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1. The new WHO 2022 and ICC proposals for the classification of myelodysplastic neoplasms. Validation based on the Düsseldorf MDS Registry and proposals for a merged classification

Author

Nachtkamp, K., Strupp, C., Vukelja, M., Kasprzak, A., Haase, D., Ganster, C., Hildebrandt, B., Betz, B., Giagounidis, A., Aul, C., Blum, S., Hofmann, W. K., Pfeilstöcker, M., Valent, P., Lübbert, M., Seidl, M., Rudelius, M., Stauder, R., Krieger, O., Götze, K. S., Bobak, J., Kündgen, A., Schulz, F., Dietrich, S., Kobbe, G., Gattermann, N., and Germing, U.

Published
2024
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7. In vivo tracking of genetically engineered, anti-HER2/neu directed natural killer cells to HER2/neu positive mammary tumors with magnetic resonance imaging

Author

Daldrup-Link, H E, Meier, R, Rudelius, M, Piontek, G, Piert, M, Metz, S, Settles, M, Uherek, C, Wels, W, Schlegel, J, and Rummeny, E J

Subjects
MR imaging, molecular imaging, iron oxides, cell targeting, NK cells
Abstract

The purpose of this study is to optimize labeling of the human natural killer (NK) cell line NK-92 with iron-oxide-based contrast agents and to monitor the in vivo distribution of genetically engineered NK-92 cells, which are directed against HER2/neu receptors, to HER2/neu positive mammary tumors with magnetic resonance (MR) imaging. Parental NK-92 cells and genetically modified HER2/neu specific NK-92scFv(FRP5)-zeta cells, expressing a chimeric antigen receptor specific to the tumor-associated ErbB2 (HER2/ neu) antigen, were labeled with ferumoxides and ferucarbotran using simple incubation, lipofection and electroporation techniques. Labeling efficiency was evaluated by MR imaging, Prussian blue stains and spectrometry. Subsequently, ferucarbotran-labeled NK-92-scFv(FRP5)-zeta n=3) or parental NK-92 cells were intravenously injected into the tail vein of six mice with HER2/neupositive NIH 3T3 mammary tumors, implanted in the mammary fat pad. The accumulation of the cells in the tumors was monitored by MR imaging before and 12 and 24 h after cell injection (p.i.). MR data were correlated with histopathology. Both the parental NK-92 and the genetically modified NK-92-scFv(FRP5)-zeta cells could be labeled with ferucarbotran and ferumoxides by lipofection and electroporation, but not by simple incubation. The intracellular cytoplasmatic iron-oxide uptake was significantly higher after labeling with ferucarbotran than ferumoxides (P

Published
2005

8. Cell tracking with gadophrin-2: a bifunctional contrast agent for MR imaging, optical imaging, and fluorescence microscopy

Author

Daldrup-Link, H E, Rudelius, M, Metz, S, Piontek, G, Pichler, B, Settles, M, Heinzmann, U, Schlegel, J, Oostendorp, RAJ, and Rummeny, E J

Subjects
gadophrin-2, optical imaging, magnetic resonance imaging, fluorescence microscopy, hematopoietic cells
Abstract

The purpose of this study was to assess the feasibility of use of gadophrin-2 to trace intravenously injected human hematopoietic cells in athymic mice, employing magnetic resonance (MR) imaging, optical imaging (OI), and fluorescence microscopy. Mononuclear peripheral blood cells from GCSF-primed patients were labeled with gadophrin-2 (Schering AG, Berlin, Germany), a paramagnetic and fluorescent metalloporphyrin, using established transfection techniques with cationic liposomes. The labeled cells were evaluated in vitro with electron microscopy and inductively coupled plasma atomic emission spectrometry. Then, 1x10(6)-3x10(8) labeled cells were injected into 14 nude Balb/c mice and the in vivo cell distribution was evaluated with MR imaging and OI before and 4, 24, and 48 h after intravenous injection (p.i.). Five additional mice served as controls: three mice were untreated controls and two mice were investigated after injection of unlabeled cells. The contrast agent effect was determined quantitatively for MR imaging by calculating signal-to-noise-ratio (SNR) data. After completion of in vivo imaging studies, fluorescence microscopy of excised organs was performed. Intracellular cytoplasmatic uptake of gadophrin-2 was confirmed by electron microscopy. Spectrometry determined an uptake of 31.56 nmol Gd per 10(6) cells. After intravenous injection, the distribution of gadophrin-2 labeled cells in nude mice could be visualized by MR, OI, and fluorescence microscopy. At 4 h p.i., the transplanted cells mainly distributed to lung, liver, and spleen, and 24 h p.i. they also distributed to the bone marrow. Fluorescence microscopy confirmed the distribution of gadophrin-2 labeled cells to these target organs. Gadophrin-2 is suited as a bifunctional contrast agent for MR imaging, OI, and fluorescence microscopy and may be used to combine the advantages of each individual imaging modality for in vivo tracking of intravenously injected hematopoietic cells.

