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51. Table S4 from The Senescence-associated Secretory Phenotype Mediates Oncogene-induced Senescence in Pediatric Pilocytic Astrocytoma

Author

Buhl, Juliane L., primary, Selt, Florian, primary, Hielscher, Thomas, primary, Guiho, Romain, primary, Ecker, Jonas, primary, Sahm, Felix, primary, Ridinger, Johannes, primary, Riehl, Dennis, primary, Usta, Diren, primary, Ismer, Britta, primary, Sommerkamp, Alexander C., primary, Martinez-Barbera, J.P., primary, Wefers, Annika K., primary, Remke, Marc, primary, Picard, Daniel, primary, Pusch, Stefan, primary, Gronych, Jan, primary, Oehme, Ina, primary, van Tilburg, Cornelis M., primary, Kool, Marcel, primary, Kuhn, Daniela, primary, Capper, David, primary, von Deimling, Andreas, primary, Schuhmann, Martin U., primary, Herold-Mende, Christel, primary, Korshunov, Andrey, primary, Brummer, Tilman, primary, Pfister, Stefan M., primary, Jones, David T.W., primary, Witt, Olaf, primary, and Milde, Till, primary

Published
2023
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52. Supplemental Table Legend from The Senescence-associated Secretory Phenotype Mediates Oncogene-induced Senescence in Pediatric Pilocytic Astrocytoma

Author

Buhl, Juliane L., primary, Selt, Florian, primary, Hielscher, Thomas, primary, Guiho, Romain, primary, Ecker, Jonas, primary, Sahm, Felix, primary, Ridinger, Johannes, primary, Riehl, Dennis, primary, Usta, Diren, primary, Ismer, Britta, primary, Sommerkamp, Alexander C., primary, Martinez-Barbera, J.P., primary, Wefers, Annika K., primary, Remke, Marc, primary, Picard, Daniel, primary, Pusch, Stefan, primary, Gronych, Jan, primary, Oehme, Ina, primary, van Tilburg, Cornelis M., primary, Kool, Marcel, primary, Kuhn, Daniela, primary, Capper, David, primary, von Deimling, Andreas, primary, Schuhmann, Martin U., primary, Herold-Mende, Christel, primary, Korshunov, Andrey, primary, Brummer, Tilman, primary, Pfister, Stefan M., primary, Jones, David T.W., primary, Witt, Olaf, primary, and Milde, Till, primary

Published
2023
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53. Figure S1, Figure S2, Figure S3, Figure S4 from The Senescence-associated Secretory Phenotype Mediates Oncogene-induced Senescence in Pediatric Pilocytic Astrocytoma

Author

Buhl, Juliane L., primary, Selt, Florian, primary, Hielscher, Thomas, primary, Guiho, Romain, primary, Ecker, Jonas, primary, Sahm, Felix, primary, Ridinger, Johannes, primary, Riehl, Dennis, primary, Usta, Diren, primary, Ismer, Britta, primary, Sommerkamp, Alexander C., primary, Martinez-Barbera, J.P., primary, Wefers, Annika K., primary, Remke, Marc, primary, Picard, Daniel, primary, Pusch, Stefan, primary, Gronych, Jan, primary, Oehme, Ina, primary, van Tilburg, Cornelis M., primary, Kool, Marcel, primary, Kuhn, Daniela, primary, Capper, David, primary, von Deimling, Andreas, primary, Schuhmann, Martin U., primary, Herold-Mende, Christel, primary, Korshunov, Andrey, primary, Brummer, Tilman, primary, Pfister, Stefan M., primary, Jones, David T.W., primary, Witt, Olaf, primary, and Milde, Till, primary

Published
2023
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54. Supplementary Materials and Methods from B-Raf Inhibitors Induce Epithelial Differentiation in BRAF-Mutant Colorectal Cancer Cells

