Search results for "C25"

showing 10 items of 566 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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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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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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Hypoxia-Inducible Factor-1α Activity as a Switch for Glioblastoma Responsiveness to Temozolomide

2018

Rationale: The activity of the transcription factor, hypoxia-inducible factor (HIF)-1?, is a common driver of a number of the pathways involved in the aggressiveness of glioblastomas (GBMs), and it has been suggested that the reduction in this activity observed, soon after the administration of temozolomide (TMZ), can be a biomarker of an early response in GBM models. As HIF-1? is a tightly regulated protein, studying the processes involved in its downregulation could shed new light on the mechanisms underlying GBM sensitivity or resistance to TMZ. Methods: The effect of HIF-1? silencing on cell responsiveness to TMZ was assessed in four genetically different human GBM cell lines by evaluat…

0301 basic medicineCancer Researchapoptosis; chaperone-mediated autophagy activity; hypoxia-inducible factor-1? silencing; temozolomide responsiveness; theranostic biomarkerBiologylcsh:RC254-28203 medical and health scienceshypoxia-inducible factor-1α silencing0302 clinical medicineGliomamedicineGene silencingViability assayTranscription factorOriginal Researchchaperone-mediated autophagy activityTemozolomideAutophagyapoptosismedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenstheranostic biomarker030104 developmental biologyHypoxia-inducible factorsOncologyApoptosis030220 oncology & carcinogenesisCancer researchtemozolomide responsivenessmedicine.drugFrontiers in Oncology
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Targeting Immune Modulators in Glioma While Avoiding Autoimmune Conditions

2021

Simple Summary Glioblastoma multiforme is a futile disease usually leading to the patient’s death within one year post-diagnosis; therefore, novel treatment options are desperately needed. In this regard, activation of the inert immune system has moved into focus in recent years. Malignant brain tumors, as well as autoimmune diseases, elicit aberrant immune responses. In this way, glioma escapes the host’s immune system and, thus, activation of the immune response in order to reduce tumor tolerance can serve as an alternative treatment option. Immune checkpoint modulators in combination with traditional therapies have gained attention in both glioma and autoimmune diseases. In this review, …

0301 basic medicineCancer Researchautoimmune disease ; immune checkpoints ; immunotherapy ; clinical trials ; Gliom ; gliomamedicine.medical_treatmentautoimmune diseaseContext (language use)Review03 medical and health sciences0302 clinical medicineImmune systemgliomaGliomamedicineRC254-282Autoimmune diseaseclinical trialsTumor microenvironmentbusiness.industryMultiple sclerosisNeoplasms. Tumors. Oncology. Including cancer and carcinogensImmunosuppressionImmunotherapybiochemical phenomena metabolism and nutritionimmune checkpointsmedicine.disease030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchimmunotherapybusinessCancers
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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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