Search results for "Oncogene"

showing 10 items of 1005 documents

Genetic alterations and oxidative metabolism in sporadic colorectal tumors from a Spanish community

1997

Deletions of loci on chromosomes 5q, 17p, 18q, and 22q, together with the incidence of p53 mutations and amplification of the double minute-2 gene were investigated in the sporadic colorectal tumors of 44 patients from a Spanish community. Chromosome deletions were analyzed by means of loss of heterozygosity analysis using a restriction fragment length polymorphism assay. Allelic losses were also detected by polymerase chain reaction (PCR)-single-stranded conformation polymorphism (SSCP) analysis of a polymorphic site in intron 2 of the p53 gene. The percentages of genetic deletions on the screened chromosomes were 39.3% (5q), 58.3% (17p), 40.9% (18q), and 40% (22q). Mutations in p53 exons …

AdultGenetic MarkersMaleGenome instabilityHeterozygoteLipid PeroxidesCancer ResearchChromosomes Human Pair 22DNA Mutational AnalysisAdenocarcinomaBiologymedicine.disease_causeLoss of heterozygosityProto-Oncogene ProteinsGene duplicationmedicineHumansMolecular BiologyGenePolymorphism Single-Stranded ConformationalAgedSequence DeletionGene AmplificationDeoxyguanosineNuclear ProteinsProto-Oncogene Proteins c-mdm2Single-strand conformation polymorphismDNA NeoplasmMiddle AgedGenes p53GlutathioneMolecular biology8-Hydroxy-2'-DeoxyguanosineChromosomes Human Pair 1SpainGenetic markerChromosomes Human Pair 5FemaleRestriction fragment length polymorphismChromosomes Human Pair 18Colorectal NeoplasmsCarcinogenesisOxidation-Reduction
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Phenotypic analysis of individuals with Costello syndrome due to HRAS p.G13C.

2011

Costello syndrome is characterized by severe failure-to-thrive, short stature, cardiac abnormalities (heart defects, tachyarrhythmia, and hypertrophic cardiomyopathy (HCM)), distinctive facial features, a predisposition to papillomata and malignant tumors, postnatal cerebellar overgrowth resulting in Chiari 1 malformation, and cognitive disabilities. De novo germline mutations in the proto-oncogene HRAS cause Costello syndrome. Most mutations affect the glycine residues in position 12 or 13, and more than 80% of patients share p.G12S. To test the hypothesis that subtle genotype-phenotype differences exist, we report the first cohort comparison between 12 Costello syndrome individuals with p…

AdultHeart Defects CongenitalMalemedicine.medical_specialtyAdolescentrasopathy.RASopathyShort statureProto-Oncogene MasArticleProto-Oncogene Proteins p21(ras)Young AdultGermline mutationSettore MED/38 - Pediatria Generale E SpecialisticaCostello syndromePregnancyInternal medicineNeoplasmsGeneticsMedicineHumansHRASChildGenetics (clinical)business.industryloose anagen hairCostello SyndromeMacrocephalyHypertrophic cardiomyopathyBrainInfantgenotype–phenotype correlationmedicine.diseaseDermatologyMagnetic Resonance ImagingMusculoskeletal AbnormalitiesEndocrinologyPhenotypeChild PreschoolFaceMutationFemalemedicine.symptombusinessMultifocal atrial tachycardiaAmerican journal of medical genetics. Part A
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The behaviour of Bcl-2, Bax and Bcl-x in Darier's disease

2002

SummaryBackground Darier's disease (DD) is a rare autosomal dominant disorder of keratinization caused by a mutation of the ATP2A2 gene. There is little information on the behaviour of Bcl-2, Bax and Bcl-x in DD. Objectives To investigate the dynamic control and the behaviour of Bax, Bcl-2 and Bcl-x in DD. We asked whether members of the Bcl-2 family might manifest their effects through modulation of intracellular calcium signalling or whether the gene that encodes the sarco/endoplasmic reticulum Ca2+ ATPase isoform 2 (SERCA2) modulates the Bcl-2 family in the regulation of apoptosis in DD. Methods Immunohistochemical methods were used. Results There was no immunoreactivity for Bcl-2 and Bc…