Published
2004

9. Cancer of unknown primary (CUP) through the lens of precision oncology – a single institution perspective

Author

Weiss, L., primary, Heinrich, K., additional, Zhang, D., additional, Dorman, K., additional, Rühlmann, K., additional, Hasselmann, K., additional, Klauschen, F., additional, Kumbrink, J., additional, Jung, A., additional, Rudelius, M., additional, Mock, A., additional, Kunz, W. G., additional, Roessler, D., additional, Beyer, G., additional, Corradini, S., additional, Heinzerling, L., additional, Haas, M., additional, von Bergwelt-Baildon, M., additional, Boeck, S., additional, Heinemann, V., additional, and Westphalen, C. B., additional

Published
2023
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10. The OTUD6B-LIN28B-MYC axis determines the proliferative state in multiple myeloma

Author

Paulmann, C., Spallek, R., Karpiuk, O., Heider, M., Schäffer, I., Zecha, J., Klaeger, S., Walzik, M., Öllinger, R., Engleitner, T., Wirth, M., Keller, U., Krönke, J., Rudelius, M., Kossatz, S., Rad, R., Kuster, B., and Bassermann, F.

Subjects
Cancer Research
Abstract

Deubiquitylases (DUBs) are therapeutically amenable components of the ubiquitin machinery that stabilize substrate proteins. Their inhibition can destabilize oncoproteins that may otherwise be undruggable. Here, we screened for DUB vulnerabilities in multiple myeloma, an incurable malignancy with dependency on the ubiquitin proteasome system and identified OTUD6B as an oncogene that drives the G1/S-transition. LIN28B, a suppressor of microRNA biogenesis, is specified as a bona fide cell cycle-specific substrate of OTUD6B. Stabilization of LIN28B drives MYC expression at G1/S, which in turn allows for rapid S-phase entry. Silencing OTUD6B or LIN28B inhibits multiple myeloma outgrowth in vivo and high OTUD6B expression evolves in patients that progress to symptomatic multiple myeloma and results in an adverse outcome of the disease. Thus, we link proteolytic ubiquitylation with post-transcriptional regulation and nominate OTUD6B as a potential mediator of the MGUS-multiple myeloma transition, a central regulator of MYC, and an actionable vulnerability in multiple myeloma and other tumors with an activated OTUD6B-LIN28B axis.

Published
2022

12. P02.03 Organization, function and gene expression of tertiary lymphoid structures in pancreatic cancer resembles lymphoid follicles in secondary lymphoid organs and their abundance is related to superior survival

Author

Lehmann, J, primary, Thelen, M, additional, Schran, S, additional, Preugszat, E, additional, Wennhold, K, additional, Garcia-Marquez, M, additional, Lohneis, P, additional, Löser, H, additional, Popp, F, additional, Kruger, S, additional, Böck, S, additional, Ormanns, S, additional, Rudelius, M, additional, von Bergwelt, M, additional, Bruns, C, additional, Quaas, A, additional, and Schlößer, H, additional

Published
2022
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16. ORGANIZATION, FUNCTION AND GENE EXPRESSION OF TERTIARY LYMPHOID STRUCTURES IN PANCREATIC CANCER RESEMBLES LYMPHOID FOLLICLES IN SECONDARY LYMPHOID ORGANS AND THEIR ABUNDANCE IS RELATED TO SUPERIOR SURVIVAL

Author

Lehmann, J., Thelen, M., Schran, S., Preugszat, E., Wennhold, K., Garcia-Marquez, M., Lohneis, P., Loeser, H., Popp, F., Kruger, S., Boeck, S., Ormanns, S., Rudelius, M., von Bergwelt, M., Bruns, C., Quaas, A., Schloesser, H., Lehmann, J., Thelen, M., Schran, S., Preugszat, E., Wennhold, K., Garcia-Marquez, M., Lohneis, P., Loeser, H., Popp, F., Kruger, S., Boeck, S., Ormanns, S., Rudelius, M., von Bergwelt, M., Bruns, C., Quaas, A., and Schloesser, H.

