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  • Catecholamines  (2)
  • GENE-EXPRESSION  (2)
  • 1
    Keywords: brain ; GENE-EXPRESSION ; HYBRIDIZATION ; TUMORS ; UNITED-STATES ; GLIOMAS ; MULTIFORME ; temozolomide ; CODON 132 MUTATION ; IDH2 MUTATIONS
    Abstract: The prognosis of glioblastoma, the most malignant type of glioma, is still poor, with only a minority of patients showing long-term survival of more than three years after diagnosis. To elucidate the molecular aberrations in glioblastomas of long-term survivors, we performed genome- and/or transcriptome-wide molecular profiling of glioblastoma samples from 94 patients, including 28 long-term survivors with 〉36 months overall survival (OS), 20 short-term survivors with 〈12 months OS and 46 patients with intermediate OS. Integrative bioinformatic analyses were used to characterize molecular aberrations in the distinct survival groups considering established molecular markers such as isocitrate dehydrogenase 1 or 2 (IDH1/2) mutations, and O(6) -methylguanine DNA methyltransferase (MGMT) promoter methylation. Patients with long-term survival were younger and more often had IDH1/2-mutant and MGMT-methylated tumors. Gene expression profiling revealed over-representation of a distinct (proneural-like) expression signature in long-term survivors that was linked to IDH1/2 mutation. However, IDH1/2-wildtype glioblastomas from long-term survivors did not show distinct gene expression profiles and included proneural, classical and mesenchymal glioblastoma subtypes. Genomic imbalances also differed between IDH1/2-mutant and IDH1/2-wildtype tumors, but not between survival groups of IDH1/2-wildtype patients. Thus, our data support an important role for MGMT promoter methylation and IDH1/2 mutation in glioblastoma long-term survival and corroborate the association of IDH1/2 mutation with distinct genomic and transcriptional profiles. Importantly, however, IDH1/2-wildtype glioblastomas in our cohort of long-term survivors lacked distinctive DNA copy number changes and gene expression signatures, indicating that other factors might have been responsible for long survival in this particular subgroup of patients.(c) 2014 UICC.
    Type of Publication: Journal article published
    PubMed ID: 24615357
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  • 2
    Keywords: GENE-EXPRESSION ; MALIGNANT GLIOMAS ; GLIOBLASTOMA ; ASTROCYTIC TUMORS ; PHASE-III TRIAL ; IDH1 mutation ; ANAPLASTIC OLIGODENDROGLIOMA ; MGMT PROMOTER METHYLATION ; FREQUENT ATRX ; ADJUVANT PROCARBAZINE
    Abstract: Cerebral gliomas of World Health Organization (WHO) grade II and III represent a major challenge in terms of histological classification and clinical management. Here, we asked whether large-scale genomic and transcriptomic profiling improves the definition of prognostically distinct entities. We performed microarray-based genome- and transcriptome-wide analyses of primary tumor samples from a prospective German Glioma Network cohort of 137 patients with cerebral gliomas, including 61 WHO grade II and 76 WHO grade III tumors. Integrative bioinformatic analyses were employed to define molecular subgroups, which were then related to histology, molecular biomarkers, including isocitrate dehydrogenase 1 or 2 (IDH1/2) mutation, 1p/19q co-deletion and telomerase reverse transcriptase (TERT) promoter mutations, and patient outcome. Genomic profiling identified five distinct glioma groups, including three IDH1/2 mutant and two IDH1/2 wild-type groups. Expression profiling revealed evidence for eight transcriptionally different groups (five IDH1/2 mutant, three IDH1/2 wild type), which were only partially linked to the genomic groups. Correlation of DNA-based molecular stratification with clinical outcome allowed to define three major prognostic groups with characteristic genomic aberrations. The best prognosis was found in patients with IDH1/2 mutant and 1p/19q co-deleted tumors. Patients with IDH1/2 wild-type gliomas and glioblastoma-like genomic alterations, including gain on chromosome arm 7q (+7q), loss on chromosome arm 10q (-10q), TERT promoter mutation and oncogene amplification, displayed the worst outcome. Intermediate survival was seen in patients with IDH1/2 mutant, but 1p/19q intact, mostly astrocytic gliomas, and in patients with IDH1/2 wild-type gliomas lacking the +7q/-10q genotype and TERT promoter mutation. This molecular subgrouping stratified patients into prognostically distinct groups better than histological classification. Addition of gene expression data to this genomic classifier did not further improve prognostic stratification. In summary, DNA-based molecular profiling of WHO grade II and III gliomas distinguishes biologically distinct tumor groups and provides prognostically relevant information beyond histological classification as well as IDH1/2 mutation and 1p/19q co-deletion status.
