Search results for "Cell Transformation"

showing 10 items of 180 documents

Do nonmelanoma skin cancers develop from extra-cutaneous stem cells?

2008

A hypothesis is presented that nonmelanoma skin cancers can develop from extra-cutaneous stem cells, and not exclusively from skin keratinocytes. This idea is supported by recent findings regarding the initiation of cancers in the digestive tract, and by a cancer stem cell model of a neoplasia. It is known that multipotent adult progenitor cells can trans-differentiate into very diverse cellular lineages and can be recruited to areas of profound tissue injury. In these settings, they might also initiate malignant transformation. Some epidemiological data and recent findings regarding mechanisms of wound healing indicate that skin cancers could also originate from bone marrow-derived or othe…

KeratinocytesCancer ResearchPathologymedicine.medical_specialtySkin NeoplasmsBone Marrow CellsCancer stem cellepidermisAnimalsHumansMedicineProgenitor cellSkin repairintegumentary systembusiness.industryStem Cellsmedicine.diseasehematopoietic stem cellsCell Transformation Neoplasticmedicine.anatomical_structureOncologyBone marrowSkin cancerStem cellbusinessKeratinocyteWound healingInternational Journal of Cancer
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Rottlerin induces a transformed phenotype in human keratinocytes.

2001

PKCdelta plays a fundamental role in cell cycle control. Consistent with its proposed tumour suppressor function, ras transfection of the human keratinocyte cell line HaCaT results in a loss of PKCdelta expression mediated by TGFalpha (Exp. Cell Res., 219, 299, 1995). To get more insight into the role of PKCdelta in keratinocytes, we investigated the effects of Rottlerin, a specific inhibitor of protein kinase Cdelta, in HaCaT cells. After Rottlerin treatment, HaCaT cells lost their cobble-stone morphology and displayed a spindle-shaped, fibroblastic phenotype. Additionally, the establishment of cell-cell contacts was prevented. This was caused by an internalization of E-cadherin and beta-c…

Keratinocytesmedia_common.quotation_subjectCellBiophysicsBiologyBiochemistryCell Linechemistry.chemical_compoundmedicineCell AdhesionHumansBenzopyransEnzyme InhibitorsProtein kinase AInternalizationMolecular BiologyProtein Kinase Cbeta Cateninmedia_commonintegumentary systemContact InhibitionAcetophenonesCell DifferentiationCell BiologyTransfectionCadherinsPhenotypeMolecular biologyCell biologyIsoenzymesHaCaTCytoskeletal ProteinsProtein Kinase C-deltamedicine.anatomical_structureCell Transformation NeoplasticPhenotypechemistryCell cultureTrans-ActivatorsRottlerinBiochemical and biophysical research communications
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Hypoxia-inducible factor 1 alpha expression increases during colorectal carcinogenesis and tumor progression

2008

Abstract Background Hypoxia-inducible factor 1 alpha (HIF-1α) is involved in processes promoting carcinogenesis of many tumors. However, its role in the development of colorectal cancer is unknown. To investigate the significance of HIF-1α during colorectal carcinogenesis and progression we examined its expression in precursor lesions constituting the conventional and serrated pathways, as well as in non-metastatic and metastatic adenocarcinomas. Methods Immunohistochemistry and Western blot is used to analyse HIF-1α expression in normal colonic mucosa, hyperplastic polyps (HPP), sessile serrated adenomas (SSA), low-grade (TA-LGD) and high-grade (TA-HGD) traditional adenomas as well as in n…

LipopolysaccharidesCancer ResearchPathologymedicine.medical_specialtyColorectal cancerColonic PolypsMouse model of colorectal and intestinal cancermedicine.disease_causelcsh:RC254-282chemistry.chemical_compoundWestern blotCell Line TumorGeneticsMedicineHumansNeoplasm Metastasismedicine.diagnostic_testbusiness.industrymedicine.diseaseHypoxia-Inducible Factor 1 alpha Subunitlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensImmunohistochemistryVascular endothelial growth factorCell Transformation NeoplasticOncologychemistryHyperplastic PolypTumor progressionDisease ProgressionImmunohistochemistrybusinessCarcinogenesisColorectal NeoplasmsPrecancerous ConditionsResearch ArticleBMC Cancer
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Transformation of primary human hepatocytes in hepatocellular carcinoma

