Search results for "medicine.disease_cause"

showing 10 items of 6035 documents

Prevention of carcinogenesis and metastasis by Artemisinin-type drugs.

2018

Artemisia annua (sweet wormwood, qinhao) is an ancient Chinese herbal remedy for pyrexia. Nowadays, artemisinin (qinghaosu) and its derivatives belong to the standard therapies against malaria worldwide, and its discovery has led to the Nobel Prize in Physiology and Medicine to Youyou Tu in 2015. While most attention has been paid to the treatment of malaria, there is increasing evidence that Artemisinin-type drugs bear a considerable potential to treat and prevent cancer. Rather than reporting on therapy of cancer, this review gives a comprehensive and timely overview on the chemopreventive effects of artemisinin and its derivatives against carcinogenesis and metastasis formation, followin…

0301 basic medicineCancer ResearchCarcinogenesisArtemisia annuaCancer metastasisArtemisia annuaBioinformaticsmedicine.disease_causeMetastasis03 medical and health sciencesAntimalarials0302 clinical medicineNeoplasmsparasitic diseasesmedicineHumansArtemisininNeoplasm MetastasisToxicity profileClinical Trials as TopicbiologyMolecular Structurebusiness.industryCancermedicine.diseasebiology.organism_classificationArtemisinins030104 developmental biologyOncology030220 oncology & carcinogenesisCarcinogenesisbusinessMalariamedicine.drugPhytotherapyCancer letters
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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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Gut vascular barrier impairment leads to intestinal bacteria dissemination and colorectal cancer metastasis to liver

2021

Metastasis is facilitated by the formation of a "premetastatic niche," which is fostered by primary tumor-derived factors. Colorectal cancer (CRC) metastasizes mainly to the liver. We show that the premetastatic niche in the liver is induced by bacteria dissemination from primary CRC. We report that tumor-resident bacteria Escherichia coli disrupt the gut vascular barrier (GVB), an anatomical structure controlling bacterial dissemination along the gut-liver axis, depending on the virulence regulator VirF. Upon GVB impairment, bacteria disseminate to the liver, boost the formation of a premetastatic niche, and favor the recruitment of metastatic cells. In training and validation cohorts of C…

0301 basic medicineCancer ResearchColorectal cancerRegulatorVirulencemedicine.disease_causeMetastasis03 medical and health sciences0302 clinical medicinemedicineHumansNeoplasm MetastasisEscherichia coliBacteriabiologybusiness.industryLiver NeoplasmsDistant recurrencebiology.organism_classificationmedicine.disease030104 developmental biologyLiverOncology030220 oncology & carcinogenesisColonic NeoplasmsCancer researchIntestinal bacteriaNeoplasm Recurrence LocalColorectal NeoplasmsbusinessBacteriaCancer Cell
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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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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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Comprehensive translational control of tyrosine kinase expression by upstream open reading frames

2016

Post-transcriptional control has emerged as a major regulatory event in gene expression and often occurs at the level of translation initiation. Although overexpression or constitutive activation of tyrosine kinases (TKs) through gene amplification, translocation or mutation are well-characterized oncogenic events, current knowledge about translational mechanisms of TK activation is scarce. Here, we report the presence of translational cis-regulatory upstream open reading frames (uORFs) in the majority of transcript leader sequences of human TK mRNAs. Genetic ablation of uORF initiation codons in TK transcripts resulted in enhanced translation of the associated downstream main protein-codin…

0301 basic medicineCancer ResearchFive prime untranslated regionKozak consensus sequenceShort CommunicationBiologymedicine.disease_causeProto-Oncogene MasGene Expression Regulation Enzymologic03 medical and health sciencesOpen Reading FramesEukaryotic translationUpstream open reading frameGeneticsmedicineHumansGene Regulatory NetworksMolecular BiologyGeneticsMutationGene Expression ProfilingTranslation (biology)Protein-Tyrosine KinasesOpen reading frame030104 developmental biologyHEK293 CellsProtein BiosynthesisHuman genomeHeLa Cells
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Growth differentiation factor 15 as a radiation-induced marker in oral carcinoma increasing radiation resistance.

2015

Background Growth differentiation factor 15 (GDF15) is involved in tumor pathogenesis of oral squamous cell carcinoma (OSCC). The aim of this study was an investigation of the potential influence of GDF15 on radioresistance of OSCC cells in vitro. Methods Oral squamous cell carcinoma cell lines were irradiated with 0, 2, or 6 Gy, and GDF15 expression in the supernatant per survived cell colony was examined with ELISA. Non-irradiated and OSCC cell lines irradiated with 6 Gy were evaluated for GDF15 expression using immunofluorescent staining. For further investigation of GDF15 effects on radioresistance, a GDF15 knockdown model in a human OSCC cell line was established, and apoptotic activit…