Published
2022

18. Zelluläre Expression von Kathepsin-Proteasen beim symptomatischen und asymptomatischen AAA

Author

Reeps, C., Lohöfer, F., Eckstein, H. H., Rudelius, M., Pelisek, J., Buhr, H. J., editor, Hölscher, A., editor, Izbicki, J. R., editor, Jauch, K. W., editor, Post, S., editor, Allgayer, H., editor, Bartsch, D. K., editor, Fries, H., editor, Ghadimi, B. M., editor, Habermann, J. K., editor, Kalthoff, H., editor, Schackert, H. K., editor, Bruns, C. J., editor, Duda, D. N., editor, Fändrich, F., editor, Heberer, M., editor, Nüssler, A. K., editor, Stark, G. B., editor, Brückner, U. B., editor, Ertel, W., editor, Faist, E., editor, Heidecke, C. D., editor, Kalff, J. C., editor, Menger, M. D., editor, Schade, U. F., editor, Vollmar, B., editor, Bechstein, W. O., editor, Klar, E., editor, Klempnauer, J., editor, Minor, T., editor, Neuhaus, P., editor, Schmidt, J., editor, Langer, S., editor, Laschke, M. W., editor, Machens, H. G., editor, Steinau, H. U., editor, Südkamp, N., editor, Vogt, P., editor, Berger, D., editor, Klinge, U., editor, Schachtrupp, A., editor, Schilling, M. K., editor, Schumpelick, V., editor, Altendorf-Hofmann, A., editor, Bollschweiler, E., editor, Bruch, H. -P., editor, Lehnert, T., editor, Lorenz, W., editor, Neugebauer, E., editor, Ohmann, C., editor, Seiler, C. M., editor, Becker, H., editor, Betzler, M., editor, Bittner, R., editor, Broelsch, C., editor, Büchler, M. W., editor, Bumm, R., editor, Dralle, H., editor, Friess, H., editor, Frilling, A., editor, Germer, C. T., editor, Hopt, U., editor, Jonas, S., editor, Jost, J., editor, Markus, B., editor, Raab, H. R., editor, Reith, H. B., editor, Schlag, P. M., editor, Teichmann, W., editor, Uhl, W., editor, Wenisch, H., editor, and Zornig, C., editor

Published
2009
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20. Clinical evolution, genetic landscape and trajectories of clonal hematopoiesis in SAMD9/SAMD9L syndromes