2015

Hepatocellular carcinoma (HCC) is the most common primary liver cancer. Currently, there is limited knowledge of neoplastic transformation of hepatocytes in HCC. In clinical practice, the high rate of HCC local recurrence suggests the presence of different hepatocyte populations within the liver and particularly in the tumor proximity. The present study investigated primary human hepatocyte cultures obtained from liver specimens of patients affected by cirrhosis and HCC, their proliferation and transformation. Liver samples were obtained from seven HCC cirrhotic patients and from three patients with normal liver (NL). Immediately after surgery, cell outgrowth and primary cultures were obtai…

Liver CirrhosisMale0301 basic medicineCancer ResearchPathologymedicine.medical_specialtyCarcinoma HepatocellularCirrhosisGlypican 3Lesion03 medical and health sciences0302 clinical medicineGlypicansAntigens NeoplasmCell MovementSettore BIO/10 - BiochimicamedicineCarcinomaHumansNeoplasm InvasivenessNeoplastic transformationAgedCell ProliferationArginasebiologySettore BIO/16 - Anatomia UmanaLiver NeoplasmsCD44Hepatocellular CarcinomaMiddle AgedFlow Cytometrymedicine.diseaseImmunohistochemistrydigestive system diseasesCell Transformation NeoplasticHyaluronan Receptors030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisHepatocellular carcinomaHepatocyteHepatocytesbiology.proteinFemalemedicine.symptomInternational Journal of Oncology
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Transcription factor NRF2 regulates miR-1 and miR-206 to drive tumorigenesis

2013

The mechanisms by which deregulated nuclear factor erythroid-2–related factor 2 (NRF2) and kelch-like ECH-associated protein 1 (KEAP1) signaling promote cellular proliferation and tumorigenesis are poorly understood. Using an integrated genomics and 13C-based targeted tracer fate association (TTFA) study, we found that NRF2 regulates miR-1 and miR-206 to direct carbon flux toward the pentose phosphate pathway (PPP) and the tricarboxylic acid (TCA) cycle, reprogramming glucose metabolism. Sustained activation of NRF2 signaling in cancer cells attenuated miR-1 and miR-206 expression, leading to enhanced expression of PPP genes. Conversely, overexpression of miR-1 and miR-206 decreased the exp…

Lung NeoplasmsCell SurvivalNF-E2-Related Factor 2Citric Acid CycleMice NudeBiologymedicine.disease_causeMiceRNA interferenceCarcinoma Non-Small-Cell LungCell Line TumormicroRNAGene expressionmedicineAnimalsHumansTranscription factor3' Untranslated RegionsCell ProliferationOligonucleotide Array Sequence AnalysisRegulation of gene expressionBinding SitesBase SequenceGeneral MedicineMolecular biologyHDAC4Cell biologyTumor BurdenGene Expression Regulation NeoplasticMicroRNAsCell Transformation NeoplasticGlucoseRNA InterferenceHistone deacetylaseCarcinogenesisTranscriptomeOxidation-ReductionNeoplasm TransplantationResearch Article
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BRAFV600E mutation, TIMP-1 upregulation, and NF-κB activation: closing the loop on the papillary thyroid cancer trilogy.