AdultKeratinocytesMaleGene isoformbcl-X ProteinApoptosisDermatologyBiologymedicine.disease_causeProto-Oncogene ProteinsATP2A2KeratinDarier's diseasemedicineHumansbcl-2-Associated X Proteinchemistry.chemical_classificationMutationEpidermis (botany)Endoplasmic reticulummedicine.diseaseProto-Oncogene Proteins c-bcl-2chemistryApoptosisImmunologyCancer researchFemaleEpidermisDarier DiseaseBritish Journal of Dermatology
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Expression and prognostic significance of insulin‑like growth factor-2 receptor in human hepatocellular carcinoma and the influence of transarterial …

2019

Hepatocellular carcinoma (HCC) is one of the most common human malignancies, the incidence of which is growing worldwide. The prognosis of HCC is very poor and it is often accompanied by a high rate of recurrence. Conventional chemotherapeutic approaches are largely inefficient. In order to develop novel effective methods for the early detection and prognosis of HCC, novel markers and therapeutic targets are urgently required. The present study focused on the effects of the expression of the tumor suppressor gene insulin‑like growth factor‑2 receptor (IGF2R) on patient survival and tumor recurrence in patients with HCC; this study paid specific attention to the influence of transarterial ch…

AdultLiver CirrhosisMale0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyCarcinoma HepatocellularCirrhosisTumor suppressor geneKaplan-Meier EstimatePolymorphism Single NucleotideDisease-Free SurvivalReceptor IGF Type 203 medical and health sciences0302 clinical medicineInternal medicinemedicineCarcinomaHumansGenetic Predisposition to DiseaseChemoembolization TherapeuticAgedAged 80 and overOncogenebusiness.industryLiver NeoplasmsCase-control studyCancerGeneral MedicineMiddle AgedPrognosismedicine.diseaseMolecular medicinedigestive system diseases030104 developmental biologyOncologyCase-Control Studies030220 oncology & carcinogenesisHepatocellular carcinomaFemaleNeoplasm Recurrence LocalbusinessFollow-Up StudiesOncology Reports
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Relation of early tumor shrinkage (ETS) observed in first‐line treatment to efficacy parameters of subsequent treatment in FIRE‐3 (AIOKRK0306)

2016

We explored the association of early tumor shrinkage (ETS) and non-ETS with efficacy of first-line and consecutive second-line treatment in patients with KRAS wild-type metastatic colorectal cancer treated in FIRE-3. Assessment of tumor shrinkage was based on the sum of longest diameters of target lesions, evaluated after 6 weeks of treatment. Shrinkage was classified as ETS (shrinkage by ≥ 20%), mETS (shrinkage by 0 to20%), mPD (minor progression0 to20%) and PD (progression ≥20%). Overall survival (OS) was 33.2 (95% CI 28.0-38.4) months in ETS patients, while non-ETS was associated with less favorable outcome (mETS 24.0 (95% CI 21.2-26.9) months, mPD 19.0 (95% CI 13.0-25.0) months, PD 12.8…

AdultMale0301 basic medicineCancer Researchmedicine.medical_specialtyBevacizumabColorectal cancerLeucovorinCetuximabKaplan-Meier Estimatemedicine.disease_causeGastroenterologyDisease-Free SurvivalProto-Oncogene Proteins p21(ras)03 medical and health sciences0302 clinical medicineInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansAgedShrinkageCetuximabbusiness.industryRemission InductionTumor shrinkageMiddle Agedmedicine.diseaseBevacizumabTreatment Outcome030104 developmental biologyOncologyFluorouracil030220 oncology & carcinogenesisFOLFIRICamptothecinFemaleFluorouracilKRASColorectal Neoplasmsbusinessmedicine.drugInternational Journal of Cancer
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Determination of somatic oncogenic mutations linked to target-based therapies using MassARRAY technology