Author

Sahoo S. S., Pastor V. B., Goodings C., Voss R. K., Kozyra E. J., Szvetnik A., Noellke P., Dworzak M., Stary J., Locatelli F., Masetti R., Schmugge M., De Moerloose B., Catala A., Kallay K., Turkiewicz D., Hasle H., Buechner J., Jahnukainen K., Ussowicz M., Polychronopoulou S., Smith O. P., Fabri O., Barzilai S., de Haas V., Baumann I., Schwarz-Furlan S., Moerloose B. D., Smith O., Haas V. D., Gohring G., Niemeyer C., Nebral K., Simonitsch-Kluppp I., Paepe P. D., Van Roy N., Campr V., Zemanova Z., Clasen-Linde E., Plesner T., Schlegelberger B., Rudelius M., Manola K., Stefanaki K., Csomor J., Andrikovics H., Betts D., O'Sullivan M., Zohar Y., Jeison M., Vito R. D., Pasquali F., Maldyk J., Haus O., Alaiz H., Kjollerstrom P., Lemos L. M., Bodova I., Cermak M., Plank L., Gazic B., Kavcic M., Podgornik H., Ros M. L., Cervera J., Gengler C., Tchinda J., Beverloo B., Leguit R., Niewisch M. R., Sauer M. G., Burkhardt B., Lang P., Bader P., Beier R., Muller I., Albert M. H., Meisel R., Schulz A., Cario G., Panda P. K., Wehrle J., Hirabayashi S., Derecka M., Durruthy-Durruthy R., Yoshimi-Noellke A., Ku M., Lebrecht D., Erlacher M., Flotho C., Strahm B., Niemeyer C. M., Wlodarski M. W., Sahoo S.S., Pastor V.B., Goodings C., Voss R.K., Kozyra E.J., Szvetnik A., Noellke P., Dworzak M., Stary J., Locatelli F., Masetti R., Schmugge M., De Moerloose B., Catala A., Kallay K., Turkiewicz D., Hasle H., Buechner J., Jahnukainen K., Ussowicz M., Polychronopoulou S., Smith O.P., Fabri O., Barzilai S., de Haas V., Baumann I., Schwarz-Furlan S., Moerloose B.D., Smith O., Haas V.D., Gohring G., Niemeyer C., Nebral K., Simonitsch-Kluppp I., Paepe P.D., Van Roy N., Campr V., Zemanova Z., Clasen-Linde E., Plesner T., Schlegelberger B., Rudelius M., Manola K., Stefanaki K., Csomor J., Andrikovics H., Betts D., O'Sullivan M., Zohar Y., Jeison M., Vito R.D., Pasquali F., Maldyk J., Haus O., Alaiz H., Kjollerstrom P., Lemos L.M., Bodova I., Cermak M., Plank L., Gazic B., Kavcic M., Podgornik H., Ros M.L., Cervera J., Gengler C., Tchinda J., Beverloo B., Leguit R., Niewisch M.R., Sauer M.G., Burkhardt B., Lang P., Bader P., Beier R., Muller I., Albert M.H., Meisel R., Schulz A., Cario G., Panda P.K., Wehrle J., Hirabayashi S., Derecka M., Durruthy-Durruthy R., Yoshimi-Noellke A., Ku M., Lebrecht D., Erlacher M., Flotho C., Strahm B., Niemeyer C.M., Wlodarski M.W., and Clinical Genetics

Subjects
Oncology, Male, medicine.medical_specialty, Monosomy, Adolescent, Somatic cell, Medizin, Bone Marrow Cells, Kaplan-Meier Estimate, General Biochemistry, Genetics and Molecular Biology, Germline, Article, Clonal Evolution, Germline mutation, SDG 3 - Good Health and Well-being, Internal medicine, medicine, Humans, Child, Germ-Line Mutation, Chromosome 7 (human), Cytopenia, clonal hemopoiesis, business.industry, Myelodysplastic syndromes, Tumor Suppressor Proteins, Intracellular Signaling Peptides and Proteins, High-Throughput Nucleotide Sequencing, Infant, General Medicine, medicine.disease, GATA2 Transcription Factor, SAMD9 and SAMD9L mutations, Pediatric Myelodysplastic syndromes, medicine.anatomical_structure, HEK293 Cells, Settore MED/38 - PEDIATRIA GENERALE E SPECIALISTICA, Child, Preschool, Myelodysplastic Syndromes, Female, Bone marrow, Clonal Hematopoiesis, Single-Cell Analysis, business
Abstract

Germline SAMD9 and SAMD9L mutations (SAMD9/9Lmut) predispose to myelodysplastic syndromes (MDS) with propensity for somatic rescue. In this study, we investigated a clinically annotated pediatric MDS cohort (n = 669) to define the prevalence, genetic landscape, phenotype, therapy outcome and clonal architecture of SAMD9/9L syndromes. In consecutively diagnosed MDS, germline SAMD9/9Lmut accounted for 8% and were mutually exclusive with GATA2 mutations present in 7% of the cohort. Among SAMD9/9Lmut cases, refractory cytopenia was the most prevalent MDS subtype (90%); acquired monosomy 7 was present in 38%; constitutional abnormalities were noted in 57%; and immune dysfunction was present in 28%. The clinical outcome was independent of germline mutations. In total, 67 patients had 58 distinct germline SAMD9/9Lmut clustering to protein middle regions. Despite inconclusive in silico prediction, 94% of SAMD9/9Lmut suppressed HEK293 cell growth, and mutations expressed in CD34+ cells induced overt cell death. Furthermore, we found that 61% of SAMD9/9Lmut patients underwent somatic genetic rescue (SGR) resulting in clonal hematopoiesis, of which 95% was maladaptive (monosomy 7 ± cancer mutations), and 51% had adaptive nature (revertant UPD7q, somatic SAMD9/9Lmut). Finally, bone marrow single-cell DNA sequencing revealed multiple competing SGR events in individual patients. Our findings demonstrate that SGR is common in SAMD9/9Lmut MDS and exemplify the exceptional plasticity of hematopoiesis in children. This analysis of a large, clinically annotated cohort of individuals with predisposition to myelodysplastic syndromes reveals insights into the genetic determinants of disease progression and their relationship with clinical manifestations and therapy outcome.

