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5. Dose modification dynamics of ponatinib in patients with chronic-phase chronic myeloid leukemia (CP-CML) from the PACE and OPTIC trials.

Author

Jabbour, Elias, Apperley, Jane, Cortes, Jorge, Rea, Delphine, Deininger, Michael, Abruzzese, Elisabetta, Chuah, Charles, DeAngelo, Daniel, Hochhaus, Andreas, Lipton, Jeffrey, Mauro, Michael, Nicolini, Franck, Pinilla-Ibarz, Javier, Rosti, Gianantonio, Rousselot, Philippe, Talpaz, Moshe, Vorog, Alexander, Ren, Xiaowei, Kantarjian, Hagop, and Shah, Neil Pravin

Subjects
Humans, Drug Resistance, Neoplasm, Leukemia, Myeloid, Chronic-Phase, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Imidazoles, Pyridazines, Fusion Proteins, bcr-abl, Protein Kinase Inhibitors, Antineoplastic Agents
Abstract

Ponatinib, the only approved all known-BCR::ABL1 inhibitor, is a third-generation tyrosine-kinase inhibitor (TKI) designed to inhibit BCR::ABL1 with or without any single resistance mutation, including T315I, and induced robust and durable responses at 45 mg/day in patients with CP-CML resistant to second-generation TKIs in the PACE trial. However, cardiovascular toxicities, including arterial occlusive events (AOEs), have emerged as treatment-related AEs within this class of TKIs. The OPTIC trial evaluated the efficacy and safety of ponatinib using a novel, response-based, dose-reduction strategy in patients with CP-CML whose disease is resistant to ≥2 TKIs or who harbor T315I. To assess the dose-response relationship and the effect on the safety of ponatinib, we examined the outcomes of patients with CP-CML enrolled in PACE and OPTIC who received 45 mg/day of ponatinib. A propensity score analysis was used to evaluate AOEs across both trials. Survival rates and median time to achieve ≤1% BCR::ABL1IS in OPTIC were similar or better than in PACE. The outcomes of patients with T315I mutations were robust in both trials. Patients in OPTIC had a lower exposure-adjusted incidence of AOEs compared with those in PACE. This analysis demonstrates that response-based dosing for ponatinib improves treatment tolerance and mitigates cardiovascular risk.

Published
2024

8. Health-related quality of life and symptoms of chronic myeloid leukemia patients after discontinuation of tyrosine kinase inhibitors: results from the EURO-SKI Trial

Author

Efficace, Fabio, Mahon, Francois-Xavier, Richter, Johan, Piciocchi, Alfonso, Cipriani, Marta, Nicolini, Franck E., Mayer, Jiri, Zackova, Daniela, Janssen, Jeroen J. W. M., Panayiotidis, Panayiotis, Vestergaard, Hanne, Koskenvesa, Perttu, Almeida, Antonio, Hjorth-Hansen, Henrik, Martinez-Lopez, Joaquin, Olsson-Strömberg, Ulla, Hochhaus, Andreas, Berger, Marc G., Etienne, Gabriel, Klamova, Hana, Faber, Edgar, Rousselot, Philippe, Pfirrmann, Markus, and Saussele, Susanne

Published
2024
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10. FRACTION: protocol of a phase II study of Fedratinib and Nivolumab combination in patients with myelofibrosis and resistance or suboptimal response to JAK-inhibitor treatment of the German MPN study group (GSG-MPN)

Author

Isfort, Susanne, von Bubnoff, Nikolas, Al-Ali, Haifa Kathrin, Becker, Heiko, Götze, Thorsten, le Coutre, Philipp, Griesshammer, Martin, Moskwa, Claudia, Wohn, Luisa, Riedel, Johanna, Palandri, Francesca, Manz, Kirsi, Hochhaus, Andreas, Döhner, Konstanze, and Heidel, Florian H.

Published
2024
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11. Asciminib monotherapy in patients with chronic-phase chronic myeloid leukemia with the T315I mutation after ≥1 prior tyrosine kinase inhibitor: 2-year follow-up results

Author

Cortes, Jorge E., Sasaki, Koji, Kim, Dong-Wook, Hughes, Timothy P., Etienne, Gabriel, Mauro, Michael J., Hochhaus, Andreas, Lang, Fabian, Heinrich, Michael C., Breccia, Massimo, Deininger, Michael, Goh, Yeow Tee, Janssen, Jeroen J.W.M., Talpaz, Moshe, de Soria, Valle Gomez Garcia, le Coutre, Philipp, DeAngelo, Daniel J., Damon, Andrea, Cacciatore, Silvia, Polydoros, Fotis, Agrawal, Nithya, and Rea, Delphine

Published
2024
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15. Management and outcome of patients with chronic myeloid leukemia in blast phase in the tyrosine kinase inhibitor era – analysis of the European LeukemiaNet Blast Phase Registry

