Search results for "Pith"

showing 10 items of 1308 documents

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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Myeloid Cell-Derived Reactive Oxygen Species Induce Epithelial Mutagenesis

2017

Increased oxidative stress has been suggested to initiate and promote tumorigenesis by inducing DNA damage and to suppress tumor development by triggering apoptosis and senescence. The contribution of individual cell types in the tumor microenvironment to these contrasting effects remains poorly understood. We provide evidence that during intestinal tumorigenesis, myeloid cell-derived H2O2 triggers genome-wide DNA mutations in intestinal epithelial cells to stimulate invasive growth. Moreover, increased reactive oxygen species (ROS) production in myeloid cells initiates tumor growth in various organs also in the absence of a carcinogen challenge in a paracrine manner. Our data identify an i…

0301 basic medicineCancer ResearchMyeloidDNA damageApoptosismedicine.disease_causeMice03 medical and health sciencesParacrine signallingmedicineAnimalsMyeloid Cellschemistry.chemical_classificationReactive oxygen speciesTumor microenvironmentChemistryEpithelial CellsHydrogen PeroxideCell BiologyMice Mutant StrainsCell biologyOxidative Stress030104 developmental biologymedicine.anatomical_structureOncologyMutagenesisMutationTumor necrosis factor alphaReactive Oxygen SpeciesCarcinogenesisOxidative stressDNA DamageSignal TransductionCancer Cell
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Cytokeratins in the Histological Diagnosis of Malignant Tumors

1994

Cytokeratins, which comprise a multigene family of 20 related polypeptides (CKs 1–20), are constituents of the intermediate filaments of epithelial cells, in which they are expressed in various combinations depending on the epithelial type and the degree of differentiation. Of these, CK 19 (400 amino acids; 44.1 kilodaltons) is an example of a widely distributed CK, being expressed in various epithelia, including many simple epithelia. In contrast, the recently identified CK 20 (424 amino acids; 48.6 kilodaltons) is essentially confined to gastrointestinal epithelia, the urothelium and Merkel cells. The differential expression of individual CKs in various types of carcinomas makes them use…

0301 basic medicineCancer ResearchPathologymedicine.medical_specialtyCellular differentiationClinical BiochemistryIntermediate FilamentsGene ExpressionBiologyEpitheliumPathology and Forensic Medicine03 medical and health sciencesCytokeratin0302 clinical medicineNeoplasmsKeratinBiomarkers TumorCarcinomamedicineHumansUrotheliumIntermediate filamentchemistry.chemical_classificationAntibodies MonoclonalCell DifferentiationEpithelial Cellsmedicine.disease030104 developmental biologymedicine.anatomical_structureOncologychemistryTumor progression030220 oncology & carcinogenesisKeratinsMerkel cellThe International Journal of Biological Markers
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Thymic Hyperplasia with Lymphoepithelial Sialadenitis (LESA)-Like Features: Strong Association with Lymphomas and Non-Myasthenic Autoimmune Diseases.

2021

Thymic hyperplasia (TH) with lymphoepithelial sialadenitis (LESA)-like features (LESA-like TH) has been described as a tumor-like, benign proliferation of thymic epithelial cells and lymphoid follicles. We aimed to determine the frequency of lymphoma and autoimmunity in LESA-like TH and performed retrospective analysis of cases with LESA-like TH and/or thymic MALT-lymphoma. Among 36 patients (21 males) with LESA-like TH (age 52 years, 32&ndash

