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Andreas E. Kulozik

Researcher at Heidelberg University

Publications -  287
Citations -  27425

Andreas E. Kulozik is an academic researcher from Heidelberg University. The author has contributed to research in topics: Nonsense-mediated decay & Gene. The author has an hindex of 71, co-authored 269 publications receiving 22982 citations. Previous affiliations of Andreas E. Kulozik include University Hospital Heidelberg & Boston Children's Hospital.

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Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma

Jeremy Schwartzentruber, +66 more
- 09 Feb 2012 - 
TL;DR: The presence of H3F3A/ATRX-DAXX/TP53 mutations was strongly associated with alternative lengthening of telomeres and specific gene expression profiles, suggesting that defects of the chromatin architecture underlie paediatric and young adult GBM pathogenesis.
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DNA methylation-based classification of central nervous system tumours

David Capper, +171 more
- 22 Mar 2018 - 
TL;DR: This work presents a comprehensive approach for the DNA methylation-based classification of central nervous system tumours across all entities and age groups, and shows that the availability of this method may have a substantial impact on diagnostic precision compared to standard methods.
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Hotspot mutations in H3F3A and IDH1 define distinct epigenetic and biological subgroups of glioblastoma.

Dominik Sturm, +82 more
- 16 Oct 2012 - 
TL;DR: It is demonstrated that each H3F3A mutation defines an epigenetic subgroup of GBM with a distinct global methylation pattern, and that they are mutually exclusive with IDH1 mutations, which characterize a third mutation-defined subgroup.
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The landscape of genomic alterations across childhood cancers

Susanne Gröbner, +185 more
- 15 Mar 2018 - 
TL;DR: The data suggest that 7–8% of the children in this cohort carry an unambiguous predisposing germline variant and that nearly 50% of paediatric neoplasms harbour a potentially druggable event, which is highly relevant for the design of future clinical trials.
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A perfect message : RNA surveillance and nonsense-mediated decay

TL;DR: It is suggested that mutated b-globin mRNA from a thalassemia patient was most of the available evidence can be integrated into a reported to be very low (Chang and Kan, 1979), forecommon model.