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  • AML STUDY-GROUP  (1)
  • Acetylcholine receptor  (1)
  • 1
    Keywords: CANCER ; EXPRESSION ; SURVIVAL ; CELL ; Germany ; GENE ; MARKER ; prognosis ; polymorphism ; single nucleotide polymorphism ; TRIAL ; AGE ; MUTATION ; SNP ; leukemia ; MARKERS ; MUTATIONS ; HIGH-RISK ; GLIOMAS ; GENE-MUTATIONS ; STUDY-GROUP ULM ; ONCOLOGY ; overall survival ; MYELOID-LEUKEMIA ; PROGNOSTIC-FACTOR ; ALLELES ; methods ; PREDICTS ; STEM ; GROUP-B ; outcome ; IDH1 ; CODON 132 ; single nucleotide ; NUCLEOPHOSMIN ; clinical oncology ; AML STUDY-GROUP ; YOUNGER ADULTS 16
    Abstract: Purpose We assessed the prognostic impact of IDH1 R132 mutations and a known single nucleotide polymorphism (SNP) located in the same exon of the IDH1 gene in patients with cytogenetically normal acute myeloid leukemia (CN-AML) in the context of other prognostic markers. Patients and Methods IDH1 exon four was directly sequenced in 275 CN-AML patients from two subsequent AML multicenter treatment trials and 120 healthy volunteers. Moreover, mutations in NPM1, FLT3, CEBPA, and WT1 were analyzed, and mRNA expression of IDH1 was quantified. Results IDH1 R132 mutations were found in 10.9% of CN-AML patients. IDH1 SNP rs11554137 was found in 12% of CN-AML patients and 11.7% of healthy volunteers. IDH1 R132 mutations had no impact on prognosis. In contrast, IDH1 SNP rs11554137 was an adverse prognostic factor for overall survival in univariate and multivariate analysis. Other significant factors were age, NPM1/FLT3 mutational status, WT1 SNP rs16754, and platelet count. The impact of IDH1 SNP rs11554137 was most pronounced in the NPM1/FLT3 high-risk patients (either NPM1 wild-type or FLT3-internal tandem duplication positive). Patients with IDH1 SNP rs11554137 had a higher expression of IDH1 mRNA than patients with two wild-type alleles. Conclusion IDH1 SNP rs11554137 but not IDH1 R132 mutations are associated with an inferior outcome in CN-AML
    Type of Publication: Journal article published
    PubMed ID: 20368538
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  • 2
    ISSN: 1432-0878
    Keywords: Synaptogenesis ; Acetylcholine receptor ; Gangliosides ; Heparan-sulphate protoglycan ; Cholinergic nerve terminal ; Torpedo marmorata
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Synaptogenesis has been studied in the electric organ of embryonic Torpedo marmorata by use of two antisera directed against components of synaptic vesicles (anti-SV) and presynaptic plasma membranes (ap-anti-TSM), respectively. The anti-SV serum was previously shown to recognize a proteoglycan specific for synaptic vesicles. The ap-anti-TSM serum was raised to plasma membranes of synaptosomes derived from the electromotor nerve terminals and affinity-purified on electric-organ gangliosides. The vesicular antigen was first detectable at the 81-mm stage of development, which is 1–2 weeks earlier than the formation of morphologically mature presynaptic terminals, but is coincident with a rise in choline acetyltransferase levels and the ability of the electric organ to generate discharges. The gangliosidic antigen recognized by the ap-anti-TSM was first detectable on the ventral electrocyte surface at the 93-mm stage of development. This indicates that specific carbohydrate epitopes, not present on the growth cones, are expressed during maturation of the nerve terminal. The nerve terminal components recognized by these sera arose pari passu with neurite coverage of the ventral surface of the electrocyte, reaching a maximum in the adult. In contrast, postsynaptic aggregates of acetylcholine receptor, rendered visible with rhodamine-labeled α-bungarotoxin, arose previous to the presynaptic antigens, reaching a maximum surface density at 110 mm and then declining in the adult.
    Type of Medium: Electronic Resource
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