Correction: High-risk additional chromosomal abnormalities at low blast counts herald death by CML

Hehlmann, Rüdiger; Voskanyan, Astghik; Lauseker, Michael; Pfirrmann, Markus; Kalmanti, Lida; Rinaldetti, Sébastien; Kohlbrenner, Katharina; Haferlach, Claudia; Schlegelberger, Brigitte; Fabarius, Alice; Seifarth, Wolfgang; Spieß, Birgit; Wuchter, Patrick; Krause, Stefan W.; Kolb, Hans Jochem; Neubauer, Andreas; Nerl, Christoph; Gratwohl, Aloïs; Baerlocher, Gabriela M.; Burchert, Andreas; Brümmendorf, Tim H.; Hasford, Jörg; Hochhaus, Andreas; Saußele, Susanne; Baccarani, Michele; Weikersthal, Ludwig Fischer von; Hahn, Michael; Schlimok, G.; Reichert, Dietmar; Janssen, J.J.W.M.; Martens, Uwe M.; Majunke, Peter; Reichert, Peter; Neben, Kai; Korsten, Stefan; Scholz, C; Oldenkott, Bernd; Heßling, Jörg; Kingreen, D.; Sperling, Christian; Schelenz, C; Blau, Igor W.; Urmersbach, A.; Ludwig, Wolf Dieter; Coutre, Philipp le; Arnold, Renate; Wit, Maurice de; Pezzutto, Antonio; Schafer, Eric S.; Schroers, Roland; Lochter, A.; Behringer, Dirk; Ko, Yoo‐Joung; Weidenhöfer, St.; Verbeek, Walter; Brossart, Peter; Trenn, Guido; Pommerien, W.; Krauter, Juergen; Doering, Gabriele; Munzinger, H.; Diekmann, C.; Hertenstein, Bernd; Stier, Sebastian; Möller-Faßbender, F.; Hänel, Mathias; Zöller, Thomas; Lamberti, Christof; Koch, Bernd; Henzel, A.; Wagner, Susanne; Schmalenbach, A.; Hoffknecht, M.; Ehninger, Gerhard; Kiani, A.; Illmer, Thomas; C, Aul; Flaßhove, Michael; Henneke, Felicitas; Simon, M.; Müller, L.; Becker, Heiko; Janz, R. F.; Eckart, Michael J.; Fuchs, Roland J.; Schlegel, Frank; Wattad, Mohammad Amen; Rudolph, R. H.; Beelen, Dietrich; Lindemann, A; Linck, D.; Wassman,; Jäger, Elke; Al-Batran, S.; Reiber, T; Waller, Christiane; Hoeffkes, Heinz-Gert; Schulz, Lucas T; Tajrobehkar, K.; Mittermüller, J.; Pralle, H.; Runde, Volker; Ap, Høyer; Tessen, H. W.; Trümper, Lorenz; Schmidt, Christian A.; Sieber, M.; Eschenburg, Henning; Depenbusch, Reinhard; Rösel, Siegfried; Lindemann, Hans‐Walter; Wolf, Hans Heinrich; Spohn, C.; Moeller, Regina; Hossfeld, Dieter K.; Zander, Axel