Search results for "P53"

showing 10 items of 303 documents

Predictive value of p53, Ki67 and TLR5 in neoplastic progression of Barrett’s esophagus: a matched case–control study

2022

Abstract Barrett’s esophagus progresses to high-grade dysplasia or cancer along the well-established metaplasia-dysplasia-adenocarcinoma sequence. The aim of this study was to evaluate the value of p53, Ki67, and toll-like receptor 5 (TLR5) in prediction of malignant progression of Barrett’s metaplasia and low-grade dysplasia. This was a retrospective matched case–control study based on Northern and Central Finland population. Patients diagnosed with esophageal high-grade dysplasia or adenocarcinoma were included. From these patients, all previous endoscopy samples were obtained along with original diagnostic HE-slides and clinical data. Age- and sex-matched patients with non-progressing Ba…

p53Esophageal NeoplasmsbiomarkkeritAdenocarcinomaPathology and Forensic MedicineimmunohistokemiaBarrett EsophagusHumansBarrett’s esophagusTLR5Molecular BiologyRetrospective StudiesMetaplasiaSurveillanceCell BiologyGeneral MedicineImmunohistochemistrydigestive system diseasesToll-Like Receptor 5antigeenitKi-67 AntigenDysplasia markerCase-Control StudiesproteiinitEsophageal adenocarcinomatarkkailuTumor Suppressor Protein p53ruokatorvisyöpäKi67Virchows Archiv
researchProduct

Digital control circuitry for the p53 dynamics in cancer cell and apoptosis

2010

Abstract Experimental work and theoretical models deduce a “digital” response of the p53 transcription factor when genomic integrity is damaged. The mutual influence of p53 and its antagonist, the Mdm2 oncogene, is closed in a feedback. This paper proposes an aerospace-based architecture for translating the p53/Mdm2/DNA damage network into a digital circuitry in which the optimal control theory is applied for obtaining the requested dynamic evolutions of some considered cell species for repairing a DNA damage. The purpose of this paper is to demonstrate the usefulness of such digital circuitry design to detect and predict the cell species dynamics for shedding light on their inner and mutua…

p53General Immunology and MicrobiologyMechanism (biology)DNA damageQH301-705.5General NeuroscienceapoptosisWiring diagramCell fate determinationBiologycellular circuitryBioinformaticsOptimal controlGeneral Biochemistry Genetics and Molecular Biologyprotein networks signallingfeedback controlCancer cellDigital controlBiology (General)General Agricultural and Biological SciencesBiological systemTranscription factorOpen Life Sciences
researchProduct

Mutations in p53 Gene Exons in a Sample from the South of Spain in Oral Cancer

2021

[Background+ Cancer is a genetic disease caused by mutations in DNA and epigenetic alterations that control gene expression. The majority of epidermoid carcinomas develop within the fields of epithelial genetic alterations. The mechanisms underlying tumorigenesis of epidermoid carcinoma are as yet unknown; therefore, precise identification of the risk factors is needed.

p53Geneticseducation.field_of_studyOral Medicine and PathologyResearchOral cancerPopulationExonCancerBiologymedicine.diseasemedicine.disease_causeChromosome 17 (human)ExonEpidermoid carcinomaDysplasiamedicineeducationCarcinogenesisGeneral DentistryGeneMutationsUNESCO:CIENCIAS MÉDICAS
researchProduct

THE HDAC INHIBITOR ITF2357 (GIVINOSTAT) AS A KEY PLAYER IN EPIGENETIC TARGETING OF MELANOMA AND COLON CANCER CELLS

2023

Histone deacetylase inhibitors (HDACIs) are epigenetic compounds that have been recently considered for their promising anti-tumor activity. The aim of this PhD thesis was to elucidate and characterize the anti-tumor effect of the HDAC inhibitor ITF2357 (Givinostat) in melanoma and colon cancer cells that are characterized by oncogenic BRAF mutations. Interestingly, data reported in this thesis demonstrate that ITF2357 exerts a remarkable anti-tumor effect in melanoma cells by inducing a switch from a pro-survival autophagy to caspase-dependent apoptosis. The thesis provides the first evidences that ITF2357 is able to target oncogenic BRAF and oncogenic p53. The ITF2357 decreasing effect on…

p53HDAC inhibitorSettore BIO/10 - BiochimicaAutophagyEpigeneticApoptosisMelanomaColon cancerBRAF
researchProduct