Author

Brioli, Annamaria, Lomaia, Elza, Fabisch, Christian, Sacha, Tomasz, Klamova, Hana, Morozova, Elena, Golos, Aleksandra, Ernst, Philipp, Olsson-Stromberg, Ulla, Zackova, Daniela, Nicolini, Franck E., Bao, Han, Castagnetti, Fausto, Patkowska, Elzbieta, Mayer, Jiri, Hirschbühl, Klaus, Podgornik, Helena, Paczkowska, Edyta, Parry, Anne, Ernst, Thomas, Voskanyan, Astghik, Szczepanek, Elzbieta, Saussele, Susanne, Franke, Georg-Nikolaus, Kiani, Alexander, Faber, Edgar, Krause, Stefan, Casado, Luis Felipe, Lewandowski, Krzysztof, Eder, Matthias, Anhut, Peter, Gil, Justyna, Südhoff, Thomas, Hebart, Holger, Heibl, Sonja, Pfirrmann, Markus, Hochhaus, Andreas, and Lauseker, Michael

Published
2024
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16. µPhos: a scalable and sensitive platform for high-dimensional phosphoproteomics

Author

Denys Oliinyk, Andreas Will, Felix R Schneidmadel, Maximilian Böhme, Jenny Rinke, Andreas Hochhaus, Thomas Ernst, Nina Hahn, Christian Geis, Markus Lubeck, Oliver Raether, Sean J Humphrey, and Florian Meier

Subjects
Drug Response, Mass Spectrometry, Phosphoproteomics, Sample Preparation, Signaling, Biology (General), QH301-705.5, Medicine (General), R5-920
Abstract

Abstract Mass spectrometry has revolutionized cell signaling research by vastly simplifying the analysis of many thousands of phosphorylation sites in the human proteome. Defining the cellular response to perturbations is crucial for further illuminating the functionality of the phosphoproteome. Here we describe µPhos (‘microPhos’), an accessible phosphoproteomics platform that permits phosphopeptide enrichment from 96-well cell culture and small tissue amounts in 90% selectivity, and excellent quantitative reproducibility. Employing highly sensitive trapped ion mobility mass spectrometry, we quantify ~17,000 Class I phosphosites in a human cancer cell line using 20 µg starting material, and confidently localize ~6200 phosphosites from 1 µg. This depth covers key signaling pathways, rendering sample-limited applications and perturbation experiments with hundreds of samples viable. We employ µPhos to study drug- and time-dependent response signatures in a leukemia cell line, and by quantifying 30,000 Class I phosphosites in the mouse brain we reveal distinct spatial kinase activities in subregions of the hippocampal formation.

Published
2024
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17. Response-guided first-line therapy and treatment of relapse in aggressive lymphoma: 10-year follow-up of the PETAL trial

Author

Wilop, S., Tometten, M., Korfel, A., Keller, U., de Wit, M., Weissinger, F., Stark, U., Behringer, D., Bückner, U., Nückel, H., Schroers, R., Trenn, G., Hertenstein, B., Bernhard, H., Heike, M., Wörns, M.-A., Kroschinsky, F., Prange-Krex, G., Giagounidis, A., Grigoleit, G. U., Selbach, J., Petrasch, S., Balleisen, J. S., Schütte, J., Dienst, A., Germing, U., Dührsen, U., von Verschuer, U., Reimer, P., Höffkes, H.-G., Runde, V., Spohn, C., Moeller, R., Dürk, H., Kofahl-Krause, D., Heuser, M., Witzens-Harig, M., Müller-Tidow, C., Martens, U. M., Strumberg, D., La Rosée, P., Hochhaus, A., Link, H., Held, G., Kneba, M., Baldus, C., Naumann, R., Chemnitz, J. M., Schulte, K., Limmroth, C., Schwarzer, A., Niederwieser, D., Platzbecker, U., Heil, G., Schwalenberg, M., Grieshammer, M., Beck, C., Stephany, M., Mesters, R., Karsten, I. E., Held, H., Mahlmann, S., Steiniger, H., Gaska, T., Südhoff, T., Kreisel-Büstgens, C., Moorahrend, E., Maschmeyer, G., Jordan, K., Kloke, O., Klein, M., Höhler, T., Grube, M., Herr, W., Hahn, D., Raghavachar, A., Schmalz, O., Fett, W., Sandmann, M., Krohn, T., Brenner, W., Plotkin, M., Franzius, C., Kotzerke, J., Hautzel, H., Bockisch, A., Hertel, A., Bengel, F. M., Haberkorn, U., Freesmeyer, M., Lützen, U., Klein, A., Kluge, R., Larisch, R., Fricke, E., Holzinger, J., Schäfer, W., Weckesser, M., Nyuyki, F., Römer, W., Brink, I., Marienhagen, J., Pöpperl, G., Jöckel, K.-H., Nonnemacher, M., Rekowski, J., Scherag, A., Neuhäuser, M., Dührsen, Ulrich, Bockisch, Andreas, Hertenstein, Bernd, Karsten, Imke E., Kroschinsky, Frank, Heuser, Michael, Hochhaus, Andreas, Höffkes, Heinz-Gert, Behringer, Dirk, Prange-Krex, Gabriele, Tometten, Mareike, Grieshammer, Martin, Grigoleit, Götz U., Schmalz, Oliver, Jordan, Karin, Bernhard, Helga, Gaska, Tobias, Giagounidis, Aristoteles, Schroers, Roland, Martens, Uwe M., Held, Gerhard, Klapper, Wolfram, Jöckel, Karl-Heinz, Nonnemacher, Michael, and Hüttmann, Andreas