0301 basic medicineCancer ResearchGrowth Differentiation Factor 15CellApoptosisEnzyme-Linked Immunosorbent AssayBiologymedicine.disease_causeReal-Time Polymerase Chain ReactionTransfectionPathology and Forensic Medicine03 medical and health sciences0302 clinical medicineRadioresistanceCell Line TumormedicineCarcinomaBiomarkers TumorHumansRNA Small InterferingMouth neoplasmSquamous Cell Carcinoma of Head and Neckmedicine.diseaseMolecular biologyNeoplasm Proteinsstomatognathic diseases030104 developmental biologymedicine.anatomical_structureOtorhinolaryngologyApoptosisCell cultureTumor progressionHead and Neck Neoplasms030220 oncology & carcinogenesisCaspasesGene Knockdown TechniquesCarcinoma Squamous CellPeriodonticsMouth NeoplasmsOral SurgeryCarcinogenesisJournal of oral pathologymedicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
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Targeting the chromosomal passenger complex subunit INCENP induces polyploidization, apoptosis and senescence in neuroblastoma

2019

Abstract Chromosomal passenger complex (CPC) has been demonstrated to be a potential target of cancer therapy by inhibiting Aurora B or survivin in different types of cancer including neuroblastoma. However, chemical inhibition of either Aurora B or survivin does not target CPC specifically due to off-target effects or CPC-independent activities of these two components. In a previous chromatin-focused siRNA screen, we found that neuroblastoma cells were particularly vulnerable to loss of INCENP, a gene encoding a key scaffolding component of the CPC. In this study, INCENP was highly expressed by neuroblastoma cells, and its expression decreased following retinoic acid–induced neuroblastoma …

0301 basic medicineCancer ResearchINCENP/CPC/Polyploidy/DNA damage/Apoptosis/SenescenceCarcinogenesisChromosomal Proteins Non-HistoneAurora B kinaseApoptosisBiologymedicine.disease_causeArticlePolyploidy03 medical and health sciencesMiceNeuroblastoma0302 clinical medicineNeuroblastomaSurvivinmedicineGene silencingAnimalsHumansneoplasmsCellular SenescenceINCENPmedicine.disease030104 developmental biologyOncologyApoptosisTumor progression030220 oncology & carcinogenesisCancer researchHeterograftsCarcinogenesis
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In silico RNA-seq and experimental analyses reveal the differential expression and splicing of EPDR1 and ZNF518B genes in relation to KRAS mutations …

2016

Several drugs used for the treatment of colorectal cancer (CRC) are targeted at the epidermal growth factor receptor, but mutations in genes of the RAS family cause resistance to these drugs. Thus, extensive research is being carried out to counterbalance this resistance. The G13D mutation of KRAS is common in humans, and we previously reported that this mutation results in the epigenetic modification of hnRNP proteins, involved in RNA splicing. As aberrant splicing often results in oncogenicity, the present study aimed to identify the genes which show altered splicing patterns in connection with the G13D KRAS mutation. To accomplish this, we first carried out an in silico analysis of RNA-s…

0301 basic medicineCancer ResearchIn silicoMutation MissenseGene ExpressionNerve Tissue ProteinsBiologymedicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health sciences0302 clinical medicinemedicineHumansProtein IsoformsComputer SimulationEpigeneticsGeneGeneticsMutationBase SequenceModels GeneticSequence Analysis RNAAlternative splicingGeneral Medicinedigestive system diseasesNeoplasm ProteinsDNA-Binding ProteinsAlternative Splicing030104 developmental biologyOncology030220 oncology & carcinogenesisRNA splicingCancer researchKRASCarcinogenesisColorectal NeoplasmsOncology reports
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Doxorubicin anti-tumor mechanisms include Hsp60 post-translational modifications leading to the Hsp60/p53 complex dissociation and instauration of re…

2017

Hsp60 is a pro-carcinogenic chaperonin in certain tumor types by interfering with apoptosis and with tumor cell death. In these tumors, it is not known whether or not doxorubicin anti-tumor effects include a blockage of the pro-carcinogenic action of this protein. We used the human lung mucoepidermoid cell line NCI-H292 and different doses of doxorubicin to measure cell viability, cell cycle progression, cell senescence indicators, Hsp60 levels and its post-translational modifications as well as the release of the chaperonin into the extracellular environment. Cell viability was reduced in relation to doxorubicin dose and this was paralleled by the appearance of cell senescence markers. Con…

0301 basic medicineCancer ResearchLung NeoplasmsChaperoninsCellApoptosismedicine.disease_causeHistones0302 clinical medicineCellular SenescenceAntibiotics AntineoplasticAcetylationG2 Phase Cell Cycle Checkpointsmedicine.anatomical_structureOncology030220 oncology & carcinogenesisCell agingIntracellularProtein BindingSignal TransductionSenescenceCyclin-Dependent Kinase Inhibitor p21animal structuresCell Survivalchemical and pharmacologic phenomenaBiologycomplex mixturesMitochondrial ProteinsDoxorubicin Hsp60 Acetylation Ubiquitination p53 Replicative senescence03 medical and health sciencesDoxorubicin; Hsp60; p53; replicative senescence; post-translational modificationsCell Line TumormedicineHumansCell Proliferationdoxorubicin p53 Hsp60Dose-Response Relationship DrugCell growthfungiUbiquitinationChaperonin 60Molecular biology030104 developmental biologyAcetylationApoptosisDoxorubicinProteolysisCancer researchCarcinoma MucoepidermoidTumor Suppressor Protein p53CarcinogenesisProtein Processing Post-Translational
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