Search results for " tumor suppressor"

showing 10 items of 64 documents

WWOX, a Chromosomal Fragile Site Gene and its Role in Cancer

2006

Allelic imbalances affecting the long arm of chromosome 16 have been extensively reported in the literature as common abnormalities observed in various carcinoma types, As a result of loss of heterozygosity (LOH) studies in breast cancer, we delimited a genomic area within chromosome 16 that demonstrated the highest frequency of abnormalities. This led us to the identification and cloning of WWOX, a candidate tumor suppressor gene (TSG) that spans a fragile region of DNA located at 16q23.3-24.1 (FRA16D: the second most active common chromosomal fragile site in the human genome). This gene encodes a protein that contains two WW domains responsible of protein-protein interactions and a short-…

GeneticsWWOXLoss of heterozygosityChromosome 16Chromosomal fragile sitemedicineCancer researchBiologyCarcinogenesismedicine.disease_causeTranscription factorGeneCandidate Tumor Suppressor Gene
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Geldanamycin and its derivatives as Hsp90 inhibitors

2012

The Hsp90 molecule, one of the most abundant heat shock proteins in mammalian cells, maintains homeostasis and prevents stress-induced cellular damage. Hsp90 is expressed under normal conditions at a level of about 1-2 Percent of total proteins, while its expression increases 2-10 fold in cancer cells. The two main constitutively expressed isoforms of Hsp90 are known as Hsp90-alpha and Hsp90-beta, and their upregulation is associated with tumor progression, invasion and formation of metastases, as well as development of drug resistance. The Hsp90 is a key target for many newly established, potent anticancer agents containing Hsp90 N-terminal ATP binding inhibitors, such as geldanamycin, and…

IndolesLactams MacrocyclicCyclin-Dependent KinaseAntineoplastic AgentsTanespimycinBenzoquinoneModels BiologicalAntineoplastic Agentchemistry.chemical_compoundDownregulation and upregulationTransforming Growth Factor betaCyclin-dependent kinaseHeat shock proteinBenzoquinonespolycyclic compoundsAnimalsHumansHSP90 Heat-Shock ProteinsbiologyAnimalTriazolesGeldanamycinHsp90Cyclin-Dependent KinasesProto-Oncogene Proteins c-rafHSP90 Heat-Shock Proteinsrc-Family KinaseschemistryTumor progressionMutationCancer cellbiology.proteinCancer researchMacrolidesMacrolideTriazoleTumor Suppressor Protein p53Animals; Antineoplastic Agents; Benzoquinones; Cyclin-Dependent Kinases; HSP90 Heat-Shock Proteins; Humans; Lactams Macrocyclic; Macrolides; Models Biological; Mutation; Novobiocin; Proto-Oncogene Proteins c-raf; Transforming Growth Factor beta; Triazoles; Tumor Suppressor Protein p53; src-Family KinasesNovobiocinHumanFrontiers in Bioscience
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Trefoil factor TFF1-induced protection of conjunctival cells from apoptosis at premitochondrial and postmitochondrial levels.

2008

PURPOSE. Goblet cells of the conjunctival epithelium synthesize and secrete TFF1 (Trefoil factor 1), a small protease-resistant peptide that, together with mucins, is responsible for the rheologic properties of the tear film. This study aimed to determine whether TFF1, whose synthesis increases in inflammatory conditions such as pterygium, could protect conjunctival cells from apoptosis. METHODS. Chang conjunctival cells, either wild-type or expressing TFF1 through stable transfection, were exposed to benzalkonium chloride (BAK) and ultraviolet (UV) irradiation to trigger apoptosis. The authors used cell fractionation to detect lipid raft‐associated proteins, coimmunoprecipitation to explor…

MESH : Cell LineMESH : Chromosomes Human Pair 21Chromosomes Human Pair 21CellApoptosisMESH: Flow CytometryMESH: Caspase 8Membrane Potentials0302 clinical medicineMESH: Mitochondrial MembranesMESH: Chromosomes Human Pair 21MESH : Membrane Potentials0303 health sciencesCaspase 8MESH : Caspase 8MESH : Benzalkonium CompoundsMESH : Tumor Suppressor ProteinsChromosome MappingFas receptorFlow CytometryXIAPMitochondriaMESH : Epithelial Cellsmedicine.anatomical_structureMESH: Epithelial Cells030220 oncology & carcinogenesisMitochondrial MembranesTrefoil Factor-1MESH : MitochondriaMESH : TransfectionBenzalkonium CompoundsConjunctivaMESH: Benzalkonium CompoundsProgrammed cell deathMESH: Enzyme ActivationMESH : ConjunctivaUltraviolet RaysMESH : Flow CytometryMESH: MitochondriaMESH: ConjunctivaCaspase 3BiologyInhibitor of apoptosisCaspase 8TransfectionCell Line03 medical and health sciencesMESH : Mitochondrial Membranesmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumansMESH: Membrane PotentialsMESH: Tumor Suppressor Proteins[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyMESH: HumansTumor Suppressor ProteinsMESH: ApoptosisMESH: TransfectionMESH : HumansEpithelial CellsMolecular biologyMESH: Cell LineEnzyme ActivationApoptosisMESH : Ultraviolet RaysMESH: Ultraviolet RaysMESH : Enzyme ActivationMESH: Chromosome MappingMESH : ApoptosisMESH : Chromosome Mapping
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PED in 2021: a major update of the protein ensemble database for intrinsically disordered proteins