Author

Herr, Ricarda, primary, Köhler, Martin, primary, Andrlová, Hana, primary, Weinberg, Florian, primary, Möller, Yvonne, primary, Halbach, Sebastian, primary, Lutz, Lisa, primary, Mastroianni, Justin, primary, Klose, Martin, primary, Bittermann, Nicola, primary, Kowar, Silke, primary, Zeiser, Robert, primary, Olayioye, Monilola A., primary, Lassmann, Silke, primary, Busch, Hauke, primary, Boerries, Melanie, primary, and Brummer, Tilman, primary

Published
2023
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55. Supplementary Table S2 from B-Raf Inhibitors Induce Epithelial Differentiation in BRAF-Mutant Colorectal Cancer Cells

Author

Herr, Ricarda, primary, Köhler, Martin, primary, Andrlová, Hana, primary, Weinberg, Florian, primary, Möller, Yvonne, primary, Halbach, Sebastian, primary, Lutz, Lisa, primary, Mastroianni, Justin, primary, Klose, Martin, primary, Bittermann, Nicola, primary, Kowar, Silke, primary, Zeiser, Robert, primary, Olayioye, Monilola A., primary, Lassmann, Silke, primary, Busch, Hauke, primary, Boerries, Melanie, primary, and Brummer, Tilman, primary

Published
2023
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56. Data from B-Raf Inhibitors Induce Epithelial Differentiation in BRAF-Mutant Colorectal Cancer Cells

Author

Herr, Ricarda, primary, Köhler, Martin, primary, Andrlová, Hana, primary, Weinberg, Florian, primary, Möller, Yvonne, primary, Halbach, Sebastian, primary, Lutz, Lisa, primary, Mastroianni, Justin, primary, Klose, Martin, primary, Bittermann, Nicola, primary, Kowar, Silke, primary, Zeiser, Robert, primary, Olayioye, Monilola A., primary, Lassmann, Silke, primary, Busch, Hauke, primary, Boerries, Melanie, primary, and Brummer, Tilman, primary

Published
2023
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57. Supplementary Figures S1-S8 from B-Raf Inhibitors Induce Epithelial Differentiation in BRAF-Mutant Colorectal Cancer Cells

Author

Herr, Ricarda, primary, Köhler, Martin, primary, Andrlová, Hana, primary, Weinberg, Florian, primary, Möller, Yvonne, primary, Halbach, Sebastian, primary, Lutz, Lisa, primary, Mastroianni, Justin, primary, Klose, Martin, primary, Bittermann, Nicola, primary, Kowar, Silke, primary, Zeiser, Robert, primary, Olayioye, Monilola A., primary, Lassmann, Silke, primary, Busch, Hauke, primary, Boerries, Melanie, primary, and Brummer, Tilman, primary

Published
2023
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58. Supplementary Figure and Table Legend from B-Raf Inhibitors Induce Epithelial Differentiation in BRAF-Mutant Colorectal Cancer Cells

Author

Herr, Ricarda, primary, Köhler, Martin, primary, Andrlová, Hana, primary, Weinberg, Florian, primary, Möller, Yvonne, primary, Halbach, Sebastian, primary, Lutz, Lisa, primary, Mastroianni, Justin, primary, Klose, Martin, primary, Bittermann, Nicola, primary, Kowar, Silke, primary, Zeiser, Robert, primary, Olayioye, Monilola A., primary, Lassmann, Silke, primary, Busch, Hauke, primary, Boerries, Melanie, primary, and Brummer, Tilman, primary

Published
2023
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60. Additional file 2 of Analysis of RAS and drug induced homo- and heterodimerization of RAF and KSR1 proteins in living cells using split Nanoluc luciferase

Author

Rohrer, Lino, Spohr, Corinna, Beha, Carina, Griffin, Ricarda, Braun, Sandra, Halbach, Sebastian, and Brummer, Tilman