Published
2024
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19. Correction: Dose modification dynamics of ponatinib in patients with chronic-phase chronic myeloid leukemia (CP-CML) from the PACE and OPTIC trials

Author

Jabbour, Elias, Apperley, Jane, Cortes, Jorge, Rea, Delphine, Deininger, Michael, Abruzzese, Elisabetta, Chuah, Charles, DeAngelo, Daniel J., Hochhaus, Andreas, Lipton, Jeffrey H., Mauro, Michael, Nicolini, Franck, Pinilla-Ibarz, Javier, Rosti, Gianantonio, Rousselot, Philippe, Shah, Neil P., Talpaz, Moshe, Vorog, Alexander, Ren, Xiaowei, and Kantarjian, Hagop

Published
2024
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22. Differential effects of dosing regimen on the safety and efficacy of dasatinib: retrospective exposure–response analysis of a Phase III study

Author

Wang X, Roy A, Hochhaus A, Kantarjian HM, Chen TT, and Shah NP

Subjects
Therapeutics. Pharmacology, RM1-950
Abstract

Xiaoning Wang,1 Amit Roy,2 Andreas Hochhaus,3 Hagop M Kantarjian,4 Tai-Tsang Chen,5 Neil P Shah6 1Discovery Medicine and Clinical Pharmacology, Bristol-Myers Squibb, Lawrenceville, NJ, USA; 2Clinical Pharmacology and Pharmacometrics, Research and Development, Bristol-Myers Squibb, Lawrenceville, NJ, USA; 3Hematology/Oncology, Jena University Hospital, Jena, Germany; 4Department of Leukemia, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA; 5Department of Global Biometric Sciences, Bristol-Myers Squibb, Wallingford, CT, USA; 6Hematology/Oncology, University of California, San Francisco School of Medicine, San Francisco, CA, USA Purpose: Dasatinib is a prototypic short half-life BCR-ABL1 tyrosine kinase inhibitor. The recommended dose of dasatinib for chronic myeloid leukemia in chronic phase was changed from 70 mg twice daily to 100 mg once daily following a Phase III dose-optimization study. To better understand the superior benefit–risk profile of dasatinib 100 mg once daily, exposure–response was characterized for efficacy (major cytogenetic response) and safety (pleural effusion). Patients and methods: Dasatinib exposure in patients with chronic myeloid leukemia in chronic phase was determined by population pharmacokinetic analysis of data from seven dasatinib clinical studies (N = 981), including the Phase III dose-optimization study (n = 567). Data from the Phase III study were then used to characterize exposure–response relationships for the four dasatinib treatment regimens investigated (100 mg once daily, 50 mg twice daily, 140 mg once daily, and 70 mg twice daily). Results: Major cytogenetic response was significantly (P < 0.01) associated with weighted average steady-state dasatinib plasma concentrations, and pleural effusion was significantly associated with trough concentration. Major cytogenetic response was also significantly associated with maintenance of uninterrupted dosing. The 100 mg once daily arm had the lowest steady-state trough concentration of the four dose arms investigated in the Phase III study, and although this arm also had the lowest weighted average steady-state dasatinib plasma concentration, it had the highest dose maintenance. Conclusion: Dasatinib dose optimization to 100 mg once daily from 70 mg twice daily significantly minimizes adverse events while maintaining efficacy by exploiting differences in the measures of exposure associated with efficacy and safety. Keywords: chronic myeloid leukemia, pharmacokinetics, major cytogenetic response, pleural effusion

Published
2013

26. Mutated IKZF1 is an independent marker of adverse risk in acute myeloid leukemia

Author

Eckardt, Jan-Niklas, Stasik, Sebastian, Röllig, Christoph, Petzold, Andreas, Sauer, Tim, Scholl, Sebastian, Hochhaus, Andreas, Crysandt, Martina, Brümmendorf, Tim H., Naumann, Ralph, Steffen, Björn, Kunzmann, Volker, Einsele, Hermann, Schaich, Markus, Burchert, Andreas, Neubauer, Andreas, Schäfer-Eckart, Kerstin, Schliemann, Christoph, Krause, Stefan W., Herbst, Regina, Hänel, Mathias, Hanoun, Maher, Kaiser, Ulrich, Kaufmann, Martin, Rácil, Zdenek, Mayer, Jiri, Oelschlägel, Uta, Berdel, Wolfgang E., Ehninger, Gerhard, Serve, Hubert, Müller-Tidow, Carsten, Platzbecker, Uwe, Baldus, Claudia D., Dahl, Andreas, Schetelig, Johannes, Bornhäuser, Martin, Middeke, Jan Moritz, and Thiede, Christian

