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13 results on '"Jöhrens, Korinna"'

1. B-cell receptor–driven MALT1 activity regulates MYC signaling in mantle cell lymphoma

Author

Dai, Beiying, Grau, Michael, Juilland, Mélanie, Klener, Pavel, Höring, Elisabeth, Molinsky, Jan, Schimmack, Gisela, Aukema, Sietse M., Hoster, Eva, Vogt, Niklas, Staiger, Annette M., Erdmann, Tabea, Xu, Wendan, Erdmann, Kristian, Dzyuba, Nicole, Madle, Hannelore, Berdel, Wolfgang E., Trneny, Marek, Dreyling, Martin, Jöhrens, Korinna, Lenz, Peter, Rosenwald, Andreas, Siebert, Reiner, Tzankov, Alexandar, Klapper, Wolfram, Anagnostopoulos, Ioannis, Krappmann, Daniel, Ott, German, Thome, Margot, and Lenz, Georg

Published
2017
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2. Prevalence, Clinical and Molecular Features, and Prognostic Value of Tetraploidy/Near-Tetraploidy in Patients with Acute Myeloid Leukemia

Author

Ruhnke, Leo, primary, Frimmel, Julia, additional, Röllig, Christoph, additional, Mohr, Brigitte, additional, Altmann, Heidi, additional, Poitz, David, additional, Zukunft, Sven, additional, Schranz, Katrin, additional, Vosberg, Sebastian, additional, Spiekermann, Karsten, additional, von Bergwelt, Michael, additional, Jost, Edgar, additional, Dressler, Sabine, additional, Schäfer-Eckart, Kerstin, additional, Chavakis, Triantafyllos, additional, Aust, Daniela, additional, Jöhrens, Korinna, additional, Baretton, Gustavo, additional, Bornhäuser, Martin, additional, Greif, Philipp A., additional, Stölzel, Friedrich, additional, Herold, Sylvia, additional, and Wagenführ, Lisa, additional

Published
2022
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6. B-Cell Receptor Driven MALT1 Activity Regulates MYC Signaling in Mantle Cell Lymphoma

Author

Dai, Beiying, primary, Grau, Michael, additional, Juilland, Mélanie, additional, Klener, Pavel, additional, Höring, Elisabeth, additional, Molinsky, Jan, additional, Schimmack, Gisela, additional, Aukema, Sietse M, additional, Vogt, Niklas, additional, Staiger, Annette M., additional, Erdmann, Tabea, additional, Xu, Wendan, additional, Erdmann, Kristian, additional, Berdel, Wolfgang E, additional, Trneny, Marek, additional, Dreyling, Martin H., additional, Jöhrens, Korinna, additional, Lenz, Peter, additional, Rosenwald, Andreas, additional, Siebert, Reiner, additional, Tzankov, Alexandar, additional, Klapper, Wolfram, additional, Anagnostopoulos, Ioannis, additional, Krappmann, Daniel, additional, Ott, German, additional, Thome, Margot, additional, and Lenz, Georg, additional

Published
2016
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7. Bone marrow T-cell infiltration during acute GVHD is associated with delayed B-cell recovery and function after HSCT

Author

Mensen, Angela, primary, Jöhrens, Korinna, additional, Anagnostopoulos, Ioannis, additional, Demski, Sonya, additional, Oey, Maike, additional, Stroux, Andrea, additional, Hemmati, Philipp, additional, Westermann, Jörg, additional, Blau, Olga, additional, Wittenbecher, Friedrich, additional, Movassaghi, Kamran, additional, Szyska, Martin, additional, Thomas, Sybill, additional, Dörken, Bernd, additional, Scheibenbogen, Carmen, additional, Arnold, Renate, additional, and Na, Il-Kang, additional

Published
2014
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8. Acute Bone Marrow GvHD Is Associated With Delayed B Cell Neogenesis and Impaired Natural Antibody Response After Allogeneic Hematopoietic Stem Cell Transplantation

Author

Mensen, Angela, primary, Jöhrens, Korinna, additional, Anagnostopoulos, Ioannis, additional, Demski, Sonya, additional, Ochs, Christoph, additional, Hemmati, Philipp, additional, Vuong, Giang Lam, additional, Rieger, Kathrin, additional, Blau, Olga, additional, Westermann, Jörg, additional, Dörken, Bernd, additional, Scheibenbogen, Carmen, additional, Arnold, Renate, additional, and Na, Il-Kang, additional

Published
2013
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9. High-Level Expression of Mastermind-Like 2 (MAML2) Contributes to Aberrant Activation of the NOTCH Signaling Pathway In Human Lymphomas

Author

Köchert, Karl, primary, Kreher, Stephan, additional, Aster, Jon C, additional, Kitagawa, Motoo, additional, Jöhrens, Korinna, additional, Anagnostopoulos, Ioannis, additional, Jundt, Franziska, additional, Stein, Harald, additional, Janz, Martin, additional, Dörken, Bernd, additional, and Mathas, Stephan, additional

Published
2010
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11. Aberrant expression of the Th2 cytokine IL-21 in Hodgkin lymphoma cells regulates STAT3 signaling and attracts Tregcells via regulation of MIP-3α