Abstract

Additional file 2: Figure S2. Side-by-side comparison of growth factor versus oncogenic KRASG12V induced BRAF-LgBiT/RAF1-SmBIT heterodimerization. HEK293T cells were transfected with either empty pMIGor pMIG/KRASG12V and the empty control vectors pLgBiT-N/pSmBit-N or the BRAF-LgBiT and RAF1-SmBiT expression vectors. Cells were either left untreated or stimulated with 100 ng/ml EGF for the indicated timepoints. Note the EGF induced increase in cells expressing BRAF-LgBiT/RAF1-SmBiT that is absent in cells transfected with the empty control vectors. Also note the consistent and highly significant increase in Nluc activity in unstimulated KRASG12V expressing cells compared to EGF stimulated cells transfected with pMIG e.V.

Published
2023
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61. Additional file 3 of Analysis of RAS and drug induced homo- and heterodimerization of RAF and KSR1 proteins in living cells using split Nanoluc luciferase

Author

Rohrer, Lino, Spohr, Corinna, Beha, Carina, Griffin, Ricarda, Braun, Sandra, Halbach, Sebastian, and Brummer, Tilman

Abstract

Additional file 3: Figure S3. Effects of more complex DIF mutations in BRAF on its heterodimerization with RAF1. HEK293T cells were transfected with either empty pLgBiT-N/pSmBiT-N control plasmidsor expression vectors encoding RAF1WT-SmBiT and the indicated BRAF-LgBiT proteins, either in combination with pMIG e.V.or pMIG KRASG12V. Cells were either treated with 10 µM Sorafenib or DMSO for 4 h prior to measurement. Shown is the mean of three to four biological replicates. HEK293T cells were transfected with either empty pLgBiT-N/pSmBiT-N control plasmids or expression vectors encoding RAF1WT-SmBiT and the indicated BRAF-LgBiT proteins, either in combination with pMIG e.V. or pMIG KRASG12V. Cells were either treated with 10 µM Sorafenib or DMSO) for 4 h prior to measurement. RAF1WT-SmBiT fusion proteins were immunoprecipitated using anti-Myc antibody. Following Western blotting, immunoprecipitatesand TCLs were probed with anti-HA and anti-Myc antibodies. Shown is a representative experiment from two biological replicates.

Published
2023
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62. Additional file 1 of Analysis of RAS and drug induced homo- and heterodimerization of RAF and KSR1 proteins in living cells using split Nanoluc luciferase

Author

Rohrer, Lino, Spohr, Corinna, Beha, Carina, Griffin, Ricarda, Braun, Sandra, Halbach, Sebastian, and Brummer, Tilman

Abstract

Additional file 1: Figure S1. Co-immunoprecipitation using anti-c-Myc antibodies confirms the enhanced heterodimerization between BRAF-LgBiT and RAF1-SmBiT as well as between RAF1-LgBiT and BRAF-SmBiT proteins in the presence of either KRASG12V or Sorafenib. HEK293T cells were co-transfected with the indicated plasmids and either pMIG empty vectoror pMIG/KRASG12V. Four hours prior to lysis, cells were treated with either 10 μM Sorafenib or the equivalent volume of DMSO. Myc-tagged RAF1-SmBiT or RAF1-LgBiT proteins were immuno-purified using anti-Myc antibody. Top: Immunoprecipitates were loaded on two gels. Purified RAF1 proteins were either detected using anti-Myc or RAF1 antibodies, while co-purified HA-tagged BRAF proteins were detected with anti-HA or anti-BRAF F7 antibodies. Note the expected increased BRAF/RAF1 heterodimerization by KRASG12V or sorafenib. Bottom: Analysis of total cellular lysates demonstrates expression of all Nluc components and confirms activation of the RAS/RAF/MEK/ERK-pathway by KRASG12V.

Published
2023
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75. Analysis of RAS and drug induced homo- and heterodimerization of RAF and KSR1 proteins in living cells using split Nanoluc luciferase.

