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18 results on '"Yosifov, Deyan Yordanov"'

2. T-bet suppresses proliferation of malignant B cells in chronic lymphocytic leukemia

Author

Roessner, Philipp M., primary, Seufert, Isabelle, additional, Chapaprieta, Vicente, additional, Jayabalan, Ruparoshni, additional, Briesch, Hannah, additional, Massoni-Badosa, Ramon, additional, Boskovic, Pavle, additional, Beckendorff, Julian, additional, Roider, Tobias, additional, Arseni, Lavinia, additional, Coelho, Mariana, additional, Chakraborty, Supriya, additional, Vaca, Alicia, additional, Sivina, Mariela, additional, Muckenhuber, Markus, additional, Rodriguez-Rodriguez, Sonia, additional, Bonato, Alice, additional, Herbst, Sophie A., additional, Zapatka, Marc, additional, Sun, Clare, additional, Kretzmer, Helene, additional, Naake, Thomas, additional, Bruch, Peter-Martin, additional, Czernilofsky, Felix, additional, ten Hacken, Elisa, additional, Schneider, Martin, additional, Helm, Dominic, additional, Yosifov, Deyan Yordanov, additional, Kauer, Joseph, additional, Danilov, Alexey V., additional, Bewarder, Moritz, additional, Heyne, Kristina, additional, Schneider, Christof, additional, Stilgenbauer, Stephan, additional, Wiestner, Adrian, additional, Mallm, Jan-Philipp, additional, Burger, Jan A., additional, Efremov, Dimitar G, additional, Lichter, Peter, additional, Dietrich, Sascha, additional, Martín-Subero, José Ignacio, additional, Rippe, Karsten, additional, and Seiffert, Martina, additional

Published
2024
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4. Oxidative stress as candidate therapeutic target to overcome microenvironmental protection of CLL

Author

Yosifov, Deyan Yordanov, Idler, Irina, Bhattacharya, Nupur, Reichenzeller, Michaela, Close, Viola, Ezerina, Daria, Scheffold, Annika, Jebaraj, Billy Michael Chelliah, Kugler, Sabrina, Bloehdorn, Johannes, Bahlo, Jasmin, Robrecht, Sandra, Eichhorst, Barbara, Fischer, Kirsten, Weigel, Anja, Busch, Hauke, Lichter, Peter, Döhner, Hartmut, Dick, Tobias P., Stilgenbauer, Stephan, and Mertens, Daniel

Published
2020
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5. Acquired BTK mutations associated with resistance to noncovalent BTK inhibitors

Author

Qi, Jialei, primary, Endres, Sascha, additional, Yosifov, Deyan Yordanov, additional, Tausch, Eugen, additional, Dheenadayalan, Rashmi Priyadharshini, additional, Gao, Xiang, additional, Müller, Annika, additional, Schneider, Christof, additional, Mertens, Daniel, additional, Gierschik, Peter, additional, Wist, Martin, additional, Jebaraj, Billy Michael Chelliah, additional, and Stilgenbauer, Stephan, additional

Published
2023
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7. Novel BTK Mutations Conferring Resistance to Non-Covalent BTK Inhibitors and Alternative Treatment Strategy

Author

Qi, Jialei, primary, Endres, Sascha, additional, Yosifov, Deyan Yordanov, additional, Tausch, Eugen, additional, Dheenadayalan, Rashmi Priyadharshini, additional, Gao, Xiang, additional, Scheffold, Annika, additional, Seyfried, Felix, additional, Meyer, Lüder, additional, Schneider, Christof, additional, Mertens, Daniel, additional, Gierschik, Peter, additional, Wist, Martin, additional, Stilgenbauer, Stephan, additional, and Jebaraj, Billy Michael Chelliah, additional

Published
2022
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8. Genetic Markers and Front Line FCR/BR Vs. Rve, Gve and Give Treatment - Outcome Results from the CLL13/GAIA Trial