2011

BRAFV600E is the most common mutation found in papillary thyroid carcinoma (PTC). Tissue inhibitor of metalloproteinases (TIMP-1) and nuclear factor (NF)-κB have been shown to play an important role in thyroid cancer. In particular, TIMP-1 binds its receptor CD63 on cell surface membrane and activates Akt signaling pathway, which is eventually responsible for its anti-apoptotic activity. The aim of our study was to evaluate whether interplay among these three factors exists and exerts a functional role in PTCs. To this purpose, 56 PTC specimens were analyzed for BRAFV600E mutation, TIMP-1 expression, and NF-κB activation. We found that BRAFV600E mutation occurs selectively in PTC nodules an…

MAPK/ERK pathwayAdultMaleProto-Oncogene Proteins B-rafCancer Researchmedicine.medical_specialtyendocrine system diseasesEndocrinology Diabetes and MetabolismThyroid cancer TIMP-1 papillary thyroid cancerMutation MissenseGlutamic AcidGene Expression Regulation EnzymologicSettore MED/13 - EndocrinologiaPapillary thyroid cancerEndocrinologyDownregulation and upregulationInternal medicinemedicineTumor Cells CulturedGene silencingHumansGene Regulatory NetworksNeoplasm InvasivenessThyroid NeoplasmsProtein kinase BThyroid cancerTissue Inhibitor of Metalloproteinase-1ChemistryAkt/PKB signaling pathwayCarcinomaNF-kappa BValineMiddle Agedmedicine.diseaseCarcinoma PapillaryUp-RegulationGene Expression Regulation NeoplasticEndocrinologyCell Transformation NeoplasticOncologyAmino Acid SubstitutionThyroid Cancer PapillaryCancer researchDisease ProgressionFemaleV600ESignal TransductionEndocrine-related cancer
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Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR inhibitors: Rationale and importance to inhibiting these pathways in human health

2011

William H. Chappell 1 , Linda S. Steelman 1,2 , Jacquelyn M. Long 2 , Ruth C. Kempf 2 , Stephen L. Abrams 1 , Richard A. Franklin 1 , Jorg Basecke 3 , Franca Stivala 4 , Marco Donia 4 , Paolo Fagone 4 , Graziella Malaponte 4 , Maria C. Mazzarino 4 , Ferdinando Nicoletti 4 , Massimo Libra 4 , Danijela Maksimovic-Ivanic 5 , Sanja Mijatovic 5 , Giuseppe Montalto 6 , Melchiorre Cervello 7 , Piotr Laidler 8 , Michele Milella 9 , Agostino Tafuri 10 , Antonio Bonati 11 , Camilla Evangelisti 12 , Lucio Cocco 12 , Alberto M. Martelli 12,13 , and James A. McCubrey 1 1 Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University 2 Department of Physics, Greenville, N…

MAPK/ERK pathwayAgingmedicine.medical_treatmentDrug ResistancerafPI3KTargeted therapycombination therapyPhosphatidylinositol 3-Kinases0302 clinical medicineTARGETED THERAPYCANCER STEM CELLSNeoplasmsCancer Stem CellsMedicineExtracellular Signal-Regulated MAP Kinases0303 health sciencesCombination TherapybiologyTOR Serine-Threonine KinasesMTORHuman health Ras inhibitors MEK ERKTargeted TherapyDiscovery and development of mTOR inhibitors3. Good healthDRUG RESISTANCECell Transformation NeoplasticOncology030220 oncology & carcinogenesismTORraf KinasesPremature agingMAP Kinase Signaling SystemReviewsSenescence03 medical and health sciencesCell Line TumorHumansPTENProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biologyMitogen-Activated Protein Kinase Kinasesbusiness.industryAKTAktagingPTEN PhosphohydrolaseRafTransplantationSENESCENCEImmunologyras Proteinsbiology.proteinCancer researchaging; akt; cancer stem cells; combination therapy; drug resistance; mtor; pi3k; raf; senescence; targeted therapybusinessProto-Oncogene Proteins c-akt
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p38α MAPK is required for contact inhibition

2005

Proliferation of nontransformed cells is regulated by cell-cell contacts, which are referred to as contact-inhibition. Despite its generally accepted importance for cell cycle control, knowledge about the intracellular signalling pathways involved in contact inhibition is scarce. In the present work we show that p38alpha mitogen-activated protein kinase (MAPK) is involved in the growth-inhibitory signalling cascade of contact inhibition in fibroblasts. p38alpha activity is increased in confluent cultures of human fibroblasts compared to proliferating cultures. Time course studies show a sustained activation of p38alpha in response to cell-cell contacts in contrast to a transient activation …

