Search results for "Protein p53"

showing 10 items of 201 documents

CEP63 deficiency promotes p53-dependent microcephaly and reveals a role for the centrosome in meiotic recombination

2015

Artículo escrito por un elevado número de autores, solo se referencian el que aparece en primer lugar, el nombre del grupo de colaboración, si le hubiere, y los autores pertenecientes a la UAM

MaleProgrammed cell deathMicrocephalyGeneral Physics and AstronomyCell Cycle ProteinsDwarfismBiologyReal-Time Polymerase Chain ReactionArticleGeneral Biochemistry Genetics and Molecular BiologyMice03 medical and health sciences0302 clinical medicineChromosome structureSpermatocytesmedicineAnimalscentrioleHomologous Recombination030304 developmental biologyRecombination GeneticfertilityGeneticsCentrosomeMeiotic recombination0303 health sciencesMultidisciplinarySperm CountProtein cep63FaciesGeneral Chemistrymedicine.diseaseBiología y Biomedicina / BiologíaImmunohistochemistryNeural stem cell3. Good healthCEP63MeiosisSeckel syndromeCentrosomeMicrocephalyTumor Suppressor Protein p53Homologous recombinationmicrocephaly ; DNA damage ; centrosome ; meiosis030217 neurology & neurosurgeryDNA Damage
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Immunohistochemical evaluation of PCNA, p53, HSP60, HSP10 and MUC-2 presence and expression in prostate carcinogenesis

2003

Background: The study of the expression of different biological markers in non-neoplastic, pre-neoplastic and neoplastic lesions of prostate could help to better understand their role in carcinogenesis and to find new diagnostic and prognostic tools. Materials and Methods: In the present work we evaluated, by immunohistochemistry, the presence and the expression of PCNA, p53, HSP60, HSP10 and MUC-2 in a series of nodular hyperplasia, low- and high-grade prostatic intraepithelial lesions and adenocarcinomas. Results: Our data confirmed that: 1) PCNA expression could be related to the grade of progression of cancer; and that 2) p53 mutation could be a late event in prostate carcinogenesis. Mo…

MaleProstatic Intraepithelial NeoplasiaMucin-2Cancer ResearchGene Expression ProfilingMucinsProstatic HyperplasiaProstateProstatic NeoplasmsCarcinogenesis; Heat-shock proteins; Prostate; Cancer Research; OncologyCell DifferentiationChaperonin 60AdenocarcinomaGenes p53ImmunohistochemistryNeoplasm ProteinsHeat-shock proteinCell Transformation NeoplasticOncologyProliferating Cell Nuclear AntigenChaperonin 10Disease ProgressionHumansTumor Suppressor Protein p53Carcinogenesi
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Identification of novel, clonally stable, somatic mutations targeting transcription factors PAX5 and NKX2-3, the epigenetic regulator LRIF1, and BRAF…

2021

Diagnosis of B-cell chronic lymphocytic leukemia (B-CLL) is usually straightforward, involving clinical, immunophenotypic (Matutes score), and (immuno)genetic analyses (to refine patient prognosis for treatment). CLL cases with atypical presentation (e.g., Matutes ≤ 3) are also encountered, and for these diseases, biology and prognostic impact are less clear. Here we report the genomic characterization of a case of atypical B-CLL in a 70-yr-old male patient; B-CLL cells showed a Matutes score of 3, chromosomal translocation t(14;18)(q32;q21) (BCL2/IGH), mutated IGHV, deletion 17p, and mutations in BCL2, NOTCH1 (subclonal), and TP53 (subclonal). Quite strikingly, a novel PAX5 mutation that w…

MaleProto-Oncogene Proteins B-rafChronic lymphocytic leukemiaCell Cycle ProteinsBiologymedicine.disease_causeSomatic evolution in cancerTranslocation GeneticEpigenesis Genetichematological neoplasmClonal Evolutionimmune system diseaseshemic and lymphatic diseasesExome SequencingmedicineHumansEpigeneticsReceptor Notch1neoplasmsLoss functionExome sequencingAgedHomeodomain ProteinsMutationPAX5 Transcription FactorGeneral Medicinemedicine.diseasePrognosisLeukemia Lymphocytic Chronic B-CellProto-Oncogene Proteins c-bcl-2MutationCancer researchPAX5Tumor Suppressor Protein p53IGHV@Rapid Cancer CommunicationTranscription FactorsCold Spring Harbor Molecular Case Studies
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p53 mutations in L3-loop zinc-binding domain, DNA-ploidy, and S phase fraction are independent prognostic indicators in colorectal cancer: A prospect…