Author

Tausch, Eugen, primary, Schneider, Christof, additional, Furstenau, Moritz, additional, Robrecht, Sandra, additional, Yosifov, Deyan Yordanov, additional, Mertens, Daniel, additional, Gregor, Michael, additional, Thornton, Patrick, additional, Staber, Philipp B., additional, Tadmor, Tamar, additional, Levin, Mark-David, additional, da Cunha-Bang, Caspar, additional, Poulsen, Christian Bjørn, additional, Illmer, Thomas, additional, Schöttker, Björn, additional, Janssens, Ann, additional, Christiansen, Ilse, additional, Noesslinger, Thomas, additional, Baumann, Michael, additional, Wendtner, Clemens-Martin, additional, Eldering, Eric, additional, Kreuzer, Karl-Anton, additional, Ritgen, Matthias, additional, Fink, Anna-Maria, additional, Fischer, Kirsten, additional, Kater, Arnon P., additional, Niemann, Carsten Utoft, additional, Hallek, Michael, additional, Eichhorst, Barbara, additional, and Stilgenbauer, Stephan, additional

Published
2022
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10. Genetic Markers and Front Line FCR/BR Vs. Rve, Gve and Give Treatment - Outcome Results from the CLL13/GAIA Trial

Author

Tausch, Eugen, Schneider, Christof, Furstenau, Moritz, Robrecht, Sandra, Yosifov, Deyan Yordanov, Mertens, Daniel, Gregor, Michael, Thornton, Patrick, Staber, Philipp B., Tadmor, Tamar, Levin, Mark-David, Da Cunha-Bang, Caspar, Poulsen, Christian Bjorn, Illmer, Thomas, Schoettker, Bjoern, Janssens, Ann, Christiansen, Ilse, Noesslinger, Thomas, Baumann, Michael, Wendtner, Clemens-Martin, Eldering, Eric, Kreuzer, Karl-Anton, Ritgen, Matthias, Fink, Anna-Maria, Fischer, Kirsten, Kater, Arnon P., Niemann, Carsten Utoft, Hallek, Michael, Eichhorst, Barbara, Stilgenbauer, Stephan, Tausch, Eugen, Schneider, Christof, Furstenau, Moritz, Robrecht, Sandra, Yosifov, Deyan Yordanov, Mertens, Daniel, Gregor, Michael, Thornton, Patrick, Staber, Philipp B., Tadmor, Tamar, Levin, Mark-David, Da Cunha-Bang, Caspar, Poulsen, Christian Bjorn, Illmer, Thomas, Schoettker, Bjoern, Janssens, Ann, Christiansen, Ilse, Noesslinger, Thomas, Baumann, Michael, Wendtner, Clemens-Martin, Eldering, Eric, Kreuzer, Karl-Anton, Ritgen, Matthias, Fink, Anna-Maria, Fischer, Kirsten, Kater, Arnon P., Niemann, Carsten Utoft, Hallek, Michael, Eichhorst, Barbara, and Stilgenbauer, Stephan

Published
2022

11. Clonal evolution in chronic lymphocytic leukemia is scant in relapsed but accelerated in refractory cases after chemo(immune) therapy

Author

Zapatka, Marc, primary, Tausch, Eugen, additional, Öztürk, Selcen, additional, Yosifov, Deyan Yordanov, additional, Seiffert, Martina, additional, Zenz, Thorsten, additional, Schneider, Christof, additional, Blöhdorn, Johannes, additional, Döhner, Hartmut, additional, Mertens, Daniel, additional, Lichter, Peter, additional, and Stilgenbauer, Stephan, additional

Published
2021
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12. Oxidative stress as candidate therapeutic target to overcome microenvironmental protection of CLL

Author

Yosifov, Deyan Yordanov, primary, Idler, Irina, additional, Bhattacharya, Nupur, additional, Reichenzeller, Michaela, additional, Close, Viola, additional, Ezerina, Daria, additional, Scheffold, Annika, additional, Jebaraj, Billy Michael Chelliah, additional, Kugler, Sabrina, additional, Bloehdorn, Johannes, additional, Bahlo, Jasmin, additional, Robrecht, Sandra, additional, Eichhorst, Barbara, additional, Fischer, Kirsten, additional, Weigel, Anja, additional, Busch, Hauke, additional, Lichter, Peter, additional, Döhner, Hartmut, additional, Dick, Tobias P., additional, Stilgenbauer, Stephan, additional, and Mertens, Daniel, additional