R.; Schafhausen, Philippe; Koster, Harry; Hollburg, Wiebke; Schmitz, N.; Dürk, Heinz; Hemeier, M.; Grote-Metke, A.; Weischer, H.; Bechtel, Brett F.; Balleisen, L.; Sosada, M.; Ho, A. D.; Petersen, Volker; Dengler, Jolanta; Bildat, Stephan; Hahn, León I. Bernstein; Dietzfelbinger, Hermann; Gröschel, W.; Bartholomäus, A.; Freier, W.; Sievers, Burkhard; Pfreundschuh, I. M.; Herrmann, Tara; Fauser, Axel A.; Menzel, Juliane; Kemmerling, M.; Hansen, Richard M.; Link, H.; Schatz, Mary Pullig; Bentz, Martin; Prümmer, Otto; Kneba, Michael; Heymanns, Jochen; Schmitz, Stephan; Scheid, Christof; Lollert, André; Neise, Michael; Planker, M.; Stauch, Martina; Schröder, M.; Kempf, Barbara; Vehling-Kaiser, U.; Kremers, Stephan; Köchling, Georg; Hartmann, Franz; Neuhaus, Thomas J.; Fetscher, Sebastian; Kämpfe, Dietrich; Heil, Gerhard; Uppenkamp, Michael; Goldmann, Britta; Huber, Timothy; Hieber, U.; Plöger, Christoph; Grießhammer, Martin; Lange, Claudia; Göttler, Bernhard; Lunscken, C.; Schiel, Xaver; Scheidegger, Claude; Stötzer, Oliver; Hitz, Henry B.; Schick, HD; Völkl, Simon; Spiekermann, Karsten; Berdel, Wolfgang E.; Hebart, Holger; Ladda, E.; Schmidt, P.M.; Burkhardt, Ute; Hentschke, S.; Falge, Christiane; Reschke, Daniel; Köhne, C. A.; Müller-Naendrup, Clemens; Sauer, Maik; Frühauf, S.; Ranft, K; Dencausse, Y.; Sandritter, Bettina; Baake, G.; Hofknecht, M.; Dengler, Robert; Edinger, Matthias; Schenk, Maryjean; Wehmeier, A.; Weidelich, H. P.; Pihusch, Rudolf; Stahlhut, Kerstin; Baldus, M.; Matzdorff, Axel; Geer, Thomas; Schanz, Stefan; Käfer, G.; Gassmann, W.; Priebe-Richter, C; Demandt, Matthias; Springer, Günther; Fiechtner, Heinrich; Denzlinger, Claudio; Schleicher, Jan; Assman, D.; Gaeckler, R.; Adam, G.; Waladkhani, Ali Reza; Rendenbach, B.; Forstbauer, Helmut; Kanz, Lothar; Jacki, Swen; Stegelmann, Frank; Kalhori, N.; Nusch, Arnd; Langer, Wolfgang; Fabbri, Muller; Brettner, Stefan; Uebelmesser, B.; Kamp, T.; Schadeck-Gressel, C.; Josten, K. U.; Klein, Oana L.; Schwerdtfeger, Rainer; Baurmann, Herrad; Strotkötter, H.; Fett, W; Raghavachar, Aruna; Maintz, Christoph; Goebler, M. C.; Schlag, Rudolf; Elsel, W.; Wernli, Martin; Heim, Dominik; Wuillemin, Walter A.; Hess, U.; Gmür, J; Mayer, Jiřı́