Published
2023
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28. Adressen

Author

Eucker, Jan, primary, Scholz, Christian W., additional, Bathon, Melanie, additional, Busse, Antonia, additional, Dieing, Annette, additional, Eucker, Jan, additional, Flath, Bernd, additional, Folprecht, Gunnar, additional, Habbel, Jan-Piet, additional, Heidel, Florian, additional, Hochhaus, Andreas, additional, Hübel, Kai, additional, Jann, Henning, additional, Jehn, Christian, additional, Klinghammer, Konrad, additional, Knauf, Wolfgang, additional, Kolb, Hans-Jochem, additional, Kroenlein, Hannes, additional, Kubasch, Anne Sophie, additional, Lüftner, Diana, additional, Meyer, Oliver, additional, Möhlig, Matthias, additional, Naumann, Ralph, additional, Nogai, Axel, additional, Ochsenreither, Sebastian, additional, Oettle, Helmut, additional, Pape, Ulrich-Frank, additional, Platzbecker, Uwe, additional, Rank, Andreas, additional, Reichardt, Peter, additional, Rick, Oliver, additional, Rieke, Damian, additional, Riess, Hanno, additional, Ruhnke, Markus, additional, Schaich, Markus, additional, Schalhorn, Andreas, additional, Schmälter, Ann-Kristin, additional, Schmidt-Graf, Friederike, additional, Schmittel, Alexander, additional, Schrezenmeier, Hubert, additional, Schulz, Carsten-Oliver, additional, Speiser, Dorothee, additional, Vogel, Arndt, additional, Baumgarten, Louisa von, additional, and Welland, Dr. med. Sabrina, additional

Published
2024
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30. Hematopoietic cell transplantation for older acute myeloid leukemia patients in first complete remission: results of a randomized phase III study

Author

Dietger Niederwieser, Dirk Hasenclever, Wolfgang Berdel, Bart J. Biemond, Haifa Al-Ali, Yves Chalandon, Michel van Gelder, Christian Junghanß, Gösta Gahrton, Mathias Hänel, Rüdiger Hehlmann, Thomas Heinicke, Andreas Hochhaus, Simona Iacobelli, Rien van Marwijk Kooy, Nicolaus Kröger, Jeroen Janssen, Madlen Jentzsch, Frank Breywisch, Mohamad Mohty, Stavroula Masouridi-Levrat, Gert Ossenkoppele, Jacob Passweg, Wolfram Pönisch, Johannes Schetelig, Christoph Schliemann, Sebastian Schwind, Matthias Stelljes, Leo F. Verdonck, Vladan Vucinic, Bob Löwenberg, and Jan Cornelissen

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Abstract

Given the selection of elderly patients with AML in first complete remission (CR1) the advantage of consolidation with allogeneic hematopoietic cell transplantation (HCT) over chemotherapy is still unclear. Newly diagnosed AML patients in CR1 aged 60-75 years were registered and a donor search initiated. After one consolidation cycle, patients with a matched donor were randomized to HCT with fludarabine/lowdose total body irradiation and cyclosporine/mycophenolate mofetil immunosuppression or conventional non-HCT. Primary outcome was restricted mean leukemia-free survival (RM-LFS) up to five years. Between 2010 and 2017, 245 patients (median age 67 years) were registered at CR1. After one consolidation, 26.9% of patients failed inclusion criteria. Of the 179 (73%) patients still on study, 75.4% had an HLA identical donor. Ten ineligible patients were excluded, and 125 randomized to HCT (n=83) or non-HCT (n=42). The primary outcome RM-LFS up to 5 years was 24.5 months (95%CI:18.9-30.1) in the HCT and 15.6 months (95%CI:10.4-20.8) in the non-HCT arm (p=0.022) due to a decrease in cumulative relapse incidence from 91.1 (95%CI:80.7-100.0) after non-HCT to 37.8 (95%CI:27.2-48.4)% after HCT (p

Published
2024
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33. Secondary-type mutations do not impact outcome in NPM1-mutated acute myeloid leukemia – implications for the European LeukemiaNet risk classification