0301 basic medicineCancer ResearchPathologymedicine.medical_specialtyPure red cell aplasia610 Medicine & healthautoimmune diseaselymphomathymitismedicine.disease_causelcsh:RC254-282SclerodermaArticleAutoimmunitysurgery03 medical and health sciences0302 clinical medicinethymusimmune system diseaseshemic and lymphatic diseasesmedicineddc:610Autoimmune diseasebusiness.industryLESAimagingHyperplasialcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseLESA; autoimmune disease; imaging; lymphoma; myasthenia; pathology; surgery; thymic epithelial tumor; thymitis; thymusSialadenitisMyasthenia gravis3. Good healthLymphomamyasthenia030104 developmental biologyOncologythymic epithelial tumor030220 oncology & carcinogenesis570 Life sciences; biologypathologybusiness
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Cancer-associated fibroblasts as abettors of tumor progression at the crossroads of EMT and therapy resistance

2019

Abstract In the last decades, the role of the microenvironment in tumor progression and therapeutic outcome has gained increasing attention. Cancer-associated fibroblasts (CAFs) have emerged as key players among stromal cells, owing to their abundance in most solid tumors and their diverse tumor-restraining/promoting roles. The interplay between tumor cells and neighboring CAFs takes place by both paracrine signals (cytokines, exosomes and metabolites) or by the multifaceted functions of the surrounding extracellular matrix. Here, we dissect the most recent identified mechanisms underlying CAF-mediated control of tumor progression and therapy resistance, which include induction of the epith…

0301 basic medicineCancer ResearchStromal cellEpithelial-Mesenchymal TransitionParacrine CommunicationAntineoplastic AgentsReviewBiologylcsh:RC254-28203 medical and health sciences0302 clinical medicineCancer-Associated FibroblastsCancer stem cellSettore MED/04 - PATOLOGIA GENERALENeoplasmsParacrine CommunicationTumor MicroenvironmentHumansEpithelial–mesenchymal transitionTumor microenvironmentCancer associated fibroblasts cancer stem cells extracellular matrix exosomes epithelial-to-mesenchymal transition.lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMicrovesiclesGene Expression Regulation Neoplastic030104 developmental biologyOncologyTumor progressionDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchDisease ProgressionMolecular MedicineCancer-Associated FibroblastsSignal Transduction
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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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The hallmarks of ovarian cancer: proliferation and cell growth

2020

Epithelial ovarian cancer (EOC) is a heterogeneous group of diseases with distinct biological and clinical behaviour. Despite the differences between them, the capability of tumour cells to continuously proliferate and avoid death is maintained among histotypes. This ability is the result of alterations at different levels, causing the deregulation of cell cycle and proliferative-related pathways. Even if the leading role is played by RB and TP53, changes in other molecular pathways are involved in the development of EOC. This ability can be exploited to generate in vitro and in vivo models resembling the conditions of tumour development in a patient. In vivo models, such as patient-derived…

0301 basic medicineCancer Researchendocrine system diseaseslcsh:MedicineBiologylcsh:RC254-282Article03 medical and health sciencesCell growth0302 clinical medicinemedicineEpithelial ovarian cancerCell proliferationHeterogeneous groupCell growthlcsh:RCell cycleEpithelial ovarian cancerlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseAnimal models030104 developmental biologyOncologyTumour development030220 oncology & carcinogenesisGenetically Engineered MouseCancer researchOvarian cancerEJC Supplements
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The role of surgery in platinum-resistant ovarian cancer: A call to the scientific community.

2021

Abstract In the last decade, a growing attention has been focused on identifying effective therapeutic strategies also in the orphan clinical setting of women with platinum-resistant disease. In this context, secondary cytoreductive surgery (SCS) remains a potential approach only in women with platinum sensitive relapse, but experimental data have been published supporting the role of SCS also in patients with platinum-resistant recurrence. In particular, surgery is emerging as a potential option in specific subgroups of women, such as those patients with low-grade serous histology, or low-volume relapse with disease located in the so-called pharmacological sanctuaries. Furthermore, contras…