2016

Somatic mutation analysis represents a useful tool in selecting personalized therapy. The aim of our study was to determine the presence of common genetic events affecting actionable oncogenes using a MassARRAY technology in patients with advanced solid tumors who were potential candidates for target-based therapies. The analysis of 238 mutations across 19 oncogenes was performed in 197 formalin-fixed paraffin-embedded samples of different tumors using the OncoCarta Panel v1.0 (Sequenom Hamburg, Germany). Of the 197 specimens, 97 (49.2%) presented at least one mutation. Forty-nine different oncogenic mutations in 16 genes were detected. Mutations in KRAS and PIK3CA were detected in 40/97 (4…

AdultMale0301 basic medicineOncologymedicine.medical_specialtyColorectal cancersomatic oncogene mutationsDNA Mutational Analysismedicine.disease_cause03 medical and health sciences0302 clinical medicineGermline mutationNeoplasmsInternal medicineHumansMedicineoncocartaPrecision MedicineGeneAgedAged 80 and overGeneticsMutationbusiness.industryHigh-Throughput Nucleotide Sequencingpersonalized medicineMiddle AgedPrecision medicinemedicine.diseaseClinical trial030104 developmental biologyOncologySpectrometry Mass Matrix-Assisted Laser Desorption-Ionization030220 oncology & carcinogenesisFemalePersonalized medicineKRASbusinessResearch PaperOncotarget
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Elevated levels of Bcl-3 inhibits Treg development and function resulting in spontaneous colitis

2017

Bcl-3 is an atypical NF-κB family member that regulates NF-κB-dependent gene expression in effector T cells, but a cell-intrinsic function in regulatory T (Treg) cells and colitis is not clear. Here we show that Bcl-3 expression levels in colonic T cells correlate with disease manifestation in patients with inflammatory bowel disease. Mice with T-cell-specific overexpression of Bcl-3 develop severe colitis that can be attributed to defective Treg cell development and function, leading to the infiltration of immune cells such as pro-inflammatory γδT cells, but not αβ T cells. In Treg cells, Bcl-3 associates directly with NF-κB p50 to inhibit DNA binding of p50/p50 and p50/p65 NF-κB dimers, t…

AdultMale0301 basic medicineP50ScienceGeneral Physics and AstronomyBiologyT-Lymphocytes RegulatoryInflammatory bowel diseaseArticleGeneral Biochemistry Genetics and Molecular BiologyYoung Adult03 medical and health sciences0302 clinical medicineImmune systemB-Cell Lymphoma 3 ProteinProto-Oncogene ProteinsGene expressionmedicineAnimalsHumansColitisMice KnockoutRegulation of gene expressionMultidisciplinaryEffectorHEK 293 cellsQNF-kappa BTranscription Factor RelANF-kappa B p50 SubunitGeneral ChemistryMiddle AgedColitismedicine.diseaseMice Inbred C57BLHEK293 Cells030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisImmunologyFemaleProtein BindingTranscription FactorsNature Communications
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A First-in-Human Phase I Study of the ATP-Competitive AKT Inhibitor Ipatasertib Demonstrates Robust and Safe Targeting of AKT in Patients with Solid …

2016

Abstract Activation of AKT signaling by PTEN loss or PIK3CA mutations occurs frequently in human cancers, but targeting AKT has been difficult due to the mechanism-based toxicities of inhibitors that target the inactive conformation of AKT. Ipatasertib (GDC-0068) is a novel selective ATP-competitive small-molecule inhibitor of AKT that preferentially targets active phosphorylated AKT (pAKT) and is potent in cell lines with evidence of AKT activation. In this phase I study, ipatasertib was well tolerated; most adverse events were gastrointestinal and grade 1–2 in severity. The exposures of ipatasertib ≥200 mg daily in patients correlated with preclinical TGI90, and pharmacodynamic studies co…