Author

Eckardt, Jan-Niklas, Bill, Marius, Rausch, Christian, Metzeler, Klaus, Spiekermann, Karsten, Stasik, Sebastian, Sauer, Tim, Scholl, Sebastian, Hochhaus, Andreas, Crysandt, Martina, Brümmendorf, Tim H., Krug, Utz, Wörmann, Bernhard, Hiddemann, Wolfgang, Görlich, Dennis, Sauerland, Cristina, Steffen, Björn, Einsele, Hermann, Neubauer, Andreas, Burchert, Andreas, Schäfer-Eckart, Kerstin, Berdel, Wolfgang E., Schliemann, Christoph, Krause, Stefan W., Hänel, Mathias, Hanoun, Maher, Kaufmann, Martin, Fransecky, Lars, Braess, Jan, Ruhnke, Leo, Schetelig, Johannes, Middeke, Jan Moritz, Serve, Hubert, Baldus, Claudia D., Platzbecker, Uwe, Müller-Tidow, Carsten, Bornhäuser, Martin, Herold, Tobias, Thiede, Christian, and Röllig, Christoph

Published
2023
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37. Correction: “The 5th edition of The World Health Organization Classification of Haematolymphoid Tumours: Lymphoid Neoplasms” Leukemia. 2022 Jul;36(7):1720–1748

Author

Alaggio, Rita, Amador, Catalina, Anagnostopoulos, Ioannis, Attygalle, Ayoma D., de Oliveira Araujo, Iguaracyra Barreto, Berti, Emilio, Bhagat, Govind, Borges, Anita Maria, Boyer, Daniel, Calaminici, Mariarita, Chadburn, Amy, Chan, John K. C., Cheuk, Wah, Chng, Wee-Joo, Choi, John K., Chuang, Shih-Sung, Coupland, Sarah E., Czader, Magdalena, Dave, Sandeep S., de Jong, Daphne, Di Napoli, Arianna, Du, Ming-Qing, Elenitoba-Johnson, Kojo S., Ferry, Judith, Geyer, Julia, Gratzinger, Dita, Guitart, Joan, Gujral, Sumeet, Harris, Marian, Harrison, Christine J., Hartmann, Sylvia, Hochhaus, Andreas, Jansen, Patty M., Karube, Kennosuke, Kempf, Werner, Khoury, Joseph, Kimura, Hiroshi, Klapper, Wolfram, Kovach, Alexandra E., Kumar, Shaji, Lazar, Alexander J., Lazzi, Stefano, Leoncini, Lorenzo, Leung, Nelson, Leventaki, Vasiliki, Li, Xiao-Qiu, Lim, Megan S., Liu, Wei-Ping, Louissaint, Jr, Abner, Marcogliese, Andrea, Medeiros, L. Jeffrey, Michal, Michael, Miranda, Roberto N., Mitteldorf, Christina, Montes-Moreno, Santiago, Morice, William, Nardi, Valentina, Naresh, Kikkeri N., Natkunam, Yasodha, Ng, Siok-Bian, Oschlies, Ilske, Ott, German, Parrens, Marie, Pulitzer, Melissa, Rajkumar, S. Vincent, Rawstron, Andrew C., Rech, Karen, Rosenwald, Andreas, Said, Jonathan, Sarkozy, Clémentine, Sayed, Shahin, Saygin, Caner, Schuh, Anna, Sewell, William, Siebert, Reiner, Sohani, Aliyah R., Suzuki, Ritsuro, Tooze, Reuben, Traverse-Glehen, Alexandra, Vega, Francisco, Vergier, Beatrice, Wechalekar, Ashutosh D., Wood, Brent, Xerri, Luc, and Xiao, Wenbin

Published
2023
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38. Immunoproteasome function maintains oncogenic gene expression in KMT2A-complex driven leukemia

Author

Nuria Tubío-Santamaría, Ashok Kumar Jayavelu, Tina M. Schnoeder, Theresa Eifert, Chen-Jen Hsu, Florian Perner, Qirui Zhang, Daniela V. Wenge, Fynn M. Hansen, Joanna M. Kirkpatrick, Nidhi Jyotsana, Steven W. Lane, Björn von Eyss, Aniruddha J. Deshpande, Michael W. M. Kühn, Juerg Schwaller, Clemens Cammann, Ulrike Seifert, Frédéric Ebstein, Elke Krüger, Andreas Hochhaus, Michael Heuser, Alessandro Ori, Matthias Mann, Scott A. Armstrong, and Florian H. Heidel

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Pharmacologic targeting of chromatin-associated protein complexes has shown significant responses in KMT2A-rearranged (KMT2A-r) acute myeloid leukemia (AML) but resistance frequently develops to single agents. This points to a need for therapeutic combinations that target multiple mechanisms. To enhance our understanding of functional dependencies in KMT2A-r AML, we have used a proteomic approach to identify the catalytic immunoproteasome subunit PSMB8 as a specific vulnerability. Genetic and pharmacologic inactivation of PSMB8 results in impaired proliferation of murine and human leukemic cells while normal hematopoietic cells remain unaffected. Disruption of immunoproteasome function drives an increase in transcription factor BASP1 which in turn represses KMT2A-fusion protein target genes. Pharmacologic targeting of PSMB8 improves efficacy of Menin-inhibitors, synergistically reduces leukemia in human xenografts and shows preserved activity against Menin-inhibitor resistance mutations. This identifies and validates a cell-intrinsic mechanism whereby selective disruption of proteostasis results in altered transcription factor abundance and repression of oncogene-specific transcriptional networks. These data demonstrate that the immunoproteasome is a relevant therapeutic target in AML and that targeting the immunoproteasome in combination with Menin-inhibition could be a novel approach for treatment of KMT2A-r AML.

