Harmonization of Biobank Education for Biobank Technicians: Identification of Learning Objectives.

The quality of biospecimens stored in a biobank depends tremendously on the technical personnel responsible for processing, storage, and release of biospecimens. Adequate training of these biobank employees would allow harmonization of correct sample handling and thus ensure a high and comparable quality of samples across biobank locations. However, in Germany there are no specific training opportunities for technical biobank staff.

F-FET PET Imaging in Differentiating Glioma Progression from Treatment-Related Changes: A Single-Center Experience.

In glioma patients, differentiation between tumor progression (TP) and treatment-related changes (TRCs) remains challenging. Difficulties in classifying imaging alterations may result in a delay or an unnecessary discontinuation of treatment. PET using -(2-F-fluoroethyl)-l-tyrosine (F-FET) has been shown to be a useful tool for detecting TP and TRCs.

A nationwide fluidics biobank of polytraumatized patients: implemented by the Network "Trauma Research" (NTF) as an expansion to the TraumaRegister DGU of the German Trauma Society (DGU).

To decrypt the complexity of the posttraumatic immune responses and to potentially identify novel research pathways for exploration, large-scale multi-center projects including not only in vivo and in vitro modeling, but also temporal sample and material collection along with clinical data capture from multiply injured patients is of utmost importance. To meet this gap, a nationwide biobank for fluidic samples from polytraumatized patients was initiated in 2013 by the task force Network "Trauma Research" (Netzwerk Traumaforschung, NTF) of the German Trauma Society (Deutsche Gesellschaft für Unfallchirurgie e.V.

Loss of cell-matrix contact increases hypoxia-inducible factor-dependent transcriptional activity in glioma cells.

In a variety of malignomas, the acquisition of a mesenchymal phenotype has been linked with anchorage-independent growth and invasiveness. To some extent, glioma cells are able to survive a loss of cell-matrix contact. We here describe that non-adherent culture of glioma cells was accompanied by an increase in hypoxia-inducible factor (HIF)-dependent, but not β-catenin/TCF-induced transcription.

Proof-of-Concept Integration of Heterogeneous Biobank IT Infrastructures into a Hybrid Biobanking Network.

Cross-institutional biobank networks hold the promise of supporting medicine by enabling the exchange of associated samples for research purposes. Various initiatives, such as BBMRI-ERIC and German Biobank Node (GBN), aim to interconnect biobanks for enabling the compilation of joint biomaterial collections. However, building software platforms to facilitate such collaboration is challenging due to the heterogeneity of existing biobank IT infrastructures and the necessary efforts for installing and maintaining additional software components.

FOXO3a orchestrates glioma cell responses to starvation conditions and promotes hypoxia-induced cell death.

Forkhead box O (FOXO) transcription factors are homeostatic regulators adjusting diverse cellular processes crucial for metabolism and survival. In gliomas, FOXOs have been shown to modulate cell death, proliferation and differentiation. Here, we investigated the role of FOXO3a in human malignant gliomas with special regard to starvation conditions.

ERGO: a pilot study of ketogenic diet in recurrent glioblastoma.

Limiting dietary carbohydrates inhibits glioma growth in preclinical models. Therefore, the ERGO trial (NCT00575146) examined feasibility of a ketogenic diet in 20 patients with recurrent glioblastoma. Patients were put on a low-carbohydrate, ketogenic diet containing plant oils.

Differential utilization of ketone bodies by neurons and glioma cell lines: a rationale for ketogenic diet as experimental glioma therapy.

Background: Even in the presence of oxygen, malignant cells often highly depend on glycolysis for energy generation, a phenomenon known as the Warburg effect. One strategy targeting this metabolic phenotype is glucose restriction by administration of a high-fat, low-carbohydrate (ketogenic) diet. Under these conditions, ketone bodies are generated serving as an important energy source at least for non-transformed cells.

Antagonism of the mammalian target of rapamycin selectively mediates metabolic effects of epidermal growth factor receptor inhibition and protects human malignant glioma cells from hypoxia-induced cell death.

Although inhibition of the epidermal growth factor receptor is a plausible therapy for malignant gliomas that, in vitro, enhances apoptosis, the results of clinical trials have been disappointing. The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that integrates starvation signals and generates adaptive responses that aim at the maintenance of energy homeostasis. Antagonism of mTOR has been suggested as a strategy to augment the efficacy of epidermal growth factor receptor inhibition by interfering with deregulated signalling cascades downstream of Akt.