Author

Rohrer, Lino, Spohr, Corinna, Beha, Carina, Griffin, Ricarda, Braun, Sandra, Halbach, Sebastian, and Brummer, Tilman

Subjects
DRUG side effects, DRUG analysis, LUCIFERASES, BRAF genes, DIMERIZATION, HOMODIMERS
Abstract

The dimerization of RAF kinases represents a key event in their activation cycle and in RAS/ERK pathway activation. Genetic, biochemical and structural approaches provided key insights into this process defining RAF signaling output and the clinical efficacy of RAF inhibitors (RAFi). However, methods reporting the dynamics of RAF dimerization in living cells and in real time are still in their infancy. Recently, split luciferase systems have been developed for the detection of protein–protein-interactions (PPIs), incl. proof-of-concept studies demonstrating the heterodimerization of the BRAF and RAF1 isoforms. Due to their small size, the Nanoluc luciferase moieties LgBiT and SmBiT, which reconstitute a light emitting holoenzyme upon fusion partner promoted interaction, appear as well-suited to study RAF dimerization. Here, we provide an extensive analysis of the suitability of the Nanoluc system to study the homo- and heterodimerization of BRAF, RAF1 and the related KSR1 pseudokinase. We show that KRASG12V promotes the homo- and heterodimerization of BRAF, while considerable KSR1 homo- and KSR1/BRAF heterodimerization already occurs in the absence of this active GTPase and requires a salt bridge between the CC-SAM domain of KSR1 and the BRAF-specific region. We demonstrate that loss-of-function mutations impairing key steps of the RAF activation cycle can be used as calibrators to gauge the dynamics of heterodimerization. This approach identified the RAS-binding domains and the C-terminal 14–3-3 binding motifs as particularly critical for the reconstitution of RAF mediated LgBiT/SmBiT reconstitution, while the dimer interface was less important for dimerization but essential for downstream signaling. We show for the first time that BRAFV600E, the most common BRAF oncoprotein whose dimerization status is controversially portrayed in the literature, forms homodimers in living cells more efficiently than its wildtype counterpart. Of note, Nanoluc activity reconstituted by BRAFV600E homodimers is highly sensitive to the paradox-breaking RAFi PLX8394, indicating a dynamic and specific PPI. We report the effects of eleven ERK pathway inhibitors on RAF dimerization, incl. third-generation compounds that are less-defined in terms of their dimer promoting abilities. We identify Naporafenib as a potent and long-lasting dimerizer and show that the split Nanoluc approach discriminates between type I, I1/2 and II RAFi. Ah1kwifp3aoZnF_eXdbERz Video Abstract [ABSTRACT FROM AUTHOR]

Published
2023
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77. LGG-27. Molecular implications of mitogen-activated protein kinase pathway inhibition by the MEK inhibitor trametinib in BRAF-fusion-driven pediatric pilocytic astrocytoma

Author

Sigaud, Romain, primary, Stefanski, Anja, additional, Selt, Florian, additional, Hielscher, Thomas, additional, Usta, Diren, additional, Kocher, Daniela, additional, Picard, Daniel, additional, Büdenbender, Isabel, additional, Remke, Marc, additional, Pfister, Stefan M, additional, Jones, David T W, additional, Brummer, Tilman, additional, Witt, Olaf, additional, and Milde, Till, additional

Published
2022
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78. LGG-17. Preventing recurrence: targeting molecular mechanisms driving tumor growth rebound after MAPKi withdrawal in pediatric low-grade glioma

Author

Kocher, Daniela, primary, Selt, Florian, additional, Valinciute, Gintvile, additional, Zaman, Julia, additional, Vonhören, David, additional, Pusch, Stefan, additional, Guiho, Romain, additional, Martinez-Barbera, Juan Pedro, additional, von Deimling, Andreas, additional, Pfister, Stefan M, additional, Jones, David T W, additional, Brummer, Tilman, additional, Witt, Olaf, additional, Milde, Till, additional, and Sigaud, Romain, additional