Published
2023
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39. The 5th edition of the World Health Organization Classification of Haematolymphoid Tumours: Lymphoid Neoplasms

Author

Alaggio, Rita, Amador, Catalina, Anagnostopoulos, Ioannis, Attygalle, Ayoma D, Araujo, Iguaracyra Barreto de Oliveira, Berti, Emilio, Bhagat, Govind, Borges, Anita Maria, Boyer, Daniel, Calaminici, Mariarita, Chadburn, Amy, Chan, John KC, Cheuk, Wah, Chng, Wee-Joo, Choi, John K, Chuang, Shih-Sung, Coupland, Sarah E, Czader, Magdalena, Dave, Sandeep S, de Jong, Daphne, Du, Ming-Qing, Elenitoba-Johnson, Kojo S, Ferry, Judith, Geyer, Julia, Gratzinger, Dita, Guitart, Joan, Gujral, Sumeet, Harris, Marian, Harrison, Christine J, Hartmann, Sylvia, Hochhaus, Andreas, Jansen, Patty M, Karube, Kennosuke, Kempf, Werner, Khoury, Joseph, Kimura, Hiroshi, Klapper, Wolfram, Kovach, Alexandra E, Kumar, Shaji, Lazar, Alexander J, Lazzi, Stefano, Leoncini, Lorenzo, Leung, Nelson, Leventaki, Vasiliki, Li, Xiao-Qiu, Lim, Megan S, Liu, Wei-Ping, Louissaint, Abner, Marcogliese, Andrea, Medeiros, L Jeffrey, Michal, Michael, Miranda, Roberto N, Mitteldorf, Christina, Montes-Moreno, Santiago, Morice, William, Nardi, Valentina, Naresh, Kikkeri N, Natkunam, Yasodha, Ng, Siok-Bian, Oschlies, Ilske, Ott, German, Parrens, Marie, Pulitzer, Melissa, Rajkumar, S Vincent, Rawstron, Andrew C, Rech, Karen, Rosenwald, Andreas, Said, Jonathan, Sarkozy, Clémentine, Sayed, Shahin, Saygin, Caner, Schuh, Anna, Sewell, William, Siebert, Reiner, Sohani, Aliyah R, Tooze, Reuben, Traverse-Glehen, Alexandra, Vega, Francisco, Vergier, Beatrice, Wechalekar, Ashutosh D, Wood, Brent, Xerri, Luc, and Xiao, Wenbin

Subjects
Cancer, Hematologic Neoplasms, Humans, Lymphoma, World Health Organization, Clinical Sciences, Oncology and Carcinogenesis, Immunology
Abstract

We herein present an overview of the upcoming 5th edition of the World Health Organization Classification of Haematolymphoid Tumours focussing on lymphoid neoplasms. Myeloid and histiocytic neoplasms will be presented in a separate accompanying article. Besides listing the entities of the classification, we highlight and explain changes from the revised 4th edition. These include reorganization of entities by a hierarchical system as is adopted throughout the 5th edition of the WHO classification of tumours of all organ systems, modification of nomenclature for some entities, revision of diagnostic criteria or subtypes, deletion of certain entities, and introduction of new entities, as well as inclusion of tumour-like lesions, mesenchymal lesions specific to lymph node and spleen, and germline predisposition syndromes associated with the lymphoid neoplasms.

Published
2022

40. The 5th edition of the World Health Organization Classification of Haematolymphoid Tumours: Myeloid and Histiocytic/Dendritic Neoplasms

Author

Khoury, Joseph D, Solary, Eric, Abla, Oussama, Akkari, Yassmine, Alaggio, Rita, Apperley, Jane F, Bejar, Rafael, Berti, Emilio, Busque, Lambert, Chan, John KC, Chen, Weina, Chen, Xueyan, Chng, Wee-Joo, Choi, John K, Colmenero, Isabel, Coupland, Sarah E, Cross, Nicholas CP, De Jong, Daphne, Elghetany, M Tarek, Takahashi, Emiko, Emile, Jean-Francois, Ferry, Judith, Fogelstrand, Linda, Fontenay, Michaela, Germing, Ulrich, Gujral, Sumeet, Haferlach, Torsten, Harrison, Claire, Hodge, Jennelle C, Hu, Shimin, Jansen, Joop H, Kanagal-Shamanna, Rashmi, Kantarjian, Hagop M, Kratz, Christian P, Li, Xiao-Qiu, Lim, Megan S, Loeb, Keith, Loghavi, Sanam, Marcogliese, Andrea, Meshinchi, Soheil, Michaels, Phillip, Naresh, Kikkeri N, Natkunam, Yasodha, Nejati, Reza, Ott, German, Padron, Eric, Patel, Keyur P, Patkar, Nikhil, Picarsic, Jennifer, Platzbecker, Uwe, Roberts, Irene, Schuh, Anna, Sewell, William, Siebert, Reiner, Tembhare, Prashant, Tyner, Jeffrey, Verstovsek, Srdan, Wang, Wei, Wood, Brent, Xiao, Wenbin, Yeung, Cecilia, and Hochhaus, Andreas

