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Your search keyword '"Talpaz, Moshe"' showing total 23 results
Start Over Author "Talpaz, Moshe" Journal leukemia & lymphoma
23 results on '"Talpaz, Moshe"'

1. Safety and efficacy of fedratinib in patients with myelofibrosis previously treated with ruxolitinib: primary analysis of FREEDOM trial

Author

Gupta, Vikas, primary, Yacoub, Abdulraheem, additional, Mesa, Ruben A., additional, Harrison, Claire N., additional, Vannucchi, Alessandro M., additional, Kiladjian, Jean-Jacques, additional, Deeg, Hans-Joachim, additional, Fazal, Salman, additional, Foltz, Lynda, additional, Mattison, Ryan J., additional, Miller, Carole B., additional, Parameswaran, Vinod, additional, Brown, Patrick, additional, Hernandez, Christopher, additional, Wang, Jia, additional, and Talpaz, Moshe, additional

Published
2024
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3. Predictive models for splenic response to JAK-inhibitor therapy in patients with myelofibrosis.

Author

Menghrajani, Kamal, Boonstra, Philip S., Mercer, Jessica A., Perkins, Cecelia, Gowin, Krisstina L., Weber, Alissa A., Mesa, Ruben, Gotlib, Jason R., Wang, Lixia, Singer, Jack W., and Talpaz, Moshe

Subjects
MYELOFIBROSIS, PREDICTION models, ALTERNATIVE medicine, SPLEEN, HEMOGLOBINS
Abstract

JAK inhibitors for myelofibrosis (MF) reduce spleen size, control constitutional symptoms, and may improve survival. We studied the clinical characteristics of 548 MF patients treated with JAK inhibitors from 2008 to 2016 to better understand predictors of splenic response. Response was defined as a 50% decrease in spleen size at early (3–4 months on therapy) and late (5–12 months) timepoints after therapy initiation. Early response positively correlated with higher doses of JAK inhibitor, baseline spleen size 5–10 cm, and hemoglobin. Early response negatively correlated with baseline spleen size >20 cm and high WBC. The strongest predictor of late response was whether a patient had a response at the earlier timepoint (OR 8.88). Our response models suggest that clinical factors can be used to predict which patients are more likely to respond to JAK inhibitors, and those who do not achieve an early response, i.e. within 3–4 months, should consider alternative treatments. [ABSTRACT FROM AUTHOR]

Published
2019
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4. Induction of p53 suppresses chronic myeloid leukemia

Author

Peterson, Luke F., primary, Lo, Miao-Chia, additional, Liu, Yihong, additional, Giannola, Diane, additional, Mitrikeska, Emilija, additional, Donato, Nicholas J., additional, Johnson, Craig N., additional, Wang, Shaomeng, additional, Mercer, Jessica, additional, and Talpaz, Moshe, additional

Published
2017
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11. Unexpected High Incidence of Severe Toxicities Associated with Alpha Interferon, Low-Dose Cytosine Arabinoside and All-Trans Retinoic Acid in Patients with Chronic Myelogenous Leukemia

Author

Sacchi, Stefano, primary, Kantarjian, Hagop M., additional, Freireich, Emil J, additional, O'brien, Susan, additional, Cortes, Jorge, additional, Rios, Mary Beth, additional, Kornblau, Steve, additional, Giles, Francis J., additional, Roller, Charles, additional, Gajewski, James, additional, and Talpaz, Moshe, additional

Published
1999
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21. New Directions in the Biology and Therapy of Chronic Myeloid Leukemia

Author

Deisseroth, Albert B., primary, Zhang, Wei, additional, Cha, Ying, additional, Yuan, Tianying, additional, Chen, Hanchun, additional, Sims, Simon, additional, Wedrychowski, Andrzej, additional, Gao, Pei-Qing, additional, Huston, Laurel, additional, Filaccio, Marylynne, additional, Claxton, David, additional, Kornblau, Steven, additional, Johnson, Elizabeth, additional, Zack Howard, O. M., additional, Andersson, Borje, additional, Giglio, Auro Del, additional, Gressot, Laurent, additional, Kantarjian, Hagop, additional, Talpaz, Moshe, additional, Khouri, Issa, additional, Champlin, Richard, additional, Andreeff, Michael, additional, Gaozza, Eugenia, additional, Seong, David, additional, Suh, Soon-Pal, additional, Ellerson, Debra, additional, Hu, Guiying, additional, and Chou, Marian, additional

Published
1992
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23. Distinct biological impact of dephosphorylation vs. downregulation of p210 Bcr-Abl : Implications for imatinib mesylate response and resistance.

Author

Kurzrock, Razelle, Talpaz, Moshe, Li, Lan, and Estrov, Zeev

Subjects
*LEUKEMIA, *CANCER, *METHANESULFONATES, *GLUCOKINASE, *IMATINIB, *ANTINEOPLASTIC agents
Abstract

Imatinib mesylate suppresses phosphorylation of its kinase target, Bcr-Abl. We hypothesized that loss of p210 Bcr-Abl (the kinase target) may lead to imatinib mesylate resistance. We studied K562 cells [chronic myelogenous leukemia (CML) blast crisis line] and MO7E/MBA-1 cells (with MBA-1 cells representing MO7E cells stably transfected with BCR-ABL ). Imatinib mesylate resistance developed when p210 Bcr-Abl expression was abolished. Furthermore, K562 cells were significantly more growth suppressed after imatinib mesylate exposure than after downregulation of Bcr-Abl expression. Signaling pathways which were functional in the absence of Bcr-Abl expression (NF-κB and mitogen-activated protein kinase activation or the growth factor pathway) were disrupted when p210 Bcr-Abl was present but dephosphorylated, suggesting that an intact, but enzymatically inactive Bcr-Abl, may interfere with critical growth/signaling pathways. Downregulation of p210 Bcr-Abl may be a mechanism by which imatinib mesylate resistance emerges. Samples from three of 15 patients with imatinib mesylate-resistant CML blast crisis had undetectable levels of p210 Bcr-Abl . We conclude that retention of a dephosphorylated p210 Bcr-Abl has a biologic impact distinct from that of downregulation/loss of p210 Bcr-Abl and, in a subset of patients, loss of the target of the kinase inhibitor may lead to imatinib mesylate resistance. [ABSTRACT FROM AUTHOR]

Published
2006
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