Oncogenic BRAF and p53 Interplay in Melanoma Cells and the Effects of the HDAC Inhibitor ITF2357 (Givinostat)

2023

Oncogenic BRAF mutations have been widely described in melanomas and promote tumour progression and chemoresistance. We previously provided evidence that the HDAC inhibitor ITF2357 (Givinostat) targets oncogenic BRAF in SK-MEL-28 and A375 melanoma cells. Here, we show that oncogenic BRAF localises to the nucleus of these cells, and the compound decreases BRAF levels in both the nuclear and cytosolic compartments. Although mutations in the tumour suppressor p53 gene are not equally frequent in melanomas compared to BRAF, the functional impairment of the p53 pathway may also contribute to melanoma development and aggressiveness. To understand whether oncogenic BRAF and p53 may cooperate, a po…

p53HDAC inhibitor; ITF2357; BRAF; melanoma; p53; apoptosisOrganic ChemistryapoptosisGeneral MedicineCatalysisComputer Science ApplicationsBRAFInorganic ChemistryHDAC inhibitorSettore BIO/10 - BiochimicaITF2357melanomaPhysical and Theoretical ChemistryMolecular BiologySpectroscopy
researchProduct

Targeting HSP90 with the small molecule inhibitor AUY922 (luminespib) as a treatment strategy against hepatocellular carcinoma

2018

Hepatocellular carcinoma (HCC) is a highly malignant tumor that responds very poorly to existing therapies, most probably due to its extraordinary inter- and intra-tumor molecular heterogeneity. The modest therapeutic response to molecular targeted agents underlines the need for new therapeutic approaches for HCC. In our study, we took advantage of well-characterized human HCC cell lines, differing in transcriptomic subtypes, DNA mutation and amplification alterations, reflecting the heterogeneity of primary HCCs, to provide a preclinical evaluation of the specific heat shock protein 90 (HSP90) inhibitor AUY922 (luminespib). Indeed, HSP90 is highly expressed in different tumor types, but it…

p53MaleCancer ResearchCellTranscriptome0302 clinical medicineHCCbeta CateninAged 80 and overLuminespibAUY922Liver NeoplasmsHep G2 CellsSorafenibMiddle AgedUp-RegulationGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyCaspases030220 oncology & carcinogenesisHepatocellular carcinomaFemaleNUPR1medicine.drugAdultSorafenibCarcinoma Hepatocellularβ-CateninMice NudeAntineoplastic AgentsSmall Molecule Libraries03 medical and health sciencesDownregulation and upregulationIn vivoCell Line TumormedicineHSP90AnimalsHumansHSP90 Heat-Shock ProteinsAgedCell growthbusiness.industryMcl-1IsoxazolesResorcinolsHCCSmedicine.diseasedigestive system diseasesMutationCancer researchTranscriptomebusinessInternational Journal of Cancer
researchProduct

Plausible Role of Estrogens in Pathogenesis, Progression and Therapy of Lung Cancer

2021

Malignant neoplasms are among the most common diseases and are responsible for the majority of deaths in the developed world. In contrast to men, available data show a clear upward trend in the incidence of lung cancer in women, making it almost as prevalent as breast cancer. Women might be more susceptible to the carcinogenic effect of tobacco smoke than men. Furthermore, available data indicate a much more frequent mutation of the tumor suppressor gene-p53 in non-small cell lung cancer (NSCLC) female patients compared to males. Another important factor, however, might lie in the female sex hormones, whose mitogenic or carcinogenic effect is well known. Epidemiologic data show a correlatio…