Published
2019
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14. NOTCH1 Signaling Is Activated in CLL By Mutations of FBXW7 and Low Expression of USP28 at 11q23

Author

Close, Viola, primary, Close, William, additional, Kugler, Sabrina Julia, additional, Reichenzeller, Michaela, additional, Yosifov, Deyan Yordanov, additional, Bloehdorn, Johannes, additional, Pan, Leiling, additional, Tausch, Eugen, additional, Westhoff, Mike-Andrew, additional, Döhner, Hartmut, additional, Stilgenbauer, Stephan, additional, Oswald, Franz, additional, and Mertens, Daniel, additional

Published
2018
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15. FBXW7mutations reduce binding of NOTCH1, leading to cleaved NOTCH1 accumulation and target gene activation in CLL

Author

Close, Viola, Close, William, Kugler, Sabrina Julia, Reichenzeller, Michaela, Yosifov, Deyan Yordanov, Bloehdorn, Johannes, Pan, Leiling, Tausch, Eugen, Westhoff, Mike-Andrew, Döhner, Hartmut, Stilgenbauer, Stephan, Oswald, Franz, and Mertens, Daniel

Abstract

NOTCH1is mutated in 10% of chronic lymphocytic leukemia (CLL) patients and is associated with poor outcome. However, NOTCH1 activation is identified in approximately one-half of CLL cases even in the absence of NOTCH1mutations. Hence, there appear to be additional factors responsible for the impairment of NOTCH1 degradation. E3-ubiquitin ligase F-box and WD40 repeat domain containing-7 (FBXW7), a negative regulator of NOTCH1, is mutated in 2% to 6% of CLL patients. The functional consequences of these mutations in CLL are unknown. We found heterozygous FBXW7mutations in 36 of 905 (4%) untreated CLL patients. The majority were missense mutations (78%) that mostly affected the WD40 substrate binding domain; 10% of mutations occurred in the first exon of the α-isoform. To identify target proteins of FBXW7 in CLL, we truncated the WD40 domain in CLL cell line HG-3 via clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein-9 (Cas9). Homozygous truncation of FBXW7resulted in an increase of activated NOTCH1 intracellular domain (NICD) and c-MYC protein levels as well as elevated hypoxia-inducible factor 1-α activity. In silico modeling predicted that novel mutations G423V and W425C in the FBXW7-WD40 domain change the binding of protein substrates. This differential binding was confirmed via coimmunoprecipitation of overexpressed FBXW7 and NOTCH1. In primary CLL cells harboring FBXW7mutations, activated NICD levels were increased and remained stable upon translation inhibition. FBXW7mutations coincided with an increase in NOTCH1 target gene expression and explain a proportion of patients characterized by dysregulated NOTCH1 signaling.

Published
2019
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18. Clonal evolution in chronic lymphocytic leukemia is scant in relapsed but accelerated in refractory cases after chemo(immune) therapy.

Author

Zapatka M, Tausch E, Öztürk S, Yosifov DY, Seiffert M, Zenz T, Schneider C, Blöhdorn J, Döhner H, Mertens D, Lichter P, and Stilgenbauer S

Subjects
Clonal Evolution genetics, Clone Cells, Humans, Longitudinal Studies, Mutation, Leukemia, Lymphocytic, Chronic, B-Cell drug therapy, Leukemia, Lymphocytic, Chronic, B-Cell genetics
Abstract

Clonal evolution is involved in the progression of chronic lymphocytic leukemia (CLL). In order to link evolutionary patterns to different disease courses, we performed a long-term longitudinal mutation profiling study of CLL patients. Tracking somatic mutations and their changes in allele frequency over time and assessing the underlying cancer cell fraction revealed highly distinct evolutionary patterns. Surprisingly, in long-term stable disease and in relapse after long-lasting clinical response to treatment, clonal shifts are minor. In contrast, in refractory disease major clonal shifts occur although there is little impact on leukemia cell counts. As this striking pattern in refractory cases is not linked to a strong contribution of known CLL driver genes, the evolution is mostly driven by treatment-induced selection of sub-clones, underlining the need for novel, non-genotoxic treatment regimens.

Published
2022
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