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Journal articles on the topic 'CML, TKI, AOEs, cytokines'

Author: Grafiati

Published: 14 March 2023

Last updated: 31 July 2025

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1

Sicuranza, Anna, Ilaria Ferrigno, Elisabetta Abruzzese