Search results for "Stability."

showing 10 items of 3015 documents

Epidemiological, clinical and molecular characterization of Lynch‐like syndrome: A population‐based study

2019

Colorectal carcinomas that are mismatch repair (MMR)‐deficient in the absence of MLH1 promoter methylation or germline mutations represent Lynch‐like syndrome (LLS). Double somatic events inactivating MMR genes are involved in the etiology of LLS tumors. Our purpose was to define the clinical and broader molecular hallmarks of LLS tumors and the population incidence of LLS, which remain poorly characterized. We investigated 762 consecutive colorectal carcinomas operated in Central Finland in 2000–2010. LLS cases were identified by a stepwise protocol based on MMR protein expression, MLH1 methylation and MMR gene mutation status. LLS tumors were profiled for CpG Island Methylator Phenotype (…

Cancer ResearchMICROSATELLITE INSTABILITYDNA mismatch repairMISMATCH-REPAIR DEFICIENCYGene mutationmedicine.disease_cause0302 clinical medicinelynch syndromeFinlandMolecular Epidemiologyeducation.field_of_studyMutationISLAND METHYLATOR PHENOTYPENONPOLYPOSIS COLORECTAL-CANCERlynch-like syndromeTUMORSLynch syndrome3. Good healthOncology030220 oncology & carcinogenesissyöpätauditColorectal NeoplasmsMutL Protein Homolog 1Lynch-like syndromeAdult3122 CancersPopulationsuolistosyövätCpG island methylator phenotypeBiologyta3111FREQUENCYMLH103 medical and health sciencesGermline mutationcolorectal carcinomaBRAF MUTATIONCOLONmedicineHumansLynchin oireyhtymäeducationneoplasmsMSIAgedRetrospective StudiesCpG Island Methylator PhenotypeMicrosatellite instabilityDNASOMATIC MUTATIONSta3122CpG Island Methylator phenotypemedicine.diseaseColorectal Neoplasms Hereditary Nonpolyposisdigestive system diseasesCOPY NUMBERMutationCancer researchInternational Journal of Cancer
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Labeling and preliminary in vivo assessment of niobium-labeled radioactive species: A proof-of-concept study.

2016

Abstract The application of radionuclide-labeled biomolecules such as monoclonal antibodies or antibody fragments for imaging purposes is called immunoscintigraphy . More specifically, when the nuclides used are positron emitters, such as zirconium-89, the technique is referred to as immuno-PET . Currently, there is an urgent need for radionuclides with a half-life which correlates well with the biological kinetics of the biomolecules under question and which can be attached to the proteins by robust labeling chemistry. 90 Nb is a promising candidate for in vivo immuno-PET , due its half-life of 14.6h and low β + energy of E mean =0.35MeV per decay. 95 Nb on the other hand, is a convenient …

Cancer ResearchPathologymedicine.medical_specialtyBiodistributionmedicine.drug_classMetaboliteNiobiumDeferoxamineMonoclonal antibody030218 nuclear medicine & medical imagingImmunoscintigraphy03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineChloridesDrug StabilityIn vivomedicineAnimalsRadiology Nuclear Medicine and imagingTissue DistributionRadioisotopesOxalatesChemistryIn vitroBevacizumab030220 oncology & carcinogenesisIsotope LabelingPositron-Emission TomographyBiophysicsMolecular MedicineSpecific activityFemaleEx vivoHalf-LifeNuclear medicine and biology
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Intestinal epithelial HuR modulates distinct pathways of proliferation and apoptosis and attenuates small intestinal and colonic tumor development.

2014

Abstract HuR is a ubiquitous nucleocytoplasmic RNA-binding protein that exerts pleiotropic effects on cell growth and tumorigenesis. In this study, we explored the impact of conditional, tissue-specific genetic deletion of HuR on intestinal growth and tumorigenesis in mice. Mice lacking intestinal expression of HuR (Hur IKO mice) displayed reduced levels of cell proliferation in the small intestine and increased sensitivity to doxorubicin-induced acute intestinal injury, as evidenced by decreased villus height and a compensatory shift in proliferating cells. In the context of Apcmin/+ mice, a transgenic model of intestinal tumorigenesis, intestinal deletion of the HuR gene caused a three-fo…

Cancer ResearchPost-translational regulationRNA-binding proteinContext (language use)ApoptosisCell Growth ProcessesBiologymedicine.disease_causeArticleAU-rich RNAMiceGene expressionIntestinal NeoplasmsmedicineAnimalsmRNA stabilityIntestinal MucosaMice KnockoutCell growthMolecular biologyPhenotypeProtein-RNA interactionSmall intestineDisease Models Animalmedicine.anatomical_structureOncologyELAV ProteinsApoptosisColonic NeoplasmsCancer researchCarcinogenesis
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Desferrioxamine as an appropriate chelator for 90Nb: Comparison of its complexation properties for M-Df-Octreotide (M=Nb, Fe, Ga, Zr)