2020

Abstract The Protein Ensemble Database (PED) (https://proteinensemble.org), which holds structural ensembles of intrinsically disordered proteins (IDPs), has been significantly updated and upgraded since its last release in 2016. The new version, PED 4.0, has been completely redesigned and reimplemented with cutting-edge technology and now holds about six times more data (162 versus 24 entries and 242 versus 60 structural ensembles) and a broader representation of state of the art ensemble generation methods than the previous version. The database has a completely renewed graphical interface with an interactive feature viewer for region-based annotations, and provides a series of descriptor…

MESH: Databases ProteinMESH: Search EngineAcademicSubjects/SCI00010[SDV.BBM.BS] Life Sciences [q-bio]/Biochemistry Molecular Biology/Structural Biology [q-bio.BM][SDV]Life Sciences [q-bio]media_common.quotation_subjectBiologycomputer.software_genreIntrinsically disordered proteins03 medical and health sciencesDatabases0302 clinical medicineInformation and Computing SciencesGeneticsFeature (machine learning)Database IssueHumansDatabases ProteinRepresentation (mathematics)Function (engineering)MESH: Tumor Suppressor Protein p53ComputingMilieux_MISCELLANEOUS030304 developmental biologymedia_commonGraphical user interfaceStructure (mathematical logic)MESH: Intrinsically Disordered Proteins0303 health sciencesMESH: HumansDatabase[SDV.BBM.BS]Life Sciences [q-bio]/Biochemistry Molecular Biology/Structural Biology [q-bio.BM]business.industryProteinBiological Sciences[SDV.BIBS]Life Sciences [q-bio]/Quantitative Methods [q-bio.QM]MetadataSearch EngineIntrinsically Disordered ProteinsState (computer science)Generic health relevanceTumor Suppressor Protein p53businesscomputer030217 neurology & neurosurgeryEnvironmental SciencesDevelopmental Biology
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p14(ARF) Prevents Proliferation of Aneuploid Cells by Inducing p53-Dependent Apoptosis.

2014

Weakening the Spindle Assembly Checkpoint by reduced expression of its components induces chromosome instability and aneuploidy that are hallmarks of cancer cells. The tumor suppressor p14(ARF) is overexpressed in response to oncogenic stimuli to stabilize p53 halting cell progression. Previously, we found that lack or reduced expression of p14(ARF) is involved in the maintenance of aneuploid cells in primary human cells, suggesting that it could be part of a pathway controlling their proliferation. To investigate this aspect further, p14(ARF) was ectopically expressed in HCT116 cells after depletion of the Spindle Assembly Checkpoint MAD2 protein that was used as a trigger for aneuploidy. …

Mad2 ProteinApoptosis; M Phase Cell Cycle Checkpoints; Mad2 Proteins; RNA Interference; Tumor Suppressor Protein p14ARF; AneuploidyApoptosiMitosisApoptosisM Phase Cell Cycle CheckpointAneuploidyHCT116 CellsSettore BIO/18 - GeneticaGene Knockout TechniquesMad2 ProteinsTumor Suppressor Protein p14ARFHumansM Phase Cell Cycle CheckpointsRNA InterferenceTumor Suppressor Protein p53Cell ProliferationJournal of cellular physiology
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Small Bowel Carcinomas in Coeliac or Crohn’s Disease: Clinico-pathological, Molecular, and Prognostic Features. A Study From the Small Bowel Cancer I…

2017

Background and aims An increased risk of small bowel carcinoma [SBC] has been reported in coeliac disease [CD] and Crohn's disease [CrD]. We explored clinico-pathological, molecular, and prognostic features of CD-associated SBC [CD-SBC] and CrD-associated SBC [CrD-SBC] in comparison with sporadic SBC [spo-SBC]. Methods A total of 76 patients undergoing surgical resection for non-familial SBC [26 CD-SBC, 25 CrD-SBC, 25 spo-SBC] were retrospectively enrolled to investigate patients' survival and histological and molecular features including microsatellite instability [MSI] and KRAS/NRAS, BRAF, PIK3CA, TP53, HER2 gene alterations. Results CD-SBC showed a significantly better sex-, age-, and st…