    Type of Publication: Journal article published
    PubMed ID: 25783747
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  • 3
    ISSN: 1432-1440
    Keywords: Catecholamines ; Octopamine ; Hepatic coma ; Sympathetic nervous system ; Katecholamine ; Octopamin ; Coma hepaticum ; Sympathisches Nervensystem
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Plasmaspiegel von Adrenalin, Noradrenalin und Octopamin wurden mit Hilfe radioenzymatischer Methoden bei neun ambulanten Zirrhose-Patienten mit Enzephalopathie und bei zehn Patienten im Coma hepaticum (Comagrad III–IV) bestimmt. Bei den Zirrhose-Patienten wurden sowohl normale als auch erhöhte Plasmaspiegel von Noradrenalin gemessen. Octopamin war im Plasma dieser Patienten sowie bei zehn gesunden Kontrollpersonen nicht nachweisbar. Erhöhte Noradrenalinspiegel im Plasma waren bei allen Patienten im Coma hepaticum vorhanden. Die Noradrenalinkonzentration im Plasma blieb auch während des Comaverlaufes erhöht oder stieg weiter an. Der Adrenalinplasmaspiegel war hingegen nicht regelmäßig erhöht. In acht der zehn Patienten war Octopamin wiederum nicht nachweisbar. Nur bei zwei Coma-Patienten konnten Octopaminspiegel bis zu 59,5 ng/ml bei gleichzeitiger Erhöhung der Noradrenalinkonzentration gefunden werden. Die Infusion der verzweigtkettigen Aminosäure L-Valin beeinflußte weder den Noradrenalin- noch den Octopaminspiegel. Die Ergebnisse sprechen dafür, daß die Aktivität des sympathischen Nervensystems im Coma hepaticum erhöht ist. Eine Akkumulierung von Octopamin ist kein charakteristischer Befund bei chronischer Lebererkrankung und hepatischem Coma. Nachdem bei zwei Coma-Patienten die Akkumulierung von Octopamin bei einer gleichzeitigen Erhöhung des Noradrenalinspiegels auftrat, erscheint eine Verdrängung von Noradrenalin durch den falschen Neurotransmitter Octopamin im noradrenergen Neuron des peripheren Sympathikus unwahrscheinlich. Die Resultate sprechen dafür, daß die Entwicklung einer Hypotension im Rahmen der Leberzirrhose und des Coma hepaticum nicht auf einen Mangel an Noradrenalin zurückzuführen ist.
    Notes: Summary Plasma levels of adrenaline, noradrenaline and octopamine were estimated by a radioenzymatic method in nine cirrhotic outpatients with encephalopathy and in ten patients with hepatic coma (coma grade III–IV). In the cirrhotic outpatients normal as well as elevated plasma levels of noradrenaline were found. Octopamine could not be detected in the plasma of these patients as well as of ten healthy volunteers. Elevated noradrenaline levels were present in all patients with hepatic coma. Plasma noradrenaline remained elevated or even further increased during the course of hepatic coma, whereas adrenaline was elevated less frequently. In eight of the ten patients with hepatic coma octopamine was again not detectable in plasma. Only in two patients high levels of octopamine up to 59.5 ng/ml could be found in addition to increased noradrenaline concentrations. The infusion of the branched chain amino acid L-valine had no influence on the plasma level of either noradrenaline or octopamine. The data indicate that the sympathetic nervous system is activated during the course of hepatic coma. An accumulation of octopamine is not a common finding in chronic liver disease and hepatic coma. Since in the two patients with elevated octopamine levels the rise in octopamine occured concomitantly with a rise in noradrenaline, a displacement of noradrenaline by the false neurotransmitter octopamine in the noradrenergic neuron of the peripheral sympathetic nervous system seems unlikely. The results indicate that the development of hypotension in the course of liver cirrhosis and hepatic coma cannot be related to a deficiency of noradrenaline.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1238
    Keywords: Severe cerebral trauma ; Midbrain syndrome ; Apallic syndrome ; Catecholamines ; Fat oxidation ; Thyroid hormones ; High caloric total parenteral alimentation (TPA)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Urinary catecholamine excretion and thyroid hormone blood level were studied in 16 patients following severe cerebral trauma. Increased excretion rates of epinephrine and norepinephrine were found. There was no significant difference in the catecholamine excretion when compared with generally traumatized patients. The relationships between catecholamine excretion, increased metabolic rates, and negative nitrogen balance indicate that in patients with a midbrain syndrome there exists an additional diencephalic metabolic factor, which leads to a rise in fat oxidation and perpetuation of catabolism. Early high caloric parenteral nutrition seems to inhibit the initial increase of catecholamine excretion and thus protects the body from an unnecessary breakdown of its own reserves. If the course is classified according to neurological stages, it can be shown that patients with a traumatic apallic syndrome in poor condition have a high increase of catecholamine excretion. Secretion of thyroid hormones is not influenced significantly by cerebral trauma.
    Type of Medium: Electronic Resource
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