Published
2022
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82. BRAF inhibitor-associated ERK activation drives development of chronic lymphocytic leukemia

Author

Yaktapour, Niuscha, Meiss, Frank, Mastroianni, Justin, Zenz, Thorsten, Andrlova, Hana, Mathew, Nimitha R., Claus, Rainer, Hutter, Barbara, Frohling, Stefan, Brors, Benedikt, Pfeifer, Dietmar, Pantic, Milena, Bartsch, Ingrid, Spehl, Timo S., Meyer, Philipp T., Duyster, Justus, Zirlik, Katja, Brummer, Tilman, and Zeiser, Robert

Subjects
Vemurafenib -- Health aspects -- Research, Protein kinases -- Physiological aspects -- Research, Chronic lymphocytic leukemia -- Development and progression -- Research, Health care industry
Abstract

Patients with [BRAFV.sup.600E/K]-driven melanoma respond to the BRAF inhibitor vemurafenib due to subsequent deactivation of the proliferative RAS/RAF/MEK/ERK pathway. In BRAF WT cells and those with mutations that activate or result in high levels of the BRAF activator RAS, BRAF inhibition can lead to ERK activation, resulting in tumorigenic transformation. We describe a patient with malignant melanoma who developed chronic lymphocytic leukemia (CLL) in the absence of RAS mutations during vemurafenib treatment. BRAF inhibition promoted patient CLL proliferation in culture and in murine xenografts and activated MEK/ERK in primary CLL cells from additional patients. BRAF inhibitor-driven ERK activity and CLL proliferation required B cell antigen receptor (BCR) activation, as inhibition of the BCR-proximal spleen tyrosine kinase (SYK) reversed ERK hyperactivation and proliferation of CLL cells from multiple patients, while inhibition of the BCR-distal Bruton tyrosine kinase had no effect. Additionally, the RAS-GTP/RAS ratio in primary CLL cells exposed to vemurafenib was reduced upon SYK inhibition. BRAF inhibition increased mortality and CLL expansion in mice harboring CLL xenografts; however, SYK or MEK inhibition prevented CLL proliferation and increased animal survival. Together, these results suggest that BRAF inhibitors promote B cell malignancies in the absence of obvious mutations in RAS or other receptor tyrosine kinases and provide a rationale for combined BRAF/MEK or BRAF/SYK inhibition., Introduction BRAF kinase inhibition has revolutionized the treatment of melanoma with somatic V600E or V600K mutations and led to improved overall survival (1). However, in tumors and normal cells with [...]

Published
2014
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90. Additional file 13 of Dynamic transcriptome analysis reveals signatures of paradoxical effect of vemurafenib on human dermal fibroblasts

Author

Corrales, Eyleen, Levit-Zerdoun, Ella, Metzger, Patrick, Kowar, Silke, Ku, Manching, Brummer, Tilman, and Boerries, Melanie

Subjects
integumentary system
Abstract

Additional file 12: Figs. S1���12. Figure S1: Differentially expressed genes in HDF after vemurafenib treatment. Figure S2: Down-regulated processes in HDF by vemurafenib treatment. Figure S3: Effect of vemurafenib on HDF motility. Figure S4: Enrichment of tumoral stroma signatures in HDF after vemurafenib treatment. Figure S5: Effect of vemurafenib on MaMel viability. Figure S6: Comparison of transcriptional profiles in BRAFWT and BRAFV600E mutant cell lines after vemurafenib treatment. Figure S7: Effect of vemurafenib on BRAFWT melanoma cell lines. Figure S8: Accessibility within promoter regions and transcription start sites (TSS) in HDF. Figure S9: Pearson correlation of chromatin accessibility and gene expression changes in HDF after vemurafenib treatment. Figure S10: Receiver operating characteristic (ROC) and precision-recall (PR) curves. Figure S11: Most significant gene-sets (KEGG pathways) showing a relation between promoter accessibility and gene expression changes after vemurafenib treatment in HDF. Figure S12: Effect of trametinib on MAPK/ERK pathway activation.