Published
2021

22. A-164 B cells are associated with aggressive Cases of Cutaneous T cell Lymphoma and a distinct spatio-temporal composition of the tumor microenviroenment.

Author

Oganesian, S., Rudelius, M., Piontek, G., Posch, C., Weigert, O., Heide, M., Krebs, S., Blum, H., Klughammer, J., Mages, S., Watter, J., Kirmaier, M., Hadzic, A., Funk, M., Tu, J., Carboniero, A., Vona, L., von Bergwelt-Baildon, M., and Theurich, S.

Subjects
*CANCER invasiveness, *CELL physiology, *TUMOR markers, *CONFERENCES & conventions, *CUTANEOUS T-cell lymphoma, *B cells
Published
2024
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25. Publisher Correction: Clinical evolution, genetic landscape and trajectories of clonal hematopoiesis in SAMD9/SAMD9L syndromes (Nature Medicine, (2021), 27, 10, (1806-1817), 10.1038/s41591-021-01511-6)

Author

Sahoo, S. S., Pastor, V. B., Goodings, C., Voss, R. K., Kozyra, E. J., Szvetnik, A., Noellke, P., Dworzak, M., Stary, J., Locatelli, Franco, Masetti, R., Schmugge, M., De Moerloose, B., Catala, A., Kallay, K., Turkiewicz, D., Hasle, H., Buechner, J., Jahnukainen, K., Ussowicz, M., Polychronopoulou, S., Smith, O. P., Fabri, O., Barzilai, S., de Haas, V., Baumann, I., Schwarz-Furlan, S., Smith, O., Haas, V. D., Gohring, G., Niemeyer, C., Nebral, K., Simonitsch-Kluppp, I., Paepe, P. D., Van Roy, N., Campr, V., Zemanova, Z., Clasen-Linde, E., Plesner, T., Schlegelberger, B., Rudelius, M., Manola, K., Stefanaki, K., Csomor, J., Andrikovics, H., Betts, D., O'Sullivan, M., Zohar, Y., Jeison, M., Vito, R. D., Pasquali, F., Maldyk, J., Haus, O., Alaiz, H., Kjollerstrom, P., Lemos, L. M., Bodova, I., Cermak, M., Plank, L., Gazic, B., Kavcic, M., Podgornik, H., Ros, M. L., Cervera, J., Gengler, C., Tchinda, J., Beverloo, B., Leguit, R., Niewisch, M. R., Sauer, M. G., Burkhardt, B., Lang, P., Bader, P., Beier, R., Muller, I., Albert, M. H., Meisel, R., Schulz, A., Cario, G., Panda, P. K., Wehrle, J., Hirabayashi, S., Derecka, M., Durruthy-Durruthy, R., Yoshimi-Noellke, A., Ku, M., Lebrecht, D., Erlacher, M., Flotho, C., Strahm, B., Niemeyer, C. M., and Wlodarski, M. W.