0301 basic medicineCancer Researchmedicine.medical_specialtymedicine.medical_treatmentContext (language use)Antineoplastic AgentsPlatinum CompoundsDiseaseHyperthermic Intraperitoneal ChemotherapyCarcinoma Ovarian Epithelial03 medical and health sciences0302 clinical medicineMedicineAnimalsHumansIn patientPlatinum resistantChemotherapybusiness.industryCytoreduction Surgical Proceduresmedicine.diseaseCombined Modality TherapySurgerySerous fluid030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisPlatinum sensitiveFemaleNeoplasm Recurrence LocalbusinessOvarian cancerBiological features Minimally invasive surgery Personalized treatment Platinum resistant Recurrent ovarian cancer Secondary cytoreductive surgerySeminars in cancer biology
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Tumor Microenvironment And Epithelial Mesenchymal Transition As Targets To Overcome Tumor Multidrug Resistance

2020

It is well established that multifactorial drug resistance hinders successful cancer treatment. Tumor cell interactions with the tumor microenvironment (TME) are crucial in epithelial-mesenchymal transition (EMT) and multidrug resistance (MDR). TME-induced factors secreted by cancer cells and cancer-associated fibroblasts (CAFs) create an inflammatory microenvironment by recruiting immune cells. CD11b+/Gr-1+ myeloid-derived suppressor cells (MDSCs) and inflammatory tumor associated macrophages (TAMs) are main immune cell types which further enhance chronic inflammation. Chronic inflammation nurtures tumor-initiating/cancer stem-like cells (CSCs), induces both EMT and MDR leading to tumor re…

0301 basic medicineCancer Researchmedicine.medical_treatmentMultidrug resistanceTargeted therapyTargeted therapy0302 clinical medicineCancer-Associated FibroblastsNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsTumor-Associated MacrophagesTumor MicroenvironmentPharmacology (medical)HypoxiaTOR Serine-Threonine KinasesSmall moleculesChemotherapy ; Hypoxia ; Inflammation ; Microenvironment ; Multidrug resistance ; Small molecules ; Targeted therapy.Drug Resistance Multiple3. Good healthDNA DemethylationGene Expression Regulation NeoplasticInfectious DiseasesOncology030220 oncology & carcinogenesisInflammation MediatorsEpithelial-Mesenchymal TransitionStromal cellMicroenvironmentBiologyProinflammatory cytokine03 medical and health sciencesCell Line TumormedicineAnimalsHumansChemotherapyEpithelial–mesenchymal transitionPharmacologyInflammationTumor microenvironmentCancerHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseHistone Deacetylase InhibitorsMultiple drug resistanceDisease Models Animal030104 developmental biologyDrug Resistance NeoplasmCancer cellCancer research
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Tight Junctions as a Key for Pathogens Invasion in Intestinal Epithelial Cells

2021

Tight junctions play a major role in maintaining the integrity and impermeability of the intestinal barrier. As such, they act as an ideal target for pathogens to promote their translocation through the intestinal mucosa and invade their host. Different strategies are used by pathogens, aimed at directly destabilizing the junctional network or modulating the different signaling pathways involved in the modulation of these junctions. After a brief presentation of the organization and modulation of tight junctions, we provide the state of the art of the molecular mechanisms leading to permeability breakdown of the gut barrier as a consequence of tight junctions’ attack by pathogens, including…

0301 basic medicineCell Membrane Permeabilitytight junction030106 microbiologyReviewBiologyInfectionsCatalysisTight JunctionsInorganic Chemistrylcsh:Chemistry03 medical and health sciencesIntestinal mucosaAnimalsHumansPhysical and Theoretical ChemistryIntestinal MucosamicroorganismsMolecular Biologylcsh:QH301-705.5SpectroscopyGut barrierTight junctionBacteriagut barrierOrganic ChemistryEpithelial CellspathogensGeneral Medicinesignaling pathwaysComputer Science ApplicationsCell biologyIntestinal Diseases030104 developmental biologylcsh:Biology (General)lcsh:QD1-999enterocytesintestinal epithelial cellsSignal transductionpermeabilitySignal TransductionInternational Journal of Molecular Sciences
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