Search results for " canc"

showing 10 items of 6172 documents

HGF/MET Axis Induces Tumor Secretion of Tenascin-C and Promotes Stromal Rewiring in Pancreatic Cancer

2021

Simple Summary It has been previously shown that activation of the MET receptor by its ligand, the hepatocyte growth factor (HGF), modulates the tumor-stroma cross-talk in models of pancreatic cancer. We now wish to cast light on the molecular mechanisms by which this ligand/receptor pair sustains the interaction between cancer cells and the tumor microenviroment. To this end, we compared data obtained by large-scale analysis of gene expression in pancreatic cancer cells grown in the presence of HGF versus cells grown in the presence of HGF and treated with specific inhibitors of HGF/MET signaling. By clustering differentially expressed genes according to functional groups, we identified ca…

0301 basic medicineCancer ResearchStromal cellpancreatic ductal adenocarcinomaArticle03 medical and health sciences0302 clinical medicinePancreatic tumorPancreatic cancerMET oncogenemedicinetumor microenvironmentmetastasisHepatocyte growth factor; MET oncogene; Metastasis; Pancreatic ductal adenocarcinoma; Tenascin C; Tumor microenvironmentRC254-282Tumor microenvironmentbiologyChemistryTenascin Ctenascin CNeoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease030104 developmental biologyhepatocyte growth factorOncology030220 oncology & carcinogenesisCancer cellHepatic stellate cellbiology.proteinCancer researchHepatocyte growth factormedicine.drugCancers
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Integrative Metabolomic and Transcriptomic Analysis for the Study of Bladder Cancer

2019

Metabolism reprogramming is considered a hallmark of cancer. The study of bladder cancer (BC) metabolism could be the key to developing new strategies for diagnosis and therapy. This work aimed to identify tissue and urinary metabolic signatures as biomarkers of BC and get further insight into BC tumor biology through the study of gene-metabolite networks and the integration of metabolomics and transcriptomics data. BC and control tissue samples (n = 44) from the same patients were analyzed by High-Resolution Magic Angle Spinning Nuclear Magnetic Resonance and microarrays techniques. Besides, urinary profiling study (n = 35) was performed in the same patients to identify a metabolomic profi…

0301 basic medicineCancer ResearchTaurinecancer biomarkersBiologycancer metabolic reprogramminglcsh:RC254-282ArticleTranscriptome03 medical and health scienceschemistry.chemical_compoundtranscriptomics0302 clinical medicineMetabolomicsmedicinemetabolic pathwaysTumor metabolomeBladder cancermedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmetabolomicsMetabolic pathway030104 developmental biologyOncologyBiochemistrychemistry030220 oncology & carcinogenesisbladder cancerCancer biomarkersDNA microarraytumor metabolome
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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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Targeting COPZ1 non-oncogene addiction counteracts the viability of thyroid tumor cells

2017

Abstract Thyroid carcinoma is generally associated with good prognosis, but no effective treatments are currently available for aggressive forms not cured by standard therapy. To find novel therapeutic targets for this tumor type, we had previously performed a siRNA-based functional screening to identify genes essential for sustaining the oncogenic phenotype of thyroid tumor cells, but not required to the same extent for the viability of normal cells (non-oncogene addiction paradigm). Among those, we found the coatomer protein complex ζ1 (COPZ1) gene, which is involved in intracellular traffic, autophagy and lipid homeostasis. In this paper, we investigated the mechanisms through which COPZ…