Subjects
Settore MED/38 - PEDIATRIA GENERALE E SPECIALISTICA, SAMD9/SAMD9L syndromes
Published
2021

26. Clinical evolution, genetic landscape and trajectories of clonal hematopoiesis in SAMD9/SAMD9L syndromes

Author

Sahoo, S. S., Pastor, V. B., Goodings, C., Voss, R. K., Kozyra, E. J., Szvetnik, A., Noellke, P., Dworzak, M., Stary, J., Locatelli, Franco, Masetti, R., Schmugge, M., De Moerloose, B., Catala, A., Kallay, K., Turkiewicz, D., Hasle, H., Buechner, J., Jahnukainen, K., Ussowicz, M., Polychronopoulou, S., Smith, O. P., Fabri, O., Barzilai, S., de Haas, V., Baumann, I., Schwarz-Furlan, S., Smith, O., Haas, V. D., Gohring, G., Niemeyer, C., Nebral, K., Simonitsch-Kluppp, I., Paepe, P. D., Van Roy, N., Campr, V., Zemanova, Z., Clasen-Linde, E., Plesner, T., Schlegelberger, B., Rudelius, M., Manola, K., Stefanaki, K., Csomor, J., Andrikovics, H., Betts, D., O'Sullivan, M., Zohar, Y., Jeison, M., Vito, R. D., Pasquali, F., Maldyk, J., Haus, O., Alaiz, H., Kjollerstrom, P., Lemos, L. M., Bodova, I., Cermak, M., Plank, L., Gazic, B., Kavcic, M., Podgornik, H., Ros, M. L., Cervera, J., Gengler, C., Tchinda, J., Beverloo, B., Leguit, R., Niewisch, M. R., Sauer, M. G., Burkhardt, B., Lang, P., Bader, P., Beier, R., Muller, I., Albert, M. H., Meisel, R., Schulz, A., Cario, G., Panda, P. K., Wehrle, J., Hirabayashi, S., Derecka, M., Durruthy-Durruthy, R., Yoshimi-Noellke, A., Ku, M., Lebrecht, D., Erlacher, M., Flotho, C., Strahm, B., Niemeyer, C. M., Wlodarski, M. W., Locatelli F. (ORCID:0000-0002-7976-3654), Sahoo, S. S., Pastor, V. B., Goodings, C., Voss, R. K., Kozyra, E. J., Szvetnik, A., Noellke, P., Dworzak, M., Stary, J., Locatelli, Franco, Masetti, R., Schmugge, M., De Moerloose, B., Catala, A., Kallay, K., Turkiewicz, D., Hasle, H., Buechner, J., Jahnukainen, K., Ussowicz, M., Polychronopoulou, S., Smith, O. P., Fabri, O., Barzilai, S., de Haas, V., Baumann, I., Schwarz-Furlan, S., Smith, O., Haas, V. D., Gohring, G., Niemeyer, C., Nebral, K., Simonitsch-Kluppp, I., Paepe, P. D., Van Roy, N., Campr, V., Zemanova, Z., Clasen-Linde, E., Plesner, T., Schlegelberger, B., Rudelius, M., Manola, K., Stefanaki, K., Csomor, J., Andrikovics, H., Betts, D., O'Sullivan, M., Zohar, Y., Jeison, M., Vito, R. D., Pasquali, F., Maldyk, J., Haus, O., Alaiz, H., Kjollerstrom, P., Lemos, L. M., Bodova, I., Cermak, M., Plank, L., Gazic, B., Kavcic, M., Podgornik, H., Ros, M. L., Cervera, J., Gengler, C., Tchinda, J., Beverloo, B., Leguit, R., Niewisch, M. R., Sauer, M. G., Burkhardt, B., Lang, P., Bader, P., Beier, R., Muller, I., Albert, M. H., Meisel, R., Schulz, A., Cario, G., Panda, P. K., Wehrle, J., Hirabayashi, S., Derecka, M., Durruthy-Durruthy, R., Yoshimi-Noellke, A., Ku, M., Lebrecht, D., Erlacher, M., Flotho, C., Strahm, B., Niemeyer, C. M., Wlodarski, M. W., and Locatelli F. (ORCID:0000-0002-7976-3654)