2014

The niobium-90 radioisotope ((90)Nb) holds considerable promise for use in immuno-PET, due to its decay parameters (t½ = 14.6h, positron yield=53%, Eß(+)(mean) = 0.35 MeV and Eß(+)(max) = 1.5 MeV). In particular, (90)Nb appears well suited to detect in vivo the pharmacokinetics of large targeting vectors (50-150 kDa). In order to be useful for immuno-PET chelators are required to both stabilize the radionuclide in terms of coordination chemistry and to facilitate the covalent attachment to the targeting vector. Different chelators were evaluated for this purpose in terms of radiolabelling efficiency and stability of the radiolabelled Nb(V) complex and in order to determine the most suitable…

Cancer ResearchStereochemistryNiobiumMetal ions in aqueous solutionKineticsOctreotideRadiation DosageCoordination complexTransmetalationDrug StabilityMaterials TestingMoleculeRadiology Nuclear Medicine and imagingChelationChelating AgentsIonsRadioisotopeschemistry.chemical_classificationChemistryMetalsCovalent bondIsotope LabelingMolecular MedicineRadiopharmaceuticalsNuclear chemistryConjugateNuclear Medicine and Biology
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RB acute loss induces centrosome amplification and aneuploidy in murine primary fibroblasts

2006

AbstractBackgroundIncorrect segregation of whole chromosomes or parts of chromosome leads to aneuploidy commonly observed in cancer. The correct centrosome duplication, assuring assembly of a bipolar mitotic spindle, is essential for chromosome segregation fidelity and preventing aneuploidy. Alteration of p53 and pRb functions by expression of HPV16-E6 and E7 oncoproteins has been associated with centrosome amplification. However, these last findings could be the result of targeting cellular proteins in addition to pRb by HPV16-E7 oncoprotein. To get a more detailed picture on the role of pRb in chromosomal instability and centrosome amplification, we analyzed the effects of the acute loss …

Cancer ResearchTime FactorsTranscription GeneticRbCentrosomes AneuploidyGene ExpressionMitosisAneuploidyBiologyRetinoblastoma Proteinlcsh:RC254-282Chromosome segregationMiceChromosome instabilityGene duplicationmedicineAnimalsCentrosome duplicationMitosisCells CulturedCentrosomeResearchGene AmplificationFibroblastsAneuploidylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseSettore BIO/18 - GeneticaSpindle checkpointOncologyCentrosomeCancer researchMolecular MedicineMolecular Cancer
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No evidence of EMAST in whole genome sequencing data from 248 colorectal cancers.

2021

Microsatellite instability (MSI) is caused by defective DNA mismatch repair (MMR), and manifests as accumulation of small insertions and deletions (indels) in short tandem repeats of the genome. Another form of repeat instability, elevated microsatellite alterations at selected tetranucleotide repeats (EMAST), has been suggested to occur in 50% to 60% of colorectal cancer (CRC), of which approximately one quarter are accounted for by MSI. Unlike for MSI, the criteria for defining EMAST is not consensual. EMAST CRCs have been suggested to form a distinct subset of CRCs that has been linked to a higher tumor stage, chronic inflammation, and poor prognosis. EMAST CRCs not exhibiting MSI have b…

Cancer Researchcongenital hereditary and neonatal diseases and abnormalities3122 Cancerscolorectal cancersuolistosyövätBiologymikrosatelliititmedicine.disease_causeGenomeDNA sequencingEMAST03 medical and health sciences0302 clinical medicineINDEL MutationGeneticsmedicineHumansGenetic TestingIndelneoplasmsGeneticsWhole genome sequencingnext generation sequencingMutationDNA-analyysiWhole Genome Sequencing1184 Genetics developmental biology physiologyMicrosatellite instabilitymedicine.diseasedigestive system diseases3. Good health030220 oncology & carcinogenesisgenome sequencing dataMicrosatellitesyöpätauditDNA mismatch repaircolorectal cancersColorectal NeoplasmsMicrosatellite RepeatsGenes, chromosomescancerREFERENCES
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Physiological mechanisms regulating the expression of endothelial-type NO synthase

