Search results for "Proto-Oncogenes"

showing 7 items of 7 documents

The MDS and EVI1 complex locus (MECOM) isoforms regulate their own transcription and have different roles in the transformation of hematopoietic stem…

2016

Transcriptional activation of the EVI1 oncogene (3q26) leads to aggressive forms of human acute myeloid leukemia (AML). However, the mechanism of EVI1-mediated leukemogenesis has not been fully elucidated. Previously, by characterizing the EVI1 promoter, we have shown that RUNX1 and ELK1 directly regulate EVI1 transcription. Intriguingly, bioinformatic analysis of the EVI1 promoter region identified the presence of several EVI1 potential binding sites. Thus, we hypothesized that EVI1 could bind to these sites regulating its own transcription. In this study, we show that there is a functional interaction between EVI1 and its promoter, and that the different EVI1 isoforms (EVI1-145kDa, EVI1-Δ…

0301 basic medicineGene isoformMECOMResponse elementBiophysicsBiologyBiochemistryCell LineMice03 medical and health scienceschemistry.chemical_compoundStructural BiologyTranscription (biology)Proto-OncogenesGeneticsAnimalsHumansProgenitor cellPromoter Regions GeneticMolecular BiologyTranscription factorGeneticsLeukemiaGene Expression Regulation LeukemicPromoterHematopoietic Stem CellsMDS1 and EVI1 Complex Locus ProteinCell biologyDNA-Binding ProteinsCell Transformation Neoplastic030104 developmental biologyRUNX1chemistryTranscription FactorsBiochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms
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Novel mutations of the MET proto-oncogene in papillary renal carcinomas.

1999

Hereditary papillary renal carcinoma (HPRC) is characterized by multiple, bilateral papillary renal carcinomas. Previously, we demonstrated missense mutations in the tyrosine kinase domain of the MET proto-oncogene in HPRC and a subset of sporadic papillary renal carcinomas. In this study, we screened a large panel of sporadic papillary renal carcinomas and various solid tumors for mutations in the MET proto-oncogene. Summarizing these and previous results, mutations of the MET proto-oncogene were detected in 17/129 sporadic papillary renal carcinomas but not in other solid tumors. We detected five novel missense mutations; three of five mutations were located in the ATP-binding region of t…

AdenomaModels MolecularCancer ResearchProtein ConformationDNA Mutational AnalysisMolecular Sequence DataHereditary Papillary Renal Cell CarcinomaBiologymedicine.disease_causeTransfectionProto-Oncogene MasReceptor tyrosine kinaseMiceAdenosine TriphosphateNeoplastic Syndromes HereditaryProto-OncogenesGeneticsCarcinomamedicineMissense mutationAnimalsHumansPoint MutationAmino Acid SequencePhosphorylationCodonMolecular BiologyKidneyMutationBinding SitesSequence Homology Amino AcidPoint mutation3T3 CellsDNA NeoplasmProto-Oncogene Proteins c-metmedicine.diseaseCarcinoma PapillaryKidney NeoplasmsNeoplasm Proteinsmedicine.anatomical_structureCell Transformation NeoplasticCancer researchbiology.proteinMutagenesis Site-DirectedTyrosine kinaseProtein Processing Post-TranslationalSequence AlignmentOncogene
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Role of Kras Status in Patients with Metastatic Colorectal Cancer Receiving First-Line Chemotherapy plus Bevacizumab: A TTD Group Cooperative Study

2012

Background: In the MACRO study, patients with metastatic colorectal cancer (mCRC) were randomised to first-line treatment with 6 cycles of capecitabine and oxaliplatin (XELOX) plus bevacizumab followed by either single-agent bevacizumab or XELOX plus bevacizumab until disease progression. An additional retrospective analysis was performed to define the prognostic value of tumour KRAS status on progression-free survival (PFS), overall survival (OS) and response rates. Methodology/Principal Findings: KRAS data (tumour KRAS status and type of mutation) were collected by questionnaire from participating centres that performed KRAS analyses. These data were then cross-referenced with efficacy da…

