated Protein KinasesBerberine; PDAC; Signal transduction inhibitors; TP5303 medical and health scienceschemistry.chemical_compound0302 clinical medicineBerberineMETFORMINAPancreatic cancerDiabetes mellitusGeneticsmedicineHumansTP53Signal transduction inhibitorMolecular BiologyCell Proliferationbusiness.industryPDACCancerAMPKmedicine.diseaseMetforminMetforminNeoplasm ProteinsPancreatic Neoplasms030104 developmental biologychemistry030220 oncology & carcinogenesisCancer cellMolecular Medicinebusinessmedicine.drugAdvances in biological regulation
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Molecular pathway activation – New type of biomarkers for tumor morphology and personalized selection of target drugs

2018

Anticancer target drugs (ATDs) specifically bind and inhibit molecular targets that play important roles in cancer development and progression, being deeply implicated in intracellular signaling pathways. To date, hundreds of different ATDs were approved for clinical use in the different countries. Compared to previous chemotherapy treatments, ATDs often demonstrate reduced side effects and increased efficiency, but also have higher costs. However, the efficiency of ATDs for the advanced stage tumors is still insufficient. Different ATDs have different mechanisms of action and are effective in different cohorts of patients. Personalized approaches are therefore needed to select the best ATD…

0301 basic medicineCancer ResearchSystems biologymutation profilingAntineoplastic AgentsComputational biologyProteomics03 medical and health sciencesNeoplasmsmicroRNABiomarkers TumorHumanscancerMedicineMolecular Targeted TherapyEpigeneticsPrecision MedicineBiomedicinebusiness.industryGene Expression ProfilingCancerbioinformaticsmedicine.diseasePrecision medicinesignaling pathwaysGene Expression Regulation NeoplasticGene expression profilingmachine learning030104 developmental biologyCommentarybusinessSignal TransductionSeminars in Cancer Biology
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Lack of a peroxiredoxin suppresses the lethality of cells devoid of electron donors by channelling electrons to oxidized ribonucleotide reductase

2017

The thioredoxin and glutaredoxin pathways are responsible of recycling several enzymes which undergo intramolecular disulfide bond formation as part of their catalytic cycles such as the peroxide scavengers peroxiredoxins or the enzyme ribonucleotide reductase (RNR). RNR, the rate-limiting enzyme of deoxyribonucleotide synthesis, is an essential enzyme relying on these electron flow cascades for recycling. RNR is tightly regulated in a cell cycle-dependent manner at different levels, but little is known about the participation of electron donors in such regulation. Here, we show that cytosolic thioredoxins Trx1 and Trx3 are the primary electron donors for RNR in fission yeast. Unexpectedly,…

0301 basic medicineCancer ResearchThioredoxin reductaseSynthesis PhaseYeast and Fungal ModelsBiochemistryElectron DonorsSchizosaccharomyces PombeThioredoxinsGlutaredoxinCell Cycle and Cell DivisionGenetics (clinical)Chemical ReactionsOxidesPeroxidesNucleic acidsChemistryRibonucleotide reductaseBiochemistryExperimental Organism SystemsCell ProcessesSchizosaccharomyces pombePhysical SciencesSynthesis phaseThioredoxinOxidation-ReductionResearch ArticleDNA Replicationlcsh:QH426-470DNA transcriptionElectron donorsBiologyDNA replicationResearch and Analysis MethodsCatalysisElectron Transport03 medical and health sciencesModel OrganismsSchizosaccharomycesRibonucleotide ReductasesOxidationGeneticsMolecular BiologyEcology Evolution Behavior and SystematicsGlutaredoxinsCell growthDNA replicationChemical CompoundsOrganismsFungiBiology and Life SciencesCell BiologyDNAPeroxiredoxinsbiology.organism_classificationYeastCell cycle and cell divisionCheckpoint Kinase 2lcsh:Genetics030104 developmental biologySchizosaccharomyces pombeGene expressionSchizosaccharomyces pombe ProteinsPeroxiredoxin
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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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Inhibition of colon cancer growth by docosahexaenoic acid involves autocrine production of TNFα

2016

IF 7.932; International audience; The omega-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) has anti-inflammatory and anti-cancer properties. Among pro-inflammatory mediators, tumor necrosis factor a (TNF alpha) plays a paradoxical role in cancer biology with induction of cancer cell death or survival depending on the cellular context. The objective of the study was to evaluate the role of TNFa in DHA-mediated tumor growth inhibition and colon cancer cell death. The treatment of human colorectal cancer cells, HCT-116 and HCT-8 cells, with DHA triggered apoptosis in autocrine TNF alpha-dependent manner. We demonstrated that DHA-induced increased content of TNF alpha mRNA occurred thr…