p53MaleLung NeoplasmsHealth Toxicology and Mutagenesismedicine.medical_treatmentlcsh:MedicineEstrogen receptorReviewNSCLCsex hormonessex hormone03 medical and health sciences0302 clinical medicineBreast cancerA549Carcinoma Non-Small-Cell LungmedicineCarcinomaestrogenNeoplasmEstrogen Receptor betaHumansLung cancerCarcinogennon-small cell lung cancer030304 developmental biology0303 health sciencesLungbusiness.industrylcsh:RPublic Health Environmental and Occupational Health17β-estradiolEstrogen Receptor alphaHormone replacement therapy (menopause)Estrogensmedicine.diseaselung adenocarcinomarespiratory tract diseaseslung cancermedicine.anatomical_structure17- estradiolReceptors Estrogen030220 oncology & carcinogenesisCancer researchFemalebusinessestrogen receptorInternational Journal of Environmental Research and Public Health
researchProduct

Molecular mechanisms of MYCN-dependent apoptosis and the MDM2-p53 pathway: an Achille’s heel to be exploited for the therapy of MYCN amplified neurob…

2012

The p53 oncosuppressor is very seldom mutated in neuroblastoma, but several mecha- nisms cooperate to its functional inactivation in this tumor. Increased MDM2 levels, due to genetic amplification or constitutive inhibition of p14ARF, significantly contribute to this event highlighting p53 reactivation as an attractive perspective for neuroblastoma treat- ment. In addition to its role in tumorigenesis, MYCN sensitizes untransformed and cancer cells to apoptosis. This is associated to a fine modulation of the MDM2-p53 pathway Indeed MYCN induces p53 and MDM2 transcription, and, by evoking a DNA damage response (DDR), it stabilizes p53 and its proapoptotic kinase Homeodomain Interacting Prote…

p53Programmed cell deathCancer ResearchHMGA1HIPK2Biologymedicine.disease_causelcsh:RC254-28203 medical and health sciencesNeuroblastoma0302 clinical medicineMDM2NeuroblastomaMYCNmedicineProtein kinase Aneoplasms030304 developmental biology0303 health sciencesKinaseHMGA1amedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensHMGA13. Good healthOncology030220 oncology & carcinogenesisCancer cellPerspective ArticleMDM2-antagonistsbiology.proteinCancer researchMdm2CarcinogenesisMDM2-antagonistFrontiers in Oncology
researchProduct

Desemmascarar el càncer: Centenars de malalties, un sol nom

2013

Tothom té una idea més o menys clara del que representa un càncer: un conjunt de cèl·lules que es divideixen sense control. Darrera aquesta imatge simplista s’amaga un dels problemes de salut més complexes i més greus que existeixen. És gràcies als avenços biomèdics dels últims vint anys que finalment estem reconeixent les grans diferències que hi ha entre els tipus de càncers coneguts, un descobriment que resultarà clau per a dissenyar teràpies més efectives en un futur proper.

p53cáncersupressors tumoralsmedicina; cáncercàncerteràpies personalitzadesGeneral Medicineoncogènmedicinacàncer; oncogèn; p53; supressors tumorals; teràpies personalitzades
researchProduct

Design, Synthesis, Chemical and Biochemical Insights Into Novel Hybrid Spirooxindole-Based p53-MDM2 Inhibitors With Potential Bcl2 Signaling Attenuat…

2021

The tumor resistance to p53 activators posed a clinical challenge. Combination studies disclosed that concomitant administration of Bcl2 inhibitors can sensitize the tumor cells and induce apoptosis. In this study, we utilized a rapid synthetic route to synthesize two novel hybrid spirooxindole-based p53-MDM2 inhibitors endowed with Bcl2 signaling attenuation. The adducts mimic the thematic features of the chemically stable potent spiro [3H-indole-3,2′-pyrrolidin]-2(1H)-ones p53-MDM2 inhibitors, while installing a pyrrole ring via a carbonyl spacer inspired by the natural marine or synthetic products that efficiently inhibit Bcl2 family functions. A chemical insight into the two synthesized…

p53human homolog of mouse double minute 2 (MDM2)ChemistryGeneral ChemistryspirooxindoleBcl 2protein–protein interaction (PPI)QD1-999Original ResearchFrontiers in Chemistry
researchProduct