2002

Although endothelial nitric oxide synthase (eNOS) is a constitutively expressed enzyme, its expression is regulated by a number of biophysical, biochemical, and hormonal stimuli, both under physiological conditions and in pathology. This review summarizes the recent findings in this field. Shear stress, growth factors (such as transforming growth factor-beta, fibroblast growth factor, vascular endothelial growth factor, and platelet-derived growth factor), hormones (such as estrogens, insulin, angiotensin II, and endothelin 1), and other compounds (such as lysophosphatidylcholine) upregulate eNOS expression. On the other hand, the cytokine tumor necrosis factor-alpha and bacterial lipopolys…

Cancer Researchmedicine.medical_specialtyNitric Oxide Synthase Type IIIPhysiologyRNA Stabilitymedicine.medical_treatmentClinical BiochemistryBiologyFibroblast growth factorBiochemistryGene Expression Regulation Enzymologicchemistry.chemical_compoundEnosInternal medicinemedicineAnimalsPromoter Regions GeneticRegulation of gene expressionBase SequenceGene Expression ProfilingGrowth factorbiology.organism_classificationActin cytoskeletonAngiotensin IICell biologyVascular endothelial growth factorEndocrinologychemistryNitric Oxide SynthaseSignal transductionSignal TransductionNitric Oxide
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Metabolic aggressiveness in benign meningiomas with chromosomal instabilities.

2010

Abstract Meningiomas are often considered benign tumors curable by surgery, but most recurrent meningiomas correspond to histologic benign tumors. Because alterations in chromosome 14 among others have suggested clinical aggressiveness and recurrence, determining both the molecular phenotype and the genetic profile may help distinguish tumors with aggressive metabolism. The aim of this study was to achieve higher specificity in the detection of meningioma subgroups by measuring chromosomal instabilities by fluorescence in situ hybridization and cytogenetics and metabolic phenotypes by high-resolution magic angle spinning spectroscopy. We studied 46 meningioma biopsies with these methodologi…

Cancer Researchmedicine.medical_specialtyPathologyMagnetic Resonance SpectroscopyBiologyMeningiomaChromosomal Instabilityotorhinolaryngologic diseasesmedicineMeningeal NeoplasmsTumor Cells CulturedHumansIn Situ Hybridization FluorescenceNeoplasm StagingChromosome Aberrationsmedicine.diagnostic_testCytogeneticsCancerChromosomemedicine.diseasePhenotypenervous system diseasesOncologyApoptosisBenign MeningiomaCytogenetic AnalysisMetabolomeMeningiomaFluorescence in situ hybridizationCancer research
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Cytogenetic analysis and metabolic profiling reveal a subgroup of benign meningiomas with chromosomal instabilities and aggressive metabolism

2010

Meningiomas add up to 30% of Central Nervous System (CNS) tumours. Atypical meningiomas show a high index of recurrence 5 years after complete resection. Sometimes, meningiomas with histological diagnosis of benign meningioma show genetics characteristics of atypical meningioma. Aberrations of chromosomes 1, 14, and 22 are the most frequently reported abnormalities in meningiomas. In this communication we used cytogenetic, FISH, and NMR metabolic profiling for a molecular characterization of a series of 46 meningiomas. Tumor samples were obtained from 46 patients with meningioma (36 benign and 12 atypical) from the Clinic Hospital of Valencia. Cytogenetic analyses were performed by short-te…

Cancer Researchmedicine.medical_specialtyPathologyTissue microarrayKaryotypeBiologymedicine.diseaseBioinformaticsCXCR4nervous system diseasesMeningiomaChromosome instabilityBenign Meningiomaotorhinolaryngologic diseasesGeneticsmedicineHistopathologyRhabdomyosarcomaneoplasmsMolecular BiologyCancer Genetics and Cytogenetics
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Impact of Different Selection Approaches for Identifying Lynch Syndrome-Related Colorectal Cancer Patients: Unity Is Strength

2022

Lynch syndrome (LS) is an inherited genetic condition associated with increased predisposition to colorectal cancer (CRC) and other tumors and is caused by germline mutations in Mismatch Repair (MMR) or EPCAM genes. The identification of LS carriers is currently based on germline testing of subjects with MMR-deficient (dMMR) tumors or fulfilling clinical criteria, but the most efficient strategies to select patients who should be offered genetic testing are yet not well defined. In order to assess the most suitable selection mode to identify LS-related CRC patients, we retrospectively collected and analyzed all clinical and molecular information of 854 CRC patients, recruited from 2013 to 2…

Cancer Researchmismatch repair genesSettore MED/06 - Oncologia MedicaMMR-deficiency[SDV]Life Sciences [q-bio]MLH1Neoplasms. Tumors. Oncology. Including cancer and carcinogenscolorectal cancerdigestive system diseasesMSH2Lynch syndromeOncologygermline mutationsmicrosatellite instabilityRC254-282Frontiers in Oncology
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