0301 basic medicineCancer ResearchTumoricidal ActionApoptosis[ SDV.CAN ] Life Sciences [q-bio]/CancerMice[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsForkhead Box Protein O3Cell cycle3. Good healthCell biologyGene Expression Regulation NeoplasticAutocrine CommunicationColonic NeoplasmsTumor-Necrosis-FactorTumor necrosis factor alphaProgrammed cell deathDocosahexaenoic AcidsHuman Colorectal-CancerGene-Expression[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiology03 medical and health sciencesGrowth factor receptorLipid-MetabolismGeneticsmedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyCell-DeathPolyunsaturated Fatty-AcidsAutocrine signallingMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyActivated Protein-KinaseTumor Necrosis Factor-alpha[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyInduced ApoptosisCancerHCT116 Cellsmedicine.diseaseXenograft Model Antitumor AssaysMicroRNAs030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsApoptosisCancer cellCancer researchPrevents Breast-Cancer
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Relevance of the natural HDAC inhibitor sulforaphane as a chemopreventive agent in urologic tumors.

2018

Due to an increased understanding of molecular biology and the genomics of cancer, new and potent agents have been approved by the Food and Drug Administration (FDA) to fight this disease. However, all of these drugs cause severe side effects and resistance inevitably develops, re-activating tumor growth and dissemination. For this reason, patients turn to natural compounds as alternative or complementary treatment options, since it has been found that natural plant products may block, inhibit, or reverse cancer development. The present review focusses on the role of the natural compound sulforaphane (SFN) as an anti-tumor agent in urologic cancer. SFN is a natural compound found in crucife…

0301 basic medicineCancer ResearchUrologic NeoplasmsApoptosisDisease03 medical and health scienceschemistry.chemical_compound0302 clinical medicineIn vivoIsothiocyanatesCell Line TumorHDAC inhibitorMedicineAnticarcinogenic AgentsHumansEpigeneticsMode of actionBiological ProductsMolecular Structurebusiness.industryCruciferous vegetablesCancermedicine.diseaseHistone Deacetylase Inhibitors030104 developmental biologyOncologychemistry030220 oncology & carcinogenesisSulfoxidesBrassicaceaeCancer researchbusinessSulforaphaneCancer letters
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Roles of TP53 in determining therapeutic sensitivity, growth, cellular senescence, invasion and metastasis.

2016

TP53 is a critical tumor suppressor gene that regulates cell cycle progression, apoptosis, cellular senescence and many other properties critical for control of normal cellular growth and death. Due to the pleiotropic effects that TP53 has on gene expression and cellular physiology, mutations at this tumor suppressor gene result in diverse physiological effects. T53 mutations are frequently detected in numerous cancers. The expression of TP53 can be induced by various agents used to treat cancer patients such as chemotherapeutic drugs and ionizing radiation. Radiation will induce Ataxia telangiectasia mutated (ATM) and other kinases that results in the phosphorylation and activation of TP53…

0301 basic medicineCancer Researchendocrine system diseasesMetastasimedicine.disease_causeMetastasisAntineoplastic AgentInvasionNeoplasmsTP53Neoplasm Metastasisbcl-2-Associated X ProteinAza CompoundProto-Oncogene ProteinApoptosis Regulatory ProteinbiologyCell CyclemiRMicroRNACell cycleCell biologyNeoplasm MetastasiGene Expression Regulation NeoplasticNutlin-3 chemosensitivityMdm2Molecular MedicineHumanSignal TransductionCyclin-Dependent Kinase Inhibitor p21Tumor suppressor genemiRsAntineoplastic AgentsCellular senescenceTP53; miRs; MDM2; Nutlin-3 chemosensitivity; Cellular senescence ; Invasion; Metastasis03 medical and health sciencesBcl-2-associated X proteinGeneticMDM2Proto-Oncogene ProteinsmicroRNAGeneticsmedicineHumansNeoplasm InvasivenessneoplasmsMolecular BiologyCell ProliferationNeoplasm InvasiveneAza CompoundsOncomirBridged Bicyclo Compounds HeterocyclicMicroRNAs030104 developmental biologyTumor progressionbiology.proteinNeoplasmTumor Suppressor Protein p53CarcinogenesisApoptosis Regulatory Proteins
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Abilities of β-Estradiol to interact with chemotherapeutic drugs, signal transduction inhibitors and nutraceuticals and alter the proliferation of pa…