Subjects
Genetics, Human Genome, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Hematologic Neoplasms, Histiocytosis, Humans, World Health Organization, Clinical Sciences, Oncology and Carcinogenesis, Immunology
Abstract

The upcoming 5th edition of the World Health Organization (WHO) Classification of Haematolymphoid Tumours is part of an effort to hierarchically catalogue human cancers arising in various organ systems within a single relational database. This paper summarizes the new WHO classification scheme for myeloid and histiocytic/dendritic neoplasms and provides an overview of the principles and rationale underpinning changes from the prior edition. The definition and diagnosis of disease types continues to be based on multiple clinicopathologic parameters, but with refinement of diagnostic criteria and emphasis on therapeutically and/or prognostically actionable biomarkers. While a genetic basis for defining diseases is sought where possible, the classification strives to keep practical worldwide applicability in perspective. The result is an enhanced, contemporary, evidence-based classification of myeloid and histiocytic/dendritic neoplasms, rooted in molecular biology and an organizational structure that permits future scalability as new discoveries continue to inexorably inform future editions.

Published
2022

41. Immunoproteasome function maintains oncogenic gene expression in KMT2A-complex driven leukemia

Author

Tubío-Santamaría, Nuria, Jayavelu, Ashok Kumar, Schnoeder, Tina M., Eifert, Theresa, Hsu, Chen-Jen, Perner, Florian, Zhang, Qirui, Wenge, Daniela V., Hansen, Fynn M., Kirkpatrick, Joanna M., Jyotsana, Nidhi, Lane, Steven W., von Eyss, Björn, Deshpande, Aniruddha J., Kühn, Michael W. M., Schwaller, Juerg, Cammann, Clemens, Seifert, Ulrike, Ebstein, Frédéric, Krüger, Elke, Hochhaus, Andreas, Heuser, Michael, Ori, Alessandro, Mann, Matthias, Armstrong, Scott A., and Heidel, Florian H.

Published
2023
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42. UBTF tandem duplications are rare but recurrent alterations in adult AML and associated with younger age, myelodysplasia, and inferior outcome

Author

Georgi, Julia-Annabell, Stasik, Sebastian, Eckardt, Jan-Niklas, Zukunft, Sven, Hartwig, Marita, Röllig, Christoph, Middeke, Jan Moritz, Oelschlägel, Uta, Krug, Utz, Sauer, Tim, Scholl, Sebastian, Hochhaus, Andreas, Brümmendorf, Tim H., Naumann, Ralph, Steffen, Björn, Einsele, Hermann, Schaich, Markus, Burchert, Andreas, Neubauer, Andreas, Schäfer-Eckart, Kerstin, Schliemann, Christoph, Krause, Stefan W., Hänel, Mathias, Noppeney, Richard, Kaiser, Ulrich, Baldus, Claudia D., Kaufmann, Martin, Müller-Tidow, Carsten, Platzbecker, Uwe, Berdel, Wolfgang E., Serve, Hubert, Ehninger, Gerhard, Bornhäuser, Martin, Schetelig, Johannes, Kroschinsky, Frank, and Thiede, Christian

Published
2023
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43. Alterations of cohesin complex genes in acute myeloid leukemia: differential co-mutations, clinical presentation and impact on outcome

Author

Eckardt, Jan-Niklas, Stasik, Sebastian, Röllig, Christoph, Sauer, Tim, Scholl, Sebastian, Hochhaus, Andreas, Crysandt, Martina, Brümmendorf, Tim H., Naumann, Ralph, Steffen, Björn, Kunzmann, Volker, Einsele, Hermann, Schaich, Markus, Burchert, Andreas, Neubauer, Andreas, Schäfer-Eckart, Kerstin, Schliemann, Christoph, Krause, Stefan W., Herbst, Regina, Hänel, Mathias, Hanoun, Maher, Kaiser, Ulrich, Kaufmann, Martin, Rácil, Zdenek, Mayer, Jiri, Cerqueira, Tiago, Kroschinsky, Frank, Berdel, Wolfgang E., Serve, Hubert, Müller-Tidow, Carsten, Platzbecker, Uwe, Baldus, Claudia D., Schetelig, Johannes, Siepmann, Timo, Bornhäuser, Martin, Middeke, Jan Moritz, and Thiede, Christian