MaleOncologyOrganoplatinum Compoundsendocrine system diseasesEpidemiologyColorectal cancer:Named Groups::Persons::Age Groups::Adult::Middle Aged [Medical Subject Headings]DeoxycytidineMetastasis:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings]Antineoplastic Combined Chemotherapy ProtocolsPathologyMedicineNeoplasm Metastasisgeneslcsh:Sciencemediana edad:Analytical Diagnostic and Therapeutic Techniques and Equipment::Therapeutics::Clinical Protocols::Antineoplastic Protocols::Antineoplastic Combined Chemotherapy Protocols [Medical Subject Headings]Aged 80 and overanciano:Chemicals and Drugs::Organic Chemicals::Organometallic Compounds::Organoplatinum Compounds [Medical Subject Headings]Cancer Risk FactorsClinical Pharmacologyprotocolos de quimioterapia antineoplásica combinadaColon AdenocarcinomaPronósticoCombination chemotherapyadultoPrognosisBevacizumabOxaliplatinpronósticoOncologyMedicineOncology Agentsmedicine.medical_specialty:Phenomena and Processes::Genetic Phenomena::Genetic Variation::Mutation [Medical Subject Headings]FluorouraciloBevacizumab:Chemicals and Drugs::Heterocyclic Compounds::Heterocyclic Compounds 1-Ring::Pyrimidines::Pyrimidine Nucleosides::Cytidine::Deoxycytidine [Medical Subject Headings]:Check Tags::Male [Medical Subject Headings]Molecular GeneticsCapecitabine:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Blood Proteins::Immunoproteins::Immunoglobulins::Antibodies::Antibodies Monoclonal::Antibodies Monoclonal Humanized [Medical Subject Headings]Gastrointestinal TumorsGenetics:Named Groups::Persons::Age Groups::Adult [Medical Subject Headings]HumansClinical TrialsBiologyneoplasmsCapecitabineAgedlcsh:R:Diseases::Neoplasms::Neoplasms by Site::Digestive System Neoplasms::Gastrointestinal Neoplasms::Intestinal Neoplasms::Colorectal Neoplasms [Medical Subject Headings]:Phenomena and Processes::Genetic Phenomena::Genetic Structures::Genome::Genome Components::Genes::Genes Neoplasm::Oncogenes::Proto-Oncogenes::Genes ras [Medical Subject Headings]medicine.diseasedigestive system diseasesOxaliplatin:Check Tags::Female [Medical Subject Headings]PharmacogeneticsMutationlcsh:QfluorouraciloMultivariate analysisDesoxicitidinahumanosCancer Treatment:Named Groups::Persons::Age Groups::Adult::Aged::Aged 80 and over [Medical Subject Headings]lcsh:Medicinemedicine.disease_causeNeoplasias colorrectalesSurgical oncologyBasic Cancer Research:Chemicals and Drugs::Heterocyclic Compounds::Heterocyclic Compounds 1-Ring::Pyrimidines::Pyrimidinones::Uracil::Fluorouracil [Medical Subject Headings]Clinical Trials (Cancer Treatment)metástasis neoplásicaMetástasis neoplásicaMultidisciplinaryMiddle AgedGenetic EpidemiologyProtocolos de quimioterapia antineoplásica combinadaFemaleAntiangiogenesis TherapyFluorouracilKRASColorectal NeoplasmsResearch Articlemedicine.drugAdultDrugs and DevicesClinical Pathologyneoplasias colorrectalesClinical Research DesignGenetic Causes of CancerAntibodies Monoclonal HumanizedAntibodiesRectal CancerAntibody TherapyDiagnostic MedicineInternal medicine:Diseases::Neoplasms::Neoplastic Processes::Neoplasm Metastasis [Medical Subject Headings]:Named Groups::Persons::Age Groups::Adult::Aged [Medical Subject Headings]mutaciónClinical GeneticsMutaciónbusiness.industryPharmacoepidemiologyCancers and NeoplasmsHuman GeneticsChemotherapy and Drug TreatmentdesoxicitidinaGenes rasanticuerposGenetics of Diseasebusinesscompuestos organoplatinoPLoS ONE
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Differential proto-oncogene mRNA induction from rats treated with peroxisome proliferators

1990

After experimental treatment of rats with clofibrate or ciprofibrate, two peroxisomes proliferators with hypolipidemic activity, RNAs were prepared from liver, kidney, heart and brain; hybridization was done with DNA probes for c-myc and c-Ha-ras oncogenes and for cyanide insensitive Acyl CoA oxidase, a peroxisomal protein. c-myc mRNA is highly abundant in liver and at a lower extent in kidney, especially after treatment with ciprofibrate; clofibrate also allows a c-myc mRNA increase, but at a lower extent. c-Ha-ras, which is already expressed in all tested tissues from control animals, is stimulated by clofibrate and ciprofibrate treatments. Comparatively these compounds stimulate the cyan…

MaleSomatic cellGenes mycBiophysicsBiologyKidneyMicrobodiesBiochemistryClofibric AcidProto-OncogenesmedicineAnimalsAcyl-CoA oxidaseClofibrateRNA MessengerMolecular BiologyHypolipidemic AgentsKidneyMessenger RNAClofibrateOncogeneFibric AcidsCell BiologyPeroxisomeMolecular biologyRats Inbred F344RatsGenes rasmedicine.anatomical_structureGene Expression RegulationLiverOrgan SpecificityAcyl-CoA OxidaseCiprofibrateOxidoreductasesmedicine.drugBiochemical and Biophysical Research Communications
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Morphological, biochemical, and molecular biological characterization of a rat rhabdomyosarcoma cell line during differentiation induction in vitro.