Male0301 basic medicineNeuroblastoma RAS viral oncogene homologOncologySurvivalReceptor ErbB-2Colorectal cancermedicine.disease_causeInflammatory bowel diseaseInflammatory bowel diseasetumour-infiltrating lymphocyteErbB-20302 clinical medicineCrohn DiseaseRetrospective StudieRisk Factors80 and overChildClass I Phosphatidylinositol 3-KinaseAged 80 and overColonic NeoplasmSettore MED/12 - GastroenterologiaCrohn's diseaseMLH1 methylationTumour-infiltrating lymphocytesGastroenterologyGeneral MedicineMiddle AgedPrognosisInflammatory bowel disease; Microsatellite instability; MLH1 promoter methylation; Survival; Tumour-infiltrating lymphocytes; Gastroenterology030220 oncology & carcinogenesisColonic NeoplasmsSurvival AnalysiKRASHumanReceptorAdultProto-Oncogene Proteins B-rafmedicine.medical_specialtyPrognosiClass I Phosphatidylinositol 3-KinasesSettore MED/08 - Anatomia PatologicaNOProto-Oncogene Proteins p21(ras)MLH1 promoter methylationYoung Adult03 medical and health sciencesInternal medicinemedicineCarcinomaHumansMLH1 methylation; inflammatory bowel disease; microsatellite instability; survival; tumour-infiltrating lymphocytesneoplasmsAgedRetrospective StudiesInflammatory bowel disease; Microsatellite instability; MLH1 promoter methylation; Survival; Tumour-infiltrating lymphocytes; Adult; Aged; Aged 80 and over; Celiac Disease; Child; Class I Phosphatidylinositol 3-Kinases; Colonic Neoplasms; Crohn Disease; Humans; Male; Microsatellite Instability; Middle Aged; Prognosis; Proto-Oncogene Proteins B-raf; Proto-Oncogene Proteins p21(ras); Receptor ErbB-2; Retrospective Studies; Risk Factors; Survival Analysis; Tumor Suppressor Protein p53; Young Adult; Gastroenterologybusiness.industryTumour-infiltrating lymphocyteRisk FactorCancerMicrosatellite instabilityinflammatory bowel disease; microsatellite instability; MLH1 promoter methylation; tumour-infiltrating lymphocytes; survivalmedicine.diseaseSurvival Analysiseye diseasesdigestive system diseasesCeliac Disease030104 developmental biologyMicrosatellite instabilityTumor Suppressor Protein p53businessJournal of Crohn's and Colitis
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Transcription intermediary factor 1γ is a tumor suppressor in mouse and human chronic myelomonocytic leukemia.

2011

Transcription intermediary factor 1γ (TIF1γ) was suggested to play a role in erythropoiesis. However, how TIF1γ regulates the development of different blood cell lineages and whether TIF1γ is involved in human hematological malignancies remain to be determined. Here we have shown that TIF1γ was a tumor suppressor in mouse and human chronic myelomonocytic leukemia (CMML). Loss of Tif1g in mouse HSCs favored the expansion of the granulo-monocytic progenitor compartment. Furthermore, Tif1g deletion induced the age-dependent appearance of a cell-autonomous myeloproliferative disorder in mice that recapitulated essential characteristics of human CMML. TIF1γ was almost undetectable in leukemic ce…

MaleAgingAntimetabolites AntineoplasticTumor suppressor geneCellular differentiationMolecular Sequence DataChronic myelomonocytic leukemiaReceptor Macrophage Colony-Stimulating FactorBiologyDecitabinechemistry.chemical_compoundMicemedicineAnimalsHumansGenes Tumor SuppressorPromoter Regions GeneticTranscription factorAgedAged 80 and overMice KnockoutBase SequenceGene Expression Regulation LeukemicCell DifferentiationLeukemia Myelomonocytic ChronicGeneral MedicineDNA MethylationMiddle Agedmedicine.diseaseTRIM33Hematopoietic Stem CellsMolecular biologyDemethylating agentHematopoiesisNeoplasm ProteinsSpecific Pathogen-Free OrganismsHaematopoiesischemistryDNA methylationCancer researchAzacitidineFemaleTranscription FactorsResearch ArticleThe Journal of clinical investigation
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SPRED1, a RAS MAPK pathway inhibitor that causes Legius syndrome, is a tumour suppressor downregulated in paediatric acute myeloblastic leukaemia

2013

Constitutional dominant loss-of-function mutations in the SPRED1 gene cause a rare phenotype referred as neurofibromatosis type 1 (NF1)-like syndrome or Legius syndrome, consisted of multiple café-au-lait macules, axillary freckling, learning disabilities and macrocephaly. SPRED1 is a negative regulator of the RAS MAPK pathway and can interact with neurofibromin, the NF1 gene product. Individuals with NF1 have a higher risk of haematological malignancies. SPRED1 is highly expressed in haematopoietic cells and negatively regulates haematopoiesis. SPRED1 seemed to be a good candidate for leukaemia predisposition or transformation. We performed SPRED1 mutation screening and expression status i…