Author

Lamprecht, Björn, Kreher, Stephan, Anagnostopoulos, Ioannis, Jöhrens, Korinna, Monteleone, Giovanni, Jundt, Franziska, Stein, Harald, Janz, Martin, Dörken, Bernd, and Mathas, Stephan

Abstract

The malignant Hodgkin/Reed-Sternberg (HRS) cells of classical Hodgkin lymphoma (HL) are derived from mature B cells, but have lost a considerable part of the B cell–specific gene expression pattern. Consequences of such a lineage infidelity for lymphoma pathogenesis are currently not defined. Here, we report that HRS cells aberrantly express the common cytokine-receptor γ-chain (γc) cytokine IL-21, which is usually restricted to a subset of CD4+T cells, and the corresponding IL-21 receptor. We demonstrate that IL-21 activates STAT3 in HRS cells, up-regulates STAT3 target genes, and protects HRS cells from CD95 death receptor–induced apoptosis. Furthermore, IL-21 is involved in up-regulation of the CC chemokine macrophage-inflammatory protein-3α (MIP-3α) in HRS cells. MIP-3α in turn attracts CCR6+CD4+CD25+FoxP3+CD127loregulatory T cells toward HRS cells, which might favor their immune escape. Together, these data support the concept that aberrant expression of B lineage–inappropriate genes plays an important role for the biology of HL tumor cells.

Published
2008
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12. Classical Hodgkin lymphoma is characterized by high constitutive expression of activating transcription factor 3 (ATF3), which promotes viability of Hodgkin/Reed-Sternberg cells

Author

Janz, Martin, Hummel, Michael, Truss, Matthias, Wollert-Wulf, Brigitte, Mathas, Stephan, Jöhrens, Korinna, Hagemeier, Christian, Bommert, Kurt, Stein, Harald, Dörken, Bernd, and Bargou, Ralf C.

Abstract

Hodgkin/Reed-Sternberg (HRS) cells of classical Hodgkin lymphoma (cHL) display unique characteristics that discriminate cHL from other B-cell lymphomas and normal B cells. Therefore, comparative gene expression profiling of Hodgkin and non-Hodgkin B cells could lead to the identification of candidate genes that are critical for the pathogenesis of cHL. We performed microarray analysis of Hodgkin and non-Hodgkin cell lines and identified activating transcription factor 3 (ATF3), a member of the cyclic AMP response element binding protein (CREB)/ATF family, as a differentially expressed candidate gene. Extensive analysis of a large panel of cell lines, primary tumor samples, and normal tissues revealed that high expression of ATF3 is found in nearly all cases of cHL and is almost exclusively restricted to it. Selective knock-down of ATF3 by RNA interference suppressed proliferation and strongly reduced viability of Hodgkin cells. Thus, overexpression of ATF3 is a molecular hallmark of cHL that contributes to the malignant growth of HRS cells. (Blood. 2006;107:2536-2539)

Published
2006
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13. B-cell receptor-driven MALT1 activity regulates MYC signaling in mantle cell lymphoma.

Author

Beiying Dai, Grau, Michael, Juilland, Mélanie, Klener, Pavel, Höring, Elisabeth, Molinsky, Jan, Schimmack, Gisela, Aukema, Sietse M., Hoster, Eva, Vogt, Niklas, Staiger, Annette M., Erdmann, Tabea, Wendan Xu, Erdmann, Kristian, Dzyuba, Nicole, Madle, Hannelore, Berdel, Wolfgang E., Trneny, Marek, Dreyling, Martin, and Jöhrens, Korinna

Subjects
*MANTLE cell lymphoma, *TALL-1 (Protein), *ANTIGEN presenting cells, *CELL receptors, *IMMUNOGLOBULIN class switching, *DIAGNOSIS, *THERAPEUTICS
Abstract

Mantle cell lymphoma (MCL) is a mature B-cell lymphoma characterized by poor clinical outcome. Recent studies revealed the importance of B-cell receptor (BCR) signaling in maintaining MCL survival. However, it remains unclear which role MALT1, an essential component of the CARD11-BCL10-MALT1 complex that links BCR signaling to the NF-κB pathway, plays in the biology of MCL. Here we show that a subset of MCLs is addicted to MALT1, as its inhibition by either RNA or pharmacologic interference induced cytotoxicity both in vitro and in vivo. Gene expression profiling following MALT1 inhibition demonstrated that MALT1 controls an MYC-driven gene expression network predominantly through increasing MYC protein stability. Thus, our analyses identify a previously unappreciated regulatory mechanism of MYC expression. Investigating primary mouse splenocytes, we could demonstrate that MALT1-induced MYC regulation is not restricted to MCL, but represents a common mechanism. MYC itself is pivotal for MCL survival because its downregulation and pharmacologic inhibition induced cytotoxicity in all MCL models. Collectively, these results provide a strong mechanistic rationale to investigate the therapeutic efficacy of targeting the MALT1-MYC axis in MCL patients. [ABSTRACT FROM AUTHOR]

Published
2017
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