2019

Improving the effects of chemotherapy and reducing the side effects are important goals in cancer research. Various approaches have been examined to enhance the effectiveness of chemotherapy. For example, signal transduction inhibitors or hormonal based approaches have been included with chemo- or radio-therapy. MIA-PaCa-2 and BxPC-3 pancreatic ductal adenocarcinoma (PDAC) cells both express the estrogen receptor (ER). The effects of β-estradiol on the growth of PDAC cells has not been examined yet the ER is expressed in PDAC cells. We have examined the effects of combining β-estradiol with chemotherapeutic drugs, signal transcription inhibitors, natural products and nutraceuticals on PDAC.…

0301 basic medicineCancer Researchendocrine system diseasesβ estradiolmedicine.medical_treatmentβ-EstradiolEstrogen receptorAntineoplastic AgentsNatural product03 medical and health sciencesFood-Drug Interactions0302 clinical medicineNutraceuticalPancreatic cancerCell Line TumorGeneticsmedicineHumansMolecular BiologyChemotherapeutic drugCell ProliferationChemotherapyNatural products?-EstradiolEstradiolbusiness.industryQUIMIOTERÁPICOSChemotherapeutic drugs; Natural products; Nutraceuticals; Pancreatic cancer; β-EstradiolPancreatic cancerMiddle Agedmedicine.diseasedigestive system diseasesPancreatic Neoplasms030104 developmental biology030220 oncology & carcinogenesisDietary SupplementsCancer researchSettore BIO/14 - FarmacologiaMolecular MedicineChemotherapeutic drugsFemaleChemotherapeutic drugsNutraceuticalsNutraceuticalSignal transductionbusinessHormoneCarcinoma Pancreatic DuctalSignal TransductionAdvances in biological regulation
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A common SNP in the UNG gene decreases ovarian cancer risk in BRCA2 mutation carriers

2018

Single nucleotide polymorphisms (SNPs) in DNA glycosylase genes involved in the base excision repair (BER) pathway can modify breast and ovarian cancer risk in BRCA1 and BRCA2 mutation carriers. We previously found that SNP rs34259 in the uracil-DNA glycosylase gene (UNG) might decrease ovarian cancer risk in BRCA2 mutation carriers. In the present study, we validated this finding in a larger series of familial breast and ovarian cancer patients to gain insights into how this UNG variant exerts its protective effect. We found that rs34259 is associated with significant UNG downregulation and with lower levels of DNA damage at telomeres. In addition, we found that this SNP is associated with…

0301 basic medicineCancer Researchmedicine.medical_specialtyendocrine system diseasesUracil-DNA glycosylaseEuropean Regional Development Fundlcsh:RC254-282Polymorphism Single Nucleotide03 medical and health sciences0302 clinical medicineBRCA2 MutationRisk FactorsPolitical scienceHealthy volunteersGeneticsmedicineHumansSNPGenetic Predisposition to DiseaseUracil-DNA Glycosidaseskin and connective tissue diseasesResearch ArticlesBRCA2 ProteinOvarian NeoplasmsNetwork onOxidative stress susceptibilityGeneral MedicineMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseBRCA2female genital diseases and pregnancy complicationsuracil‐DNA glycosylase030104 developmental biologyCancer risk modifierOncology030220 oncology & carcinogenesisFamily medicineMutationMolecular MedicineDNA damageFemaleChristian ministryTelomere damageOvarian cancerHuman cancerResearch Article
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Interrelationship between miRNA and splicing factors in pancreatic ductal adenocarcinoma

2021

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers because of diagnosis at late stage and inherent/acquired chemoresistance. Recent advances in genomic profiling and biology of this disease have not yet been translated to a relevant improvement in terms of disease management and patient’s survival. However, new possibilities for treatment may emerge from studies on key epigenetic factors. Deregulation of microRNA (miRNA) dependent gene expression and mRNA splicing are epigenetic processes that modulate the protein repertoire at the transcriptional level. These processes affect all aspects of PDAC pathogenesis and have great potential to unravel new therapeutic targets…

0301 basic medicineCancer Researchsplicing deregulationinteractionDiseaseBiologymedicine.disease_causeinteraction; miRNA; PDAC; splicing deregulation; splicing modulation03 medical and health sciencesSplicing factor0302 clinical medicineDownregulation and upregulationCell Line TumormicroRNAGene expressionmedicineHumansEpigeneticsMolecular BiologymiRNAPDACDNA MethylationGene Expression Regulation NeoplasticPancreatic NeoplasmsRepressor ProteinsMicroRNAs030104 developmental biology030220 oncology & carcinogenesisRNA splicingCancer researchKRASRNA Splicing Factorssplicing modulationCarcinoma Pancreatic Ductal
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