0301 basic medicineCancer ResearchTime FactorsCOPZ1ApoptosisCOPZ1Thyroid cancerThyroid NeoplasmThyroidRNAi TherapeuticCell death; COPZ1; Non-oncogene addiction; Thyroid carcinoma; Animals; Apoptosis; Autophagy; Cell Line Tumor; Cell Survival; Coatomer Protein; Endoplasmic Reticulum Stress; Female; Gene Expression Regulation Neoplastic; Humans; Mice Nude; RNA Interference; Signal Transduction; Thyroid Neoplasms; Time Factors; Transfection; Tumor Burden; Unfolded Protein Response; Xenograft Model Antitumor Assays; RNAi Therapeutics; Oncology; Cancer ResearchEndoplasmic Reticulum StressOncogene AddictionTumor BurdenGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyFemaleRNA InterferenceNon-oncogene addictionHumanSignal TransductionCell deathProgrammed cell deathXenograft Model Antitumor AssayTime FactorCell SurvivalMice NudeBiologyTransfectionCoatomer ProteinThyroid carcinomaThyroid carcinoma03 medical and health sciencesCell Line TumorAutophagymedicineAnimalsHumansThyroid NeoplasmsEndoplasmic Reticulum StreAnimalAutophagyApoptosimedicine.diseaseXenograft Model Antitumor AssaysRNAi Therapeutics030104 developmental biologyImmunologyUnfolded Protein ResponseCancer researchUnfolded protein response
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Artesunate Inhibits Growth of Sunitinib-Resistant Renal Cell Carcinoma Cells through Cell Cycle Arrest and Induction of Ferroptosis

2020

Although innovative therapeutic concepts have led to better treatment of advanced renal cell carcinoma (RCC), efficacy is still limited due to the tumor developing resistance to applied drugs. Artesunate (ART) has demonstrated anti-tumor effects in different tumor entities. This study was designed to investigate the impact of ART (1&ndash

0301 basic medicineCancer ResearchTraditional Chinese Medicine (TCM) growth inhibition ferroptosis reactive oxygen species (ROS)Cell cycle checkpointBiologyurologic and male genital diseasesreactive oxygen species (ROS)lcsh:RC254-282Articlegrowth inhibition03 medical and health scienceschemistry.chemical_compound0302 clinical medicinerenal cell carcinoma (RCC)medicineClonogenic assayCytotoxicityartesunate (ART)SunitinibTraditional Chinese Medicine (TCM)Cell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensferroptosissunitib resistance030104 developmental biologyOncologychemistryCell cultureApoptosis030220 oncology & carcinogenesisCancer researchGrowth inhibitionmedicine.drugCancers
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The organoid era permits the development of new applications to study glioblastoma

2020

Simple Summary Glioblastoma is the most lethal primary adult brain tumor. The great number of mutations involved and the aggressiveness of glioblastoma render this type of cancer especially difficult to investigate. To address this problem, cerebral organoids have emerged as promising tools to investigate brain biology and to recapitulates the major steps involved in glioblastoma tumorigenesis. This review focuses on methods of cerebral organoid development, describes the protocols used for inducing glioblastoma, the approach used to derive glioblastoma organoids directly from patients’ biopsies and discusses their limitations and potential future direction. Abstract Glioblastoma (GB) is th…

0301 basic medicineCancer ResearchTranslational researchContext (language use)ReviewStem cellsBiologylcsh:RC254-28203 medical and health sciences0302 clinical medicineGenome editingGliomaOrganoidmedicinePreclinical cancer modelsPrecision medicineCancerTranslational researchlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasePrecision medicineBiobankOrganoids030104 developmental biologyTumoroidsOncologyGlioblastomaNeuroscience030217 neurology & neurosurgeryCancers
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NOTCH3 expression is linked to breast cancer seeding and distant metastasis

2018

Background Development of distant metastases involves a complex multistep biological process termed the invasion-metastasis cascade, which includes dissemination of cancer cells from the primary tumor to secondary organs. NOTCH developmental signaling plays a critical role in promoting epithelial-to-mesenchymal transition, tumor stemness, and metastasis. Although all four NOTCH receptors show oncogenic properties, the unique role of each of these receptors in the sequential stepwise events that typify the invasion-metastasis cascade remains elusive. Methods We have established metastatic xenografts expressing high endogenous levels of NOTCH3 using estrogen receptor alpha-positive (ERα+) MCF…