MaleCancer ResearchAdolescentLoss of HeterozygosityFrameshift mutationGene productLoss of heterozygosityPrecursor B-Cell Lymphoblastic Leukemia-Lymphomahemic and lymphatic diseasesGeneticsmedicineHumansGenes Tumor SuppressorNeurofibromatosisChildMolecular BiologyAdaptor Proteins Signal TransducingLegius syndromeNeurofibromin 1biologyCafe-au-Lait SpotsInfant NewbornIntracellular Signaling Peptides and ProteinsMacrocephalyInfantMembrane Proteinsmedicine.diseaseNeurofibromin 1Gene Expression Regulation NeoplasticLeukemia Myeloid AcuteHaematopoiesisGenes rasChild PreschoolMutationCancer researchbiology.proteinFemalemedicine.symptomOncogene
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Whole-exome sequencing and targeted gene sequencing provide insights into the role of PALB2 as a male breast cancer susceptibility gene

2016

Male breast cancer (MBC) is a rare disease whose etiology appears to be largely associated with genetic factors. BRCA1 and BRCA2 mutations account for about 10% of all MBC cases. Thus, a fraction of MBC cases are expected to be due to genetic factors not yet identified. To further explain the genetic susceptibility for MBC, whole-exome sequencing (WES) and targeted gene sequencing were applied to high-risk, BRCA1/2 mutation-negative MBC cases.Germ-line DNA of 1 male and 2 female BRCA1/2 mutation-negative breast cancer (BC) cases from a pedigree showing a first-degree family history of MBC was analyzed with WES. Targeted gene sequencing for the validation of WES results was performed for 48 …

MaleCancer ResearchDNA Mutational AnalysisBreast NeoplasmsBreast Neoplasms MaleDNA Mutational AnalysiGenetic susceptibility; Male breast cancer; N-acetyltransferase 1 (NAT1); Partner and localizer of BRCA2 (PALB2); Whole-exome sequencing; Oncology; Cancer ResearchGenetic susceptibilityHumansExomeGenetic Predisposition to DiseaseN-acetyltransferase 1 (NAT1)genetic susceptibility; male breast cancer; N-acetyltransferase 1 (NAT1); partner and localizer of BRCA2 (PALB2); whole-exome sequencing; BRCA1 Protein; BRCA2 Protein; Breast Neoplasms; Breast Neoplasms Male; Case-Control Studies; DNA Mutational Analysis; Exome; Fanconi Anemia Complementation Group N Protein; Female; Genetic Predisposition to Disease; Humans; Italy; Male; Mutation; Nuclear Proteins; Pedigree; Tumor Suppressor Proteins; Oncology; Cancer ResearchNuclear ProteinBRCA2 ProteinTumor Suppressor ProteinBRCA1 ProteinTumor Suppressor ProteinsPartner and localizer of BRCA2 (PALB2)Nuclear ProteinsPedigreeMale breast cancerItalyOncologyCase-Control StudiesWhole-exome sequencingMutationFemaleCase-Control StudieFanconi Anemia Complementation Group N ProteinBreast NeoplasmHuman
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The associated expression of Maspin and Bax proteins as a potential prognostic factor in intrahepatic cholangiocarcinoma

2006

Abstract Background Maspin, a member of the serpin family, is a suppressor of tumor growth, an inhibitor of angiogenesis and an inducer of apoptosis. Maspin induces apoptosis by increasing Bax, a member of the Bcl-2 family of apoptosis-regulating proteins. In this exploratory study, we investigated the associated expression of Maspin and Bax proteins as a potential prognostic factor in intrahepatic cholangiocarcinoma (IHCCA). Methods Twenty-two paraffin-embedded samples were analyzed by immunohistochemical methods using Maspin, Bax and CD34 antibodies. Maspin was scored semiquantitatively (HSCORE). Apoptosis was assessed using an antibody against cleaved caspase-3. Results The strong relati…

MaleCancer ResearchPathologymedicine.medical_specialtyAngiogenesisApoptosisCaspase 3Kaplan-Meier EstimateSerpinlcsh:RC254-282law.inventionCholangiocarcinomaBcl-2-associated X proteinlawBiomarkers TumorGeneticsmedicineHumansGenes Tumor SuppressorSerpinsIntrahepatic CholangiocarcinomaAgedbcl-2-Associated X ProteinbiologyCaspase 3business.industryMicrocirculationLiver NeoplasmsMaspinMiddle AgedPrognosislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensNeoplasm ProteinsEnzyme ActivationOncologyApoptosisCancer researchbiology.proteinSuppressorFemalebusinessResearch ArticleBMC Cancer
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