MAPK/ERK pathwayCancer ResearchContact InhibitionCell growthp38 mitogen-activated protein kinasesCell Culture TechniquesContact inhibitionFibroblastsBiologyCell biologyMitogen-Activated Protein Kinase 14Cell Transformation Neoplasticmedicine.anatomical_structureCell cultureNeoplasmsGeneticsmedicineHumansSignal transductionProtein kinase AFibroblastMolecular BiologyCell ProliferationSignal TransductionOncogene
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Emerging Raf inhibitors

2009

The Raf/MAPK kinase/extracellular-signal-regulated kinase pathway is often activated by genetic alterations in upstream signaling molecules. An integral component of this pathway, BRAF, is also activated by mutation, especially in melanoma and thyroid cancers. The Raf/MAPK kinase/extracellular-signal-regulated kinase pathway has profound effects on proliferative, apoptotic and differentiation pathways as well as the sensitivity and resistance to chemotherapeutic drugs.This review discusses targeting of Raf which could control abnormal proliferation in cancer and other proliferative diseases. The important roles that genetics plays in the response of patients to Raf inhibitors is also evalua…

MAPK/ERK pathwayProto-Oncogene Proteins B-rafCell signalingMAP Kinase Signaling SystemSignal transductionrafmedicine.disease_causemekerkmedicineHumanscancerPharmacology (medical)raf inhibitorsExtracellular Signal-Regulated MAP KinasesMelanomaProtein Kinase InhibitorsPharmacologyapoptosis cancer ERK proliferative disorderssignal transductionMitogen-Activated Protein Kinase KinasesApoptosis; Cancer; ERK; Kinases; MEK; Proliferative disorders; Protein phosphorylation; Raf; Raf inhibitors; Signal transductionMutationproliferative disordersapoptosis; cancer; erk; kinases; mek; proliferative disorders; protein phosphorylation; raf; raf inhibitors; signal transduction read more: http://informahealthcare.com/doi/abs/10.1517/14728210903232633business.industryKinaseMelanomaapoptosisCancermedicine.diseaseXenograft Model Antitumor Assaysprotein phosphorylationCell Transformation Neoplastickinasessignal transduction read more: http://informahealthcare.com/doi/abs/10.1517/14728210903232633ApoptosisDrug Resistance NeoplasmCancer researchSignal transductionMitogen-Activated Protein Kinasesbusiness
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Expression of spindle assembly checkpoint proteins BubR1 and Mad2 expression as potential biomarkers of malignant transformation of oral leukoplakia:…

2021

Background The Spindle Assembly Checkpoint (SAC) is a surveillance mechanism essential to ensure the accuracy of chromosome segregation during mitosis. Our aim was to evaluate the expression of SAC proteins in oral carcinogenesis, and to assess their potential in predicting malignant transformation of oral leukoplakia. Material and Methods We analysed the immunoexpression of BubR1, Mad2, Bub3, and Spindly proteins in 64 oral biopsies from 52 oral leukoplakias and 12 normal tissues. Univariate and multivariate analysis were performed to evaluate predictive factors for malignant transformation (MT). Results We observed that BubR1 and Mad2 were more highly expressed in high dysplasia grade les…

Mad2BUB3medicine.disease_causeMalignant transformationOral Cancer and Potentially malignant disordersmedicineoral dysplasiawnt ligandsHumansGeneral DentistryMitosisUNESCO:CIENCIAS MÉDICASLeukoplakiadestruction complexbusiness.industryResearchoral cancermedicine.disease?-cateninSpindle checkpointstomatognathic diseasesCell Transformation NeoplasticOtorhinolaryngologyDysplasiaMad2 ProteinsCancer researchM Phase Cell Cycle CheckpointsSurgeryLeukoplakia OralbusinessCarcinogenesisBiomarkersMedicina Oral, Patología Oral y Cirugía Bucal
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