0301 basic medicineCancer ResearchTransplantation HeterologousNotch signaling pathwayEstrogen receptorMice NudeBreast NeoplasmsTriple Negative Breast NeoplasmsTumor stemneCentrosome amplificationTumor stemnessMetastasilcsh:RC254-282MetastasisMetastasis03 medical and health sciences0302 clinical medicineBreast cancerNeoplasm SeedingBreast cancerSurgical oncologyCell Line TumormedicineAnimalsHumansCell Self RenewalReceptor Notch3business.industryGene Expression ProfilingMiddle Agedmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrimary tumorSurvival Analysis3. Good healthChromosomal instabilityGene Expression Regulation NeoplasticSettore BIO/18 - Genetica030104 developmental biologyOncology030220 oncology & carcinogenesisCancer cellCancer researchMCF-7 CellsFemaleRNA InterferencebusinessBrain metastasisResearch ArticleBreast Cancer Research
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Potential Molecular Players of the Tumor Microenvironment in Extracranial Pediatric Solid Tumors

2020

Pediatric cancers are rare malignancies worldwide and represent around 1% of all new cancer diagnoses [...]

0301 basic medicineCancer ResearchTumor microenvironmentbusiness.industryCancermedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenslcsh:RC254-28203 medical and health sciences030104 developmental biology0302 clinical medicineEditorialn/aOncology030220 oncology & carcinogenesisCancer researchMedicinebusinessCancers
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Aberrant splicing of the tumor suppressor CYLD promotes the development of chronic lymphocytic leukemia via sustained NF-κB signaling

2017

The pathogenesis of chronic lymphocytic leukemia (CLL) has been linked to constitutive NF-κB activation but the underlying mechanisms are poorly understood. Here we show that alternative splicing of the negative regulator of NF-κB and tumor suppressor gene CYLD regulates the pool of CD5+ B cells through sustained canonical NF-κB signaling. Reinforced canonical NF-κB activity leads to the development of B1 cell-associated tumor formation in aging mice by promoting survival and proliferation of CD5+ B cells, highly reminiscent of human B-CLL. We show that a substantial number of CLL patient samples express sCYLD, strongly implicating a role for it in human B-CLL. We propose that our new CLL-l…

0301 basic medicineCancer ResearchTumor suppressor geneCell SurvivalRNA SplicingChronic lymphocytic leukemia2720 Hematology610 Medicine & healthBiologyCD5 Antigenslaw.inventionPathogenesisMice03 medical and health sciencesimmune system diseaseslawhemic and lymphatic diseasesmedicineAnimalsHumans10239 Institute of Laboratory Animal Science1306 Cancer ResearchGenes Tumor SuppressorGeneCell ProliferationB-LymphocytesAlternative splicingNF-kappa BUbiquitinationHematologymedicine.diseaseLeukemia Lymphocytic Chronic B-CellDeubiquitinating Enzyme CYLDLeukemia030104 developmental biologyOncologyImmunologyCancer research570 Life sciences; biologySuppressor2730 OncologyCD5Signal TransductionLeukemia
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Editorial: Cell Stress, Metabolic Reprogramming, and Cancer

2018

0301 basic medicineCancer Researchantioxidant responseAntioxidant response; Ataxia-telangiectasia mutated; Cancer; Epithelial-to-mesenchymal transition; Glutamine; Hypoxia-inducible factor 1 alpha; L-lactate; Mitochondria; Oncology; Cancer ResearchMetabolic reprogrammingMitochondrionBiologylcsh:RC254-28203 medical and health sciencesHypoxia-Inducible Factor 1-AlphamedicinecancerGlycolysisEpithelial–mesenchymal transitionataxia-telangiectasia mutatedCancerL-lactatemedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensGlutaminemitochondriaCell stress030104 developmental biologyEditorialOncologyCancer researchglutaminehypoxia-inducible factor 1 alphaepithelial-to-mesenchymal transition
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