2002

p53 gene alterations are among the most common events observed in colorectal cancer,and are accompanied frequently by DNA aneuploidy and high proliferative activity. The prognostic significance of such mutations remains controversial. We prospectively evaluated the prognostic significance of p53 mutations, DNA-ploidy, and S phase fraction (SPF) in a consecutive series of 160 colorectal cancer patients (median follow-up 71 months). Tumor DNA was screened for p53 mutations by PCR/single-strand conformational polymorphism/sequencing. DNA-ploidy and SPF were assessed by DNA flow cytometry. p53 mutations were detected in 68 of 160 (42.5%) cases. In 56% (38 of 68) of these, p53 mutations were fou…

MaleSettore MED/06 - Oncologia Medicaprotein p53S PhaseBiomarkers TumorHumansProspective StudiesCodonAgedPloidiesPolymorphism GeneticDNA NeoplasmExonsDNAMiddle AgedGenes p53PrognosisSurvival AnalysisProtein Structure TertiaryItalyMultivariate AnalysisMutationFemaleCarrier ProteinsColorectal NeoplasmsFollow-Up Studies
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Anaplastic Wilms' tumour, a subtype displaying poor prognosis, harbours p53 gene mutations

1994

The genetics of Wilms' tumour (WT), a paediatric malignancy of the kidney, is complex. Inactivation of the tumour suppressor gene, WT1, is associated with tumour aetiology in approximately 10-15% of WTs. Chromosome 17p changes have been noted in cytogenetic studies of WTs, prompting us to screen 140 WTs for p53 mutations. When histopathology reports were available, p53 mutations were present in eight of eleven anaplastic WTs, a tumour subtype associated with poor prognosis. Amplification of MDM2, a gene whose product binds and sequesters p53, was excluded. Our results indicate that p53 alterations provide a molecular marker for anaplastic WTs.

MaleTumor suppressor geneDNA Mutational AnalysisMolecular Sequence DataGene mutationBiologyMalignancymedicine.disease_causePolymerase Chain ReactionWilms TumorProto-Oncogene ProteinsGeneticsmedicineHumansAmino Acid SequenceGeneAllelesMutationBase SequencefungiNuclear ProteinsCell DifferentiationProto-Oncogene Proteins c-mdm2Wilms' tumorGenes p53Prognosismedicine.diseaseKidney NeoplasmsNeoplasm ProteinsGene Expression Regulation Neoplasticbody regionsGenetic markerbiology.proteinCancer researchMdm2FemaleTumor Suppressor Protein p53Nature Genetics
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Anti-aging activity of the Ink4/Arf locus.

2009

The proteins encoded by the Ink4/Arf locus, p16Ink4a, p19Arf and p15Ink4b are major tumour suppressors that oppose aberrant mitogenic signals. The expression levels of the locus are progressively increased during aging and genome-wide association studies have linked the locus to a number of aging-associated diseases and frailty in humans. However, direct measurement of the global impact of the Ink4/Arf locus on organismal aging and longevity was lacking. In this work, we have examined the fertility, cancer susceptibility, aging and longevity of mice genetically modified to carry one (Ink4/Arf-tg) or two (Ink4/Arf-tg/tg) intact additional copies of the locus. First, increased gene dosage of …

Malemedicine.medical_specialtyAgingDNA damageTransgenemedia_common.quotation_subjectLongevityGene DosageLocus (genetics)Mice TransgenicBiologyGene dosagelaw.inventionMicelawInternal medicineNeoplasmsmedicineAnimalsGenes Tumor SuppressorSpermatogenesisGeneCyclin-Dependent Kinase Inhibitor p16Infertility Malemedia_commonCell ProliferationCell growthLongevityCell BiologyImmunity InnateMice Inbred C57BLEndocrinologyCancer researchSuppressorTumor Suppressor Protein p53Aging cell
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Apoptosis in malignant glioma cells triggered by the temozolomide-induced DNA lesion O6-methylguanine

2006

Methylating drugs such as temozolomide (TMZ) are widely used in the treatment of brain tumours (malignant gliomas). The mechanism of TMZ-induced glioma cell death is unknown. Here, we show that malignant glioma cells undergo apoptosis following treatment with the methylating agents N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and TMZ. Cell death determined by colony formation and apoptosis following methylation is greatly stimulated by p53. Transfection experiments with O(6)-methylguanine-DNA methyltransferase (MGMT) and depletion of MGMT by O(6)-benzylguanine showed that, in gliomas, the apoptotic signal originates from O(6)-methylguanine (O(6)MeG) and that repair of O(6)MeG by MGMT prevent…

MethylnitronitrosoguanidineCancer ResearchProgrammed cell deathFas Ligand ProteinGuanineDNA repairFas-Associated Death Domain ProteinBlotting WesternApoptosisBiologymedicine.disease_causeO(6)-Methylguanine-DNA MethyltransferaseGliomaTemozolomideTumor Cells CulturedGeneticsmedicineHumansDNA Breaks Double-StrandedRNA Small InterferingAntineoplastic Agents AlkylatingneoplasmsMolecular BiologyTumor Stem Cell AssayCell ProliferationTemozolomideBrain NeoplasmsCell CycleGliomaCell cycleFlow CytometryFas receptormedicine.diseaseDacarbazineProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesCancer researchTumor Suppressor Protein p53CarcinogenesisDNA Damagemedicine.drugOncogene
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Apoptosis induced by MNNG in human TK6 lymphoblastoid cells is p53 and Fas/CD95/Apo-1 related.