AdultMale0301 basic medicineProto-Oncogene Proteins c-aktAdministration OralPharmacologyIpatasertibDrug Administration SchedulePiperazines03 medical and health sciences0302 clinical medicineCell Line TumorNeoplasmsHumansPTENMedicineProtein Kinase InhibitorsProtein kinase BPI3K/AKT/mTOR pathwayAgedbiologybusiness.industryMiddle AgedXenograft Model Antitumor AssaysSmall moleculePyrimidines030104 developmental biologyOncologyCell culture030220 oncology & carcinogenesisPharmacodynamicsbiology.proteinFemalebusinessProto-Oncogene Proteins c-akt
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A constitutive BCL2 down-regulation aggravates the phenotype of PKD1-mutant-induced polycystic kidney disease

2017

IF 5.340; International audience; The main identified function of BCL2 protein is to prevent cell death by apoptosis. Mice knock-out for Bcl2 demonstrate growth retardation, severe polycystic kidney disease (PKD), gray hair and lymphopenia, and die prematurely after birth. Here, we report a 40-year-old male referred to for abdominal and thoracic aortic dissection with associated aortic root aneurysm, PKD, lymphocytopenia with a history of T cell lymphoblastic lymphoma, white hair since the age of 20, and learning difficulties. PKD, which was also detected in the father and sister, was related to an inherited PKD1 mutation. The combination of PKD with gray hair and lymphocytopenia was also r…

AdultMale0301 basic medicineTRPP Cation Channelsphenotypebcl2 geneBiologymicro rnaMice03 medical and health sciencesdown-regulationsymptom aggravating factorshemic and lymphatic diseasest-lymphocyteGene expressionGeneticsmedicinePolycystic kidney diseaseAnimalsHumansGenetic Predisposition to Disease[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsgenesMolecular BiologyGeneGenetics (clinical)Exome sequencingMice KnockoutPKD1apoptosisExonsGeneral MedicinePolycystic Kidney Autosomal Dominantmedicine.diseasePhenotypePedigreeUp-Regulation3. Good healthMicroRNAs030104 developmental biologyMRNA SequencingProto-Oncogene Proteins c-bcl-2[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsImmunologyCancer researchLymphocytopeniapolycystic kidney diseasesbcl-2 proteinHuman Molecular Genetics
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Single-Nucleotide Polymorphism Array-Based Karyotyping of Acute Promyelocytic Leukemia

2014

Acute promyelocytic leukemia (APL) is characterized by the t(15;17)(q22;q21), but additional chromosomal abnormalities (ACA) and other rearrangements can contribute in the development of the whole leukemic phenotype. We hypothesized that some ACA not detected by conventional techniques may be informative of the onset of APL. We performed the high-resolution SNP array (SNP-A) 6.0 (Affymetrix) in 48 patients diagnosed with APL on matched diagnosis and remission sample. Forty-six abnormalities were found as an acquired event in 23 patients (48%): 22 duplications, 23 deletions and 1 Copy-Neutral Loss of Heterozygocity (CN-LOH), being a duplication of 8(q24) (23%) and a deletion of 7(q33-qter) (…

AdultMaleAcute promyelocytic leukemiamedicine.medical_specialtyAdolescentOncogene Proteins FusionMicroarrayslcsh:MedicineLoss of HeterozygosityChromosomal translocationBiologyResearch and Analysis MethodsPolymorphism Single NucleotideTranslocation GeneticHematologic Cancers and Related DisordersLoss of heterozygosityYoung AdultLeukemia Promyelocytic AcuteLeukemiasGene duplicationMedicine and Health SciencesmedicineHumanslcsh:ScienceAgedChromosome AberrationsChromosomes Human Pair 15Multidisciplinarylcsh:RBreakpointCytogeneticsBiology and Life SciencesComputational BiologyHematologyMiddle AgedPrognosismedicine.diseaseMolecular biologyLeukemiaBioassays and Physiological AnalysisKaryotypingCancer researchlcsh:QFemaleResearch ArticleChromosomes Human Pair 17SNP arrayPLoS ONE
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