Abstract

Germline SAMD9 and SAMD9L mutations (SAMD9/9Lmut) predispose to myelodysplastic syndromes (MDS) with propensity for somatic rescue. In this study, we investigated a clinically annotated pediatric MDS cohort (n = 669) to define the prevalence, genetic landscape, phenotype, therapy outcome and clonal architecture of SAMD9/9L syndromes. In consecutively diagnosed MDS, germline SAMD9/9Lmut accounted for 8% and were mutually exclusive with GATA2 mutations present in 7% of the cohort. Among SAMD9/9Lmut cases, refractory cytopenia was the most prevalent MDS subtype (90%); acquired monosomy 7 was present in 38%; constitutional abnormalities were noted in 57%; and immune dysfunction was present in 28%. The clinical outcome was independent of germline mutations. In total, 67 patients had 58 distinct germline SAMD9/9Lmut clustering to protein middle regions. Despite inconclusive in silico prediction, 94% of SAMD9/9Lmut suppressed HEK293 cell growth, and mutations expressed in CD34+ cells induced overt cell death. Furthermore, we found that 61% of SAMD9/9Lmut patients underwent somatic genetic rescue (SGR) resulting in clonal hematopoiesis, of which 95% was maladaptive (monosomy 7 ± cancer mutations), and 51% had adaptive nature (revertant UPD7q, somatic SAMD9/9Lmut). Finally, bone marrow single-cell DNA sequencing revealed multiple competing SGR events in individual patients. Our findings demonstrate that SGR is common in SAMD9/9Lmut MDS and exemplify the exceptional plasticity of hematopoiesis in children.

Published
2021

31. Panel-guided personalized medicine in metastatic breast and gynecological cancer: First experiences at the CCC Munich and clinically relevant changes over time

Author

Sultova, E, additional, CB, Westphalen, additional, Jung, A, additional, Kirchner, T, additional, Mayr, D, additional, Rudelius, M, additional, Ormanns, S, additional, Kumbrink, J, additional, Heinemann, V, additional, Metzeler, K, additional, PA, Greif, additional, Trillsch, F, additional, Mahner, S, additional, Harbeck, N, additional, and Würstlein, R, additional

Published
2020
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32. P09.03 Cathepsin S alterations induce a tumor-promoting immune microenvironment in follicular lymphoma

Author

Hildebrand, JA, primary, Bararia, D, additional, Stolz, S, additional, Häbe, S, additional, Osorio-Barrios, F, additional, Bartoschek, MD, additional, Gaitzsch, E, additional, Jurinovic, V, additional, Rautter, K, additional, Ludwig, C, additional, Bultmann, S, additional, Leonhardt, H, additional, Eustermann, S, additional, Hopfner, K, additional, Hiddemann, W, additional, Bergwelt, M, additional, Schmidt-Supprian, M, additional, Sárosi, MB, additional, Rudelius, M, additional, Passerini, V, additional, Mautner, J, additional, and Weigert, O, additional

Published
2020
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33. Personalisierte Medizin bei metastasierten Brust- und gynäkologischen Krebserkrankungen. Erste Ergebnisse in CCC LMU München

Author

Sultova, E, additional, Westphalen, B, additional, Jung, A, additional, Kirchner, T, additional, Mayr, D, additional, Rudelius, M, additional, Ormanns, S, additional, Kumbrink, J, additional, Heinemann, V, additional, Metzeler, K, additional, Greif, P A, additional, Trillsch, F, additional, Mahner, S, additional, Harbeck, N, additional, and Wuerstlein, R, additional

Published
2020
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38. PS1309 A NOVEL NPM-ALK-DRIVEN MODEL OF CD30+ T-CELL LYMPHOMA

Author

Shoumariyeh, K., primary, Schneider, N., additional, Ehrenfeld, S., additional, Redhaber, D., additional, Poggio, T., additional, Klingeberg, C., additional, Kreutmair, S., additional, Rudelius, M., additional, Fend, F., additional, Illert, A.L., additional, Duyster, J., additional, and Miething, C., additional

Published
2019
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39. PF311 ISOLATED PRIMARY ADRENAL LYMPHOMA (IPAL) - AN EMERGING LYMPHOMA ENTITY? RESULTS OF A RETROSPECTIVE MULTICENTER STUDY

Author

Majidi, F., primary, Martino, S., additional, Kondakci, M., additional, Haase, M., additional, Chortis, V., additional, Arlt, W., additional, Ronchi, C.L., additional, Fassnacht, M., additional, Laurent, C., additional, Petit, J.-M., additional, Casasnovas, O., additional, Habra, M.A., additional, Kanji, A., additional, Salvatori, R., additional, Ho, A., additional, Spyroglou, A., additional, Beuschlein, F., additional, Villa, D., additional, Limvorapitak, W., additional, Wahlin, B., additional, Gimm, O., additional, Rudelius, M., additional, Schott, M., additional, Germing, U., additional, Haas, R., additional, and Gattermann, N., additional