doi:10.1038/s41375-020-01039-7

Cited by 5 publications

(2 citation statements)

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“…Both cell lines are Philadelphia chromosome positive and produce BCR-ABL1 protein, but K562 is characterized as erythroleukemia [21], whereas KU812 is characterized as a basophilic precursor [22]. Although BCR-ABL1's transcript level in KU812 is lower than K562 [23], KU812 has high-risk additional chromosomal abnormalities (e.g., i(17q), +19, +der(9)t(9;22)) [24]. Cells were plated at 2 × 10 5 cells/mL and maintained in RPMI 1640 medium (GIBCO, Brooklyn, NY, USA) supplemented with 10% fetal bovine serum (GIBCO), and stored at 37 • C in a humidified atmosphere containing 5% CO 2 .…”

Section: Cell Culture and Tkismentioning

confidence: 99%

miR-494 in Extracellular Vesicles as a Potent Biomarker of Chronic Myeloid Leukemia Treatment with Tyrosine Kinase Inhibitors

Shibuta

Shimizu

Takada

et al. 2022

Hemato

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Extracellular vesicles (EVs) are nano-sized particles released from cells and transferring molecules (proteins, lipids and nucleic acids such as mRNA, tRNA and miRNA) to recipient cells. Surface antigens and components are important for the functions as cell-to-cell communication of EVs. Thus, EVs are useful biomarkers for various diseases including leukemias and other types of malignancies. We evaluated whether miRNAs in EVs released from chronic myelogenous leukemia (CML) cells could be used for diagnosis. Microarray analysis of miRNAs in EVs obtained from the culture supernatants of two CML cell lines showed that miR-494 and miR-373-5p were significantly decreased by tyrosine kinase inhibitor for BCR-ABL1. Validation analysis with Taqman-based qRT-PCR of whole serum obtained patients with CML in the chronic phase (n = 5) did not show a significant difference in miR-494 levels compared to the CML accelerated phase and blast crisis patients (n = 5). However, the levels of miR-494 were 2.9-fold higher in the accelerated phase or blast crisis than in the chronic phase (p < 0.05). These results indicate that it is important to measure miR-494 using only EVs rather than whole serum. Our data suggest that EV-miR-494 is a useful biomarker of CML progression and evaluation of response to tyrosine kinase inhibitors.

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Section: Cell Culture and Tkismentioning

confidence: 99%

miR-494 in Extracellular Vesicles as a Potent Biomarker of Chronic Myeloid Leukemia Treatment with Tyrosine Kinase Inhibitors

Shibuta

Shimizu

Takada

et al. 2022

Hemato

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“…In later stages of the disease (accelerated phase and blast crisis), differentiation is reduced and expansion of immature progenitors is observed. Additional clonal karyotypic abnormalities are typically only observed during the accelerated and blast crisis phases ( Hehlmann et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Predictive nonlinear modeling of malignant myelopoiesis and tyrosine kinase inhibitor therapy

Rodriguez

Iniguez

Jena

et al. 2023

eLife

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Chronic myeloid leukemia (CML) is a blood cancer characterized by dysregulated production of maturing myeloid cells driven by the product of the Philadelphia chromosome, the BCR-ABL1 tyrosine kinase. Tyrosine kinase inhibitors (TKI) have proved effective in treating CML but there is still a cohort of patients who do not respond to TKI therapy even in the absence of mutations in the BCR-ABL1 kinase domain that mediate drug resistance. To discover novel strategies to improve TKI therapy in CML, we developed a nonlinear mathematical model of CML hematopoiesis that incorporates feedback control and lineage branching. Cell-cell interactions were constrained using an automated model selection method together with previous observations and new in vivo data from a chimeric BCR-ABL1 transgenic mouse model of CML. The resulting quantitative model captures the dynamics of normal and CML cells at various stages of the disease and exhibits variable responses to TKI treatment, consistent with those of CML patients. The model predicts that an increase in the proportion of CML stem cells in the bone marrow would decrease the tendency of the disease to respond to TKI therapy, in concordance with clinical data and confirmed experimentally in mice. The model further suggests that, under our assumed similarities between normal and leukemic cells, a key predictor of refractory response to TKI treatment is an increased maximum probability of self-renewal of normal hematopoietic stem cells. We use these insights to develop a clinical prognostic criterion to predict the efficacy of TKI treatment and to design strategies to improve treatment response. The model predicts that stimulating the differentiation of leukemic stem cells while applying TKI therapy can significantly improve treatment outcomes.

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Which Second-Line Tyrosine Kinase Inhibitor(s) for Chronic Myeloid Leukemia?

Schwab

Luger

2023

Curr. Treat. Options in Oncol.

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Correction: High-risk additional chromosomal abnormalities at low blast counts herald death by CML

Cited by 5 publications

References 0 publications

miR-494 in Extracellular Vesicles as a Potent Biomarker of Chronic Myeloid Leukemia Treatment with Tyrosine Kinase Inhibitors

miR-494 in Extracellular Vesicles as a Potent Biomarker of Chronic Myeloid Leukemia Treatment with Tyrosine Kinase Inhibitors

Predictive nonlinear modeling of malignant myelopoiesis and tyrosine kinase inhibitor therapy

Which Second-Line Tyrosine Kinase Inhibitor(s) for Chronic Myeloid Leukemia?

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