Published
2021
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91. Sensitivity and resistance of oncogenic RAS-driven tumors to dual MEK and ERK inhibition

Author

Catalano, Antonella, Adlesic, Mojca, Kaltenbacher, Thorsten, Klar, Rhena F. U., Albers, Joachim, Seidel, Philipp, Brandt, Laura P., Hejhal, Tomas, Busenhart, Philipp, Röhner, Niklas, Zodel, Kyra, Fritsch, Kornelia, Wild, Peter Johannes, Duyster, Justus, Fritsch, Ralph, Brummer, Tilman, Frew, Ian, Catalano, Antonella, Adlesic, Mojca, Kaltenbacher, Thorsten, Klar, Rhena F. U., Albers, Joachim, Seidel, Philipp, Brandt, Laura P., Hejhal, Tomas, Busenhart, Philipp, Röhner, Niklas, Zodel, Kyra, Fritsch, Kornelia, Wild, Peter Johannes, Duyster, Justus, Fritsch, Ralph, Brummer, Tilman, and Frew, Ian

Abstract

Simple Summary: Mutations in RAS-family genes frequently cause different types of human cancers. Inhibitors of the MEK (mitogen-activated protein kinase) and ERK (extracellular signal-regulated kinase) protein kinases that function downstream of RAS proteins have shown some clinical benefits when used for the treatment of these cancers, but drug resistance frequently emerges. Here we show that combined treatment with MEK and ERK inhibitors blocks the emergence of resistance to either drug alone. However, if cancer cells have already developed resistance to MEK inhibitors or to ERK inhibitors, the combined therapy is frequently ineffective. These findings imply that these inhibitors should be used together for cancer therapy. We also show that drug resistance involves complex patterns of rewiring of cellular kinase signaling networks that do not overlap between each different cancer cell line. Nonetheless, we show that MAP4K4 is required for efficient cell proliferation in several different MEK/ERK inhibitor resistant cancer cell lines, uncovering a potential new therapeutic target. Abstract: Oncogenic mutations in RAS family genes arise frequently in metastatic human cancers. Here we developed new mouse and cellular models of oncogenic HrasG12V-driven undifferentiated pleomorphic sarcoma metastasis and of KrasG12D-driven pancreatic ductal adenocarcinoma metastasis. Through analyses of these cells and of human oncogenic KRAS-, NRAS- and BRAF-driven cancer cell lines we identified that resistance to single MEK inhibitor and ERK inhibitor treatments arise rapidly but combination therapy completely blocks the emergence of resistance. The prior evolution of resistance to either single agent frequently leads to resistance to dual treatment. Dual MEK inhibitor plus ERK inhibitor therapy shows anti-tumor efficacy in an HrasG12V-driven autochthonous sarcoma model but features of drug resistance in vivo were also evident. Array-based kinome activity profiling revealed an abse

Published
2021

93. Oncogenic FAM131B–BRAF fusion resulting from 7q34 deletion comprises an alternative mechanism of MAPK pathway activation in pilocytic astrocytoma

Author

Cin, Huriye, Meyer, Claus, Herr, Ricarda, Janzarik, Wibke G., Lambert, Sally, Jones, David T. W., Jacob, Karine, Benner, Axel, Witt, Hendrik, Remke, Marc, Bender, Sebastian, Falkenstein, Fabian, Van Anh, Ton Nu, Olbrich, Heike, von Deimling, Andreas, Pekrun, Arnulf, Kulozik, Andreas E., Gnekow, Astrid, Scheurlen, Wolfram, Witt, Olaf, Omran, Heymut, Jabado, Nada, Collins, V. Peter, Brummer, Tilman, Marschalek, Rolf, Lichter, Peter, Korshunov, Andrey, and Pfister, Stefan M.

