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Jörn D. Beck

Researcher at University of Erlangen-Nuremberg

Publications -  47
Citations -  2019

Jörn D. Beck is an academic researcher from University of Erlangen-Nuremberg. The author has contributed to research in topics: Breakpoint & Gene. The author has an hindex of 22, co-authored 47 publications receiving 1921 citations. Previous affiliations of Jörn D. Beck include University of Hamburg.

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Malignant peripheral neuroectodermal tumors. A retrospective analysis of 42 patients.

TL;DR: In patients with primary chemotherapy after biopsy‐proven diagnosis, the responsiveness of this disease to chemotherapy could be demonstrated, and Combination chemotherapy containing anthracyclines and high doses of alkylating agents appeared superior.
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CNS late-effects after ALL therapy in childhood. Part III: neuropsychological performance in long-term survivors of childhood ALL: impairments of concentration, attention, and memory.

TL;DR: The neuropsychological function is defined and which central nervous system functions are impaired following the German ALL-BFM and COALL protocols for CNS-negative patients are described to support the strategy of avoiding prophylactic CNS irradiation in low risk patients.
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High-dose methotrexate in pediatric acute lymphoblastic leukemia: impact of ABCC2 polymorphisms on plasma concentrations.

TL;DR: The adenosine triphosphate‐binding cassette (ABC) class transporter ABCC2 (MRP2 [multidrug resistance related protein 2] or cMOAT [canalicular multispecific organic anion transporter]).
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Osteonecrosis: a treatment related toxicity in childhood acute lymphoblastic leukemia (ALL)--experiences from trial ALL-BFM 95.

TL;DR: A group‐wide evaluation was performed to determine incidence, risk factors, and morbidity for ON, due to spontaneous reporting of affected patients with ON.
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Exon/intron structure of the human ALL‐1 (MLL) gene involved in translocations to chromosomal region 11q23 and acute leukaemias

TL;DR: A set of genomic fragments was isolated that represent a total of 35 exons encompassing > 95% of the protein‐coding region and the 3′‐non‐translated region of the All‐1 gene and form the basis for a greater understanding of the translocations and other structural alterations of the gene that conserve the open reading frame and thus produce presumably oncogenic variants of the ALL‐1 protein.