Published
2023
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44. Treatment of chronic-phase chronic myeloid leukemia in patients randomized to dasatinib or imatinib after suboptimal responses to three months of imatinib therapy: final 5-year results from DASCERN

Author

Jorge E. Cortes, Qian Jiang, Jianxiang Wang, Jianyu Weng, Huanling Zhu, Xiaoli Liu, Andreas Hochhaus, Dong-Wook Kim, Jerald Radich, Michael Savona, Patricia Martin-Regueira, Oumar Sy, and Giuseppe Saglio

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Abstract

Early molecular response (EMR) at 3 months is predictive of improved overall survival (OS) and progression-free survival (PFS) in patients with chronic myeloid leukemia in the chronic phase (CML-CP). Although about one-third of patients treated with first-line imatinib do not achieve EMR, long-term OS and PFS are still observed in most patients. DASCERN (NCT01593254) is a prospective, phase IIb, randomized trial evaluating a switch to dasatinib in patients who have not achieved EMR after 3 months of treatment with first-line imatinib. Early analysis demonstrated an improved major molecular response (MMR) rate at 12 months with dasatinib versus imatinib (29% vs. 13%, P=0.005). Here, we report results from the final 5-year follow-up. In total, 174 patients were randomized to dasatinib and 86 to remain on imatinib. Forty-six (53%) patients who remained on imatinib but subsequently experienced failure were allowed to cross over to dasatinib per protocol. At a minimum follow-up of 60 months, the cumulative MMR rate was significantly higher in patients randomized to dasatinib versus imatinib (77% vs. 44%, P

Published
2024
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45. Time from diagnosis to treatment has no impact on survival in newly diagnosed acute myeloid leukemia treated with venetoclax-based regimens

Author

David Baden, Sven Zukunft, Gema Hernandez, Nadine Wolgast, Sophie Steinhauser, Alexander Pohlmann, Christoph Schliemann, Jan-Henrik Mikesch, Bjorn Steffen, Tim Sauer, Maher Hanoun, Kerstin Schafer-Eckart, Stefan W. Krause, Mathias Hanel, Hermann Einsele, Edgar Jost, Tim H. Brummendorf, Sebastian Scholl, Andreas Hochhaus, Andreas Neubauer, Andreas Burchert, Martin Kaufmann, Dirk Niemann, Markus Schaich, Wolfgang Blau, Alexander Kiani, Martin Gorner, Ulrich Kaiser, Johannes Kullmer, Thomas Weber, Wolfgang E Berdel, Gerhard Ehninger, Carsten Muller-Tidow, Uwe Platzbecker, Hubert Serve, Martin Bornhauser, Christoph Rollig, Claudia D Baldus, and Lars Fransecky

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Abstract

In newly diagnosed acute myeloid leukemia, immediate initiation of treatment is standard of care. However, deferral of antileukemic therapy may be indicated to assess comorbidities or pre-therapeutic risk factors. We explored the impact of time from diagnosis to treatment on outcomes in newly diagnosed acute myeloid leukemia undergoing venetoclax-based therapy in two distinct cohorts. By querying the Study Alliance Leukemia database and the global health network TriNetX, we identified 138 and 717 patients respectively with an average age of 76 and 72 years who received venetoclax-based firstline therapy. When comparing patients who started treatment earlier or later than 10 days after initial diagnosis, no significant difference in median overall survival was observed - neither in the SAL cohort (7.7 vs. 9.6 months, p=.42) nor in the TriNetX cohort (7.5 vs. 7.2 months, p=.41). Similarly, severe infections, bleeding, and thromboembolic events were equally observed between early and later treatments, both in the overall patient groups and specific subgroups (age ≥75 years or leukocytes ≥20x109/L). This retrospective analysis indicates that delaying the start of venetoclax-based therapy in newly diagnosed acute myeloid leukemia might be a safe option for selected patients, provided that close clinical monitoring is performed.

Published
2024
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47. Step-in dosing of bosutinib in pts with chronic phase chronic myeloid leukemia (CML) after second-generation tyrosine kinase inhibitor (TKI) therapy: results of the Bosutinib Dose Optimization (BODO) Study

Author

Isfort, Susanne, Manz, Kirsi, Teichmann, Lino L., Crysandt, Martina, Burchert, Andreas, Hochhaus, Andreas, Saussele, Susanne, Kiani, Alexander, Göthert, Joachim R., Illmer, Thomas, Schafhausen, Philippe, Al-Ali, Haifa Kathrin, Stegelmann, Frank, Hänel, Mathias, Pfeiffer, Tim, Giagounidis, Aristoteles, Franke, Georg-Nikolaus, Koschmieder, Steffen, Fabarius, Alice, Ernst, Thomas, Warnken-Uhlich, Mareille, Wolber, Uta, Kohn, Denise, Pfirrmann, Markus, Wolf, Dominik, and Brümmendorf, Tim H.

Published
2023
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