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Raphael Koch

Researcher at University of Göttingen

Publications -  38
Citations -  1616

Raphael Koch is an academic researcher from University of Göttingen. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 13, co-authored 23 publications receiving 1180 citations. Previous affiliations of Raphael Koch include Harvard University.

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Exosomal evasion of humoral immunotherapy in aggressive B-cell lymphoma modulated by ATP-binding cassette transporter A3

TL;DR: It is shown that lymphoma exosomes shield target cells from antibody attack and that exosome biogenesis is modulated by the lysosome-related organelle-associated ATP-binding cassette (ABC) transporter A3 (ABCA3), and mechanisms of cancer cell resistance to drugs and antibodies are linked in an ABCA3-dependent pathway of exosomal secretion.
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The Public Repository of Xenografts Enables Discovery and Randomized Phase II-like Trials in Mice

Elizabeth C. Townsend, +98 more
- 11 Apr 2016 - 
TL;DR: It is demonstrated that large studies of acute leukemia PDXs that mimic human randomized clinical trials can characterize drug efficacy and generate transcriptional, functional, and proteomic biomarkers in both treatment-naive and relapsed/refractory disease.
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AZD4573 Is a Highly Selective CDK9 Inhibitor That Suppresses MCL-1 and Induces Apoptosis in Hematologic Cancer Cells.

TL;DR: It demonstrated rapid induction of apoptosis and subsequent cell death broadly across hematologic cancer models in vitro, and MCL-1 depletion in a dose- and time-dependent manner was identified as a major mechanism through which AZD4573 induces cell death in tumor cells.
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Intracellular ABC transporter A3 confers multidrug resistance in leukemia cells by lysosomal drug sequestration.

TL;DR: Analysis of the intrinsic drug efflux capacity of leukemic stem cells found the ABC transporter A3 (ABCA3) to be expressed consistently in acute myeloid leukemia (AML) samples and identified subcellular drug sequestration mediated by the genuinely intracellular ABCA3 as being a clinically relevant mechanism of intrinsic MDR.