Published
2019
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44. V729: Immunomodulatory drugs mediate both anti-tumor activity and teratotoxocity via destabilization of CD147 and MCT1

Author

Eichner, R., Heider, M., Germing, U., Langer, C., Knop, S., Einsele, H., Peschel, C., Keller, U., Schmid, Bettina, Götze, K. S., Küster, B., Bassermann, F, Fernández-Sáiz, V., van Bebber, Frauke, Garz, A.-K., Lemeer, Rudelius, M., Targosz, B.-S., Jacobs, L., and Platzbecker, U.

Subjects
ddc:350
Abstract

Introduction: Immunomodulatory drugs (IMiDs) as thalidomide, lenalidomide and pomalidomide, have immunomodulatory, anti-proliferative, anti-angiogenic and teratotoxic effects and are key treatment components for hematologic malignancies such as multiple myeloma (MM)and del(5q) myelodysplastic syndrome (MDS). IMiDs bind to Cereblon(CRBN), a substrate receptor of CRL4 ubiquitin ligases, to mediate anti-cancer and teratotoxic effects. Recently, IKZF1/3 and CK1-alpha wereidentified as substrates, which are degraded upon IMiD-induced bindingto CRBN. However, both the physiological function of CRBN, as well as acommon mechanism by which IMiDs exert their versatile effects, remainlargely elusive.

Published
2016

45. JAM-A as a prognostic factor and new therapeutic target in multiple myeloma

Author

Solimando, A G, primary, Brandl, A, additional, Mattenheimer, K, additional, Graf, C, additional, Ritz, M, additional, Ruckdeschel, A, additional, Stühmer, T, additional, Mokhtari, Z, additional, Rudelius, M, additional, Dotterweich, J, additional, Bittrich, M, additional, Desantis, V, additional, Ebert, R, additional, Trerotoli, P, additional, Frassanito, M A, additional, Rosenwald, A, additional, Vacca, A, additional, Einsele, H, additional, Jakob, F, additional, and Beilhack, A, additional

Published
2017
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46. Non-Invasive Beurteilung der Chemokin Receptor 4 (CXCR4) Expression in Gastroenteropankreatischen Neuroendokrinen Tumoren

Author

Weich, A, additional, Werner, RA, additional, Higuchi, T, additional, Schmid, JS, additional, Schirbel, A, additional, Lassmann, M, additional, Wild, V, additional, Rudelius, M, additional, Kudlich, T, additional, Herrmann, K, additional, Scheurlen, M, additional, Buck, AK, additional, Kropf, S, additional, Wester, HJ, additional, and Lapa, C, additional

Published
2017
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50. Protein Kinase C-beta-Dependent Activation of NF-kappa B in Stromal Cells Is Indispensable for the Survival of Chronic Lymphocytic Leukemia B Cells In Vivo

Author

Lutzny, G., Kocher, T., Schmidt-Supprian, M., Rudelius, M., Klein-Hitpass, L., Finch, A., Duerig, J., Wagner, M., Haferlach, C., Kohlmann, A., Schnittger, S., Seifert, M., Wanninger, S., Zaborsky, N., Oostendorp, R., Ruland, J., Leitges, M., Kuhnt, T., Schaefer, Y., Lampl, B., Peschel, C., Egle, A., and Ringshausen, I.

Subjects
hemic and lymphatic diseases
Abstract

Tumor cell survival critically depends on heterotypic communication with benign cells in the microenvironrnent. Here, we describe a survival signaling pathway activated in stromal cells by contact to B cells from patients with chronic lymphocytic leukemia (CLL). The expression of protein kinase C (PKC)-beta II and the subsequent activation of NF-kappa B in bone marrow stromal cells are prerequisites to support the survival of malignant B cells. PKC-beta knockout mice are insusceptible to CLL transplantations, underscoring the in vivo significance of the PKC-beta II-NF-kappa B signaling pathway in the tumor microenvironment. Upregulated stromal PKG-beta II in biopsies from patients with CLL, acute lymphoblastic leukemia, and mantle cell lymphoma suggests that this pathway may commonly be activated in a variety of hematological malignancies.

Published
2013

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