1990

BA-HAN-1C is a clonal rat rhabdomyosarcoma cell line consisting of proliferating mononuclear tumor cells, some of which spontaneously fuse to form terminally differentiated postmitotic myotubelike giant cells. Exposure to retinoic acid resulted in an inhibition of proliferation and a marked increase in cellular differentiation. The number of myotubelike giant cells significantly increased, and about 30% of the mononuclear tumor cells exhibited morphological features of rhabdomyogenic differentiation which were not observed in the mononuclear cells of untreated cultures. Morphological differentiation was paralleled by an increase in total creatine kinase activity as a biochemical marker of d…

Proto-OncogenesCell divisionHealth Toxicology and MutagenesisCellular differentiationTretinoinBiologyCell LineTretinoinProto-OncogenesRhabdomyosarcomaTumor Cells CulturedmedicineAnimalsRhabdomyosarcomaPublic Health Environmental and Occupational HealthCell Differentiationmedicine.diseaseMolecular biologyIn vitroRatsGene Expression Regulation NeoplasticCell cultureRat RhabdomyosarcomaCell DivisionResearch Articlemedicine.drugEnvironmental Health Perspectives
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Uniform response of c-raf expression to differentiation induction and inhibition of proliferation in a rat rhabdomyosarcoma cell line

1990

The clonal rat rhabdomyosarcoma cell line BA-HAN-1C is composed of proliferating mononuclear cells, some of which spontaneously fuse to terminally differentiated myotube-like giant cells. Both the induction of differentiation by retinoic acid (RA) and by sodium butyrate (NaBut), as well as the inhibition of proliferation by fetal calf serum (FCS)-depleted medium uniformly resulted in the same effects. There was a significant (p less than 0.001) inhibition of proliferation and induction of cellular differentiation, as evidenced by a significant (p less than 0.05) increase in creatine kinase activity. Furthermore, after exposure to RA-supplemented or FCS-depleted medium, a significant (p less…

medicine.medical_specialtyCellular differentiationRetinoic acidTretinoinBiologyPeripheral blood mononuclear cellCell Fusionchemistry.chemical_compoundInternal medicineProto-OncogenesRhabdomyosarcomaTumor Cells CulturedmedicineAnimalsRNA MessengerRNA Neoplasmc-RafCreatine KinaseMessenger RNACell DifferentiationSodium butyrateBlotting NorthernMolecular biologyRatsGene Expression Regulation NeoplasticButyratesMicroscopy ElectronEndocrinologychemistryGiant cellCell cultureButyric AcidCell DivisionVirchows Archiv B Cell Pathology Including Molecular Pathology
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Specific mutations of the RET proto-oncogene are related to disease phenotype in MEN 2A and FMTC.

1994

We have analysed 118 families with inherited medullary thyroid carcinoma (MTC) for mutations of the RET proto-oncogene. These included cases of multiple endocrine neoplasia types 2A (MEN 2A) and 2B (MEN 2B) and familial MTC (FMTC). Mutations at one of 5 cysteines in the extracellular domain were found in 97% of patients with MEN 2A and 86% with FMTC but not in MEN 2B patients or normal controls. 84% of the MEN2A mutations affected codon 634. MEN 2A patients with a Cys634 to Arg substitution had a greater risk of developing parathyroid disease than those with other codon 634 mutations. Our data show a strong correlation between disease phenotype and the nature and position of the RET mutatio…

medicine.medical_specialtyendocrine system diseasesOncogene RETDNA Mutational AnalysisMolecular Sequence DataMultiple endocrine neoplasia type 2RET proto-oncogeneBiologymedicine.disease_causeProto-Oncogene MasInternal medicineProto-Oncogene ProteinsProto-OncogenesGeneticsmedicineDrosophila ProteinsHumansPoint MutationThyroid NeoplasmsMultiple endocrine neoplasiaDNA PrimersMutationBase SequencePoint mutationMultiple Endocrine NeoplasiaProto-Oncogene Proteins c-retReceptor Protein-Tyrosine KinasesExonsmedicine.diseasePhenotypeEndocrinologyPhenotypeProto-Oncogene Proteins c-retCarcinoma MedullaryCancer researchNature genetics
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