Search results for "Receptor Protein-Tyrosine Kinases"

showing 4 items of 44 documents

Activation of TRK Genes in Ewingʼs Sarcoma Trk A Receptor Expression Linked to Neural Differentiation

1997

Trk receptors have been identified by immunohistochemical methods in primitive neuroectodermal tumor (PNET)/Ewing's sarcoma (ES). However, the presence of different members of the Trk family of receptors in PNET/ES has not been specified. We have examined whether Trk A, B, and C receptors are specifically expressed in ES both with and without features of neural differentiation. Ten ES tumors (five primary tumors of bone and five extraosseous tumors transplanted into nude mice) were investigated for expression of Trk receptors by immunohistochemistry and reverse transcription-polymerase chain reaction. One primary ES and the five grafted ES tumors exhibited signs of neural differentiation; t…

animal structuresReceptor expressionReceptors Nerve Growth FactorSarcoma EwingBiologyPathology and Forensic MedicineMiceProto-Oncogene ProteinsmedicineAnimalsNeuroectodermal Tumors PrimitiveReceptor trkCReceptor trkAReceptorReceptor Ciliary Neurotrophic FactorMolecular BiologyNeuronsMembrane ProteinsReceptor Protein-Tyrosine KinasesEwing's sarcomaCell DifferentiationCell BiologyProtein-Tyrosine Kinasesmedicine.diseaseMolecular biologyGene Expression Regulation Neoplasticenzymes and coenzymes (carbohydrates)nervous systemTrk receptorPrimitive neuroectodermal tumorembryonic structuresImmunohistochemistrySarcomaImmunostainingDiagnostic Molecular Pathology
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Expression of neurotrophins, GDNF, and their receptors in rat thyroid tissue

1999

Levels of mRNA for neurotrophins (brain-derived neurotrophic factor, BDNF; neurotrophin 3, NT-3; neurotrophin 4, NT-4) and their receptors (trkA, trkB, trkC) and for glial cell line-derived neurotrophic factor (GDNF) and its receptors (ret, GDNFR-alpha) were measured in rat thyroid tissue by ribonuclease protection assays. In thyroid tissue the NT-3 mRNA level was threefold lower and the NT-4 mRNA level sixfold higher than those detected in adult rat hippocampus, while BDNF mRNA was undetectable. Very low levels of mRNA for truncated trkB and trkC receptors and no catalytic trkA, trkB or trkC were found. In conclusion NT-3 and NT-4, but not the corresponding functional receptors, are expres…

endocrine systemmedicine.medical_specialtyGlial Cell Line-Derived Neurotrophic Factor ReceptorsHistologyendocrine system diseasesThyroid GlandGene ExpressionNerve Tissue ProteinsReceptors Nerve Growth FactorNeurotrophin-3Tropomyosin receptor kinase AFollicular cellPathology and Forensic MedicineNeurotrophin 3Proto-Oncogene ProteinsInternal medicinemedicineGlial cell line-derived neurotrophic factorAnimalsDrosophila ProteinsHumansLow-affinity nerve growth factor receptorReceptor trkCGlial Cell Line-Derived Neurotrophic FactorNerve Growth FactorsRNA MessengerReceptor trkAReceptor Ciliary Neurotrophic FactorbiologyBrain-Derived Neurotrophic FactorProto-Oncogene Proteins c-retReceptor Protein-Tyrosine KinasesCell BiologyRatsCell biologyEndocrinologynervous systemProto-Oncogene Proteins c-retbiology.proteinGDNF family of ligandsNeurotrophinCell and Tissue Research
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Aberrant copy numbers of ALK gene is a frequent genetic alteration in neuroblastomas.

2009

A total of 50 neuroblastomas were assessed for frequency of ALK gene copy number aberrations by interphase fluorescence in situ hybridization using a break-apart fluorescence in situ hybridization probe. The data were compared with status of MYCN, 11q, 17q, and 1p36. We observed ALK aberrations (amplification, 1 of 45; gain, 15 of 45 and loss/imbalance, 11 of 45) in a total of 27 (60%) of 45 neuroblastomas. Synchronic MYCN and ALK aberrations accounted for 23 of 45 (51%) tumors; however, MYCN alterations were also detected in 11 (60%) of 18 tumors without ALK aberrations. Our data suggest that copy number aberrations of the ALK gene is a frequent genetic event in the development of neurobla…

medicine.medical_specialtyPathologyGene DosageBiologyPathology and Forensic MedicineNeuroblastomahemic and lymphatic diseasesNeuroblastomamedicineAnaplastic lymphoma kinaseHumansAnaplastic Lymphoma KinaseCopy number aberrationneoplasmsIn Situ Hybridization FluorescenceOncogene ProteinsN-Myc Proto-Oncogene Proteinmedicine.diagnostic_testGenetic AlterationCancerNuclear ProteinsReceptor Protein-Tyrosine KinasesAnatomical pathologyProtein-Tyrosine Kinasesmedicine.diseaseTissue Array AnalysisCancer researchAutonomic neuropathyFluorescence in situ hybridizationHuman 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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