2003

Agents inducing O(6)-methylguanine (O(6)MeG) in DNA, such as N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), are not only highly mutagenic and carcinogenic but also cytotoxic because of the induction of apoptosis. In CHO fibroblasts, apoptosis triggered by O(6)MeG requires cell proliferation and MutSalpha-dependent mismatch repair and is related to the induction of DNA double-strand breaks (DSBs). Furthermore, it is mediated by Bcl-2 degradation and does not require p53 for which the cells were mutated [Cancer Res. 60 (2000) 5815]. Here we studied cytotoxicity and apoptosis induced by MNNG in a pair of human lymphoblastoid cells expressing wild-type p53 (TK6) and mutant p53 (WTK1) and show tha…

MethylnitronitrosoguanidineCell SurvivalHealth Toxicology and MutagenesisApoptosisCHO CellsBiologyCell LineBcl-2-associated X proteinCricetinaeProto-Oncogene ProteinsGeneticsCytotoxic T cellAnimalsHumansfas Receptorbcl-2-Associated X ProteinMitogen-Activated Protein Kinase 1Cell growthLymphoblastFas receptorMolecular biologyKineticsCell killingProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisbiology.proteinTumor Suppressor Protein p53DNA DamageMutation research
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O6-methylguanine DNA methyltransferase and p53 status predict temozolomide sensitivity in human malignant glioma cells

2006

Temozolomide (TMZ) is a methylating agent which prolongs survival when administered during and after radiotherapy in the first-line treatment of glioblastoma and which also has significant activity in recurrent disease. O6-methylguanine DNA methyltransferase (MGMT) is a DNA repair enzyme attributed a role in cancer cell resistance to O6-alkylating agent-based chemotherapy. Using a panel of 12 human glioma cell lines, we here defined the sensitivity to TMZ in acute cytotoxicity and clonogenic survival assays in relation to MGMT, mismatch repair and p53 status and its modulation by dexamethasone, irradiation and BCL-X(L). We found that the levels of MGMT expression were a major predictor of T…

MethyltransferaseCell Survivalbcl-X ProteinBcl-xLTransfectionBiochemistryDNA methyltransferaseO(6)-Methylguanine-DNA MethyltransferaseCellular and Molecular NeuroscienceCell Line TumorGliomaTemozolomidemedicineHumansCytotoxicityAntineoplastic Agents AlkylatingneoplasmsTumor Stem Cell AssayTemozolomideCell DeathbiologyGliomamedicine.diseaseCarmustinedigestive system diseasesDacarbazineEnzyme ActivationGene Expression Regulation NeoplasticCancer cellbiology.proteinCancer researchDNA mismatch repairTumor Suppressor Protein p53medicine.drugJournal of Neurochemistry
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Genes, Ageing and Longevity in Humans: Problems, Advantages and Perspectives.

2006

Many epidemiological data indicate the presence of a strong familial component of longevity that is largely determined by genetics, and a number of possible associations between longevity and allelic variants of genes have been described. A breakthrough strategy to get insight into the genetics of longevity is the study of centenarians, the best example of successful ageing. We review the main results regarding nuclear genes as well as the mitochondrial genome, focusing on the investigations performed on Italian centenarians, compared to those from other countries. These studies produced interesting results on many putative "longevity genes". Nevertheless, many discrepancies are reported, l…

Mitochondrial DNAAgingProteasome Endopeptidase ComplexNuclear geneApolipoproteins geneticsInsulin-Like Growth Factor I geneticsmedia_common.quotation_subjectApolipoprotein E4LongevityBiologyGenetic polymorphisms ageing longevity centenarians association studies mitochondrial DNABiochemistryDNA MitochondrialInflammation geneticsApolipoprotein E4 geneticsCytokines geneticsAnimalsHumansAlleleInsulin-Like Growth Factor ILongevity geneticsGenemedia_commonGenetic associationGeneticsAged 80 and overInflammationPolymorphism GeneticAryldialkylphosphataseSuperoxide DismutaseLongevitySuperoxide Dismutase geneticsGeneral MedicineClusterin geneticsPoly(ADP-ribose) Polymerases geneticsAging geneticsApolipoproteinsClusterinTumor Suppressor Protein p53 geneticsGenesEvolutionary biologyTraitCytokinesGene poolPoly(ADP-ribose) PolymerasesTumor Suppressor Protein p53Aryldialkylphosphatase geneticsDNA Mitochondrial geneticsProteasome Endopeptidase Complex physiology
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