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Der deutsche Markt für Venture Capital (VC) ist trotz erfreulicher Fortschritte insbesondere in den letzten drei Jahren im Vergleich zum weltweit größten VC-Markt in den USA unterentwickelt. Venture Capital-Investitionen beliefen sich in Deutschland im Jahr 1996 auf 0,04% des Bruttoinlandsproduktes, weniger als ein Drittel des U.S.-amerikanischen Niveaus. Obwohl seither ein deutlicher Anstieg zu verzeichnen ist, hat der deutsche VC-Markt mit einem Fondsvolumen von ca. 18,6 Milliarden DM nach jüngsten Angaben nur etwa ein Achtel der Größe des amerikanischen Marktes.
Aim: Pharmacoresistance is a major burden in epilepsy treatment. We aimed to identify genetic biomarkers in response to specific antiepileptic drugs (AEDs) in genetic generalized epilepsies (GGE). Materials & methods: We conducted a genome-wide association study (GWAS) of 3.3 million autosomal SNPs in 893 European subjects with GGE – responsive or nonresponsive to lamotrigine, levetiracetam and valproic acid. Results: Our GWAS of AED response revealed suggestive evidence for association at 29 genomic loci (p <10-5) but no significant association reflecting its limited power. The suggestive associations highlight candidate genes that are implicated in epileptogenesis and neurodevelopment. Conclusion: This first GWAS of AED response in GGE provides a comprehensive reference of SNP associations for hypothesis-driven candidate gene analyses in upcoming pharmacogenetic studies.
Burkitt lymphoma (BL) is the most common B-cell lymphoma in children. Within the International Cancer Genome Consortium (ICGC), we performed whole genome and transcriptome sequencing of 39 sporadic BL. Here, we unravel interaction of structural, mutational, and transcriptional changes, which contribute to MYC oncogene dysregulation together with the pathognomonic IG-MYC translocation. Moreover, by mapping IGH translocation breakpoints, we provide evidence that the precursor of at least a subset of BL is a B-cell poised to express IGHA. We describe the landscape of mutations, structural variants, and mutational processes, and identified a series of driver genes in the pathogenesis of BL, which can be targeted by various mechanisms, including IG-non MYC translocations, germline and somatic mutations, fusion transcripts, and alternative splicing.