Published
2011
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95. Oncogenic KrasG12D Activation in the Nonhematopoietic Bone Marrow Microenvironment Causes Myelodysplastic Syndrome in Mice

Author

Osswald, Lena, primary, Hamarsheh, Shaima'a, additional, Uhl, Franziska Maria, additional, Andrieux, Geoffroy, additional, Klein, Claudius, additional, Dierks, Christine, additional, Duquesne, Sandra, additional, Braun, Lukas M., additional, Schmitt-Graeff, Annette, additional, Duyster, Justus, additional, Boerries, Melanie, additional, Brummer, Tilman, additional, and Zeiser, Robert, additional

Published
2021
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96. LGG-04. MULTIOMIC ANALYSIS OF MAPK PATHWAY ACTIVITY IN PEDIATRIC PILOCYTIC ASTROCYTOMA

Author

Sigaud, Romain, primary, Selt, Florian, additional, Hielscher, Thomas, additional, Stefanski, Anja, additional, Overbeck, Nina, additional, Usta, Diren, additional, Kocher, Daniela, additional, Remke, Marc, additional, Picard, Daniel, additional, Pfister, Stefan M, additional, Jones, David T W, additional, Brummer, Tilman, additional, Witt, Olaf, additional, and Milde, Till, additional

Published
2021
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97. Sensitivity and Resistance of Oncogenic RAS-Driven Tumors to Dual MEK and ERK Inhibition

Author

Catalano, Antonella, primary, Adlesic, Mojca, additional, Kaltenbacher, Thorsten, additional, Klar, Rhena F. U., additional, Albers, Joachim, additional, Seidel, Philipp, additional, Brandt, Laura P., additional, Hejhal, Tomas, additional, Busenhart, Philipp, additional, Röhner, Niklas, additional, Zodel, Kyra, additional, Fritsch, Kornelia, additional, Wild, Peter J., additional, Duyster, Justus, additional, Fritsch, Ralph, additional, Brummer, Tilman, additional, and Frew, Ian J., additional

Published
2021
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98. Transitioning the Molecular Tumor Board from Proof of Concept to Clinical Routine: A German Single-Center Analysis

Author

Hoefflin, Rouven, primary, Lazarou, Adriana, additional, Hess, Maria Elena, additional, Reiser, Meike, additional, Wehrle, Julius, additional, Metzger, Patrick, additional, Frey, Anna Verena, additional, Becker, Heiko, additional, Aumann, Konrad, additional, Berner, Kai, additional, Boeker, Martin, additional, Buettner, Nico, additional, Dierks, Christine, additional, Duque-Afonso, Jesus, additional, Eisenblaetter, Michel, additional, Erbes, Thalia, additional, Fritsch, Ralph, additional, Ge, Isabell Xiang, additional, Geißler, Anna-Lena, additional, Grabbert, Markus, additional, Heeg, Steffen, additional, Heiland, Dieter Henrik, additional, Hettmer, Simone, additional, Kayser, Gian, additional, Keller, Alexander, additional, Kleiber, Anita, additional, Kutilina, Alexandra, additional, Mehmed, Leman, additional, Meiss, Frank, additional, Poxleitner, Philipp, additional, Rawluk, Justyna, additional, Ruf, Juri, additional, Schäfer, Henning, additional, Scherer, Florian, additional, Shoumariyeh, Khalid, additional, Tzschach, Andreas, additional, Peters, Christoph, additional, Brummer, Tilman, additional, Werner, Martin, additional, Duyster, Justus, additional, Lassmann, Silke, additional, Miething, Cornelius, additional, Boerries, Melanie, additional, Illert, Anna L., additional, and von Bubnoff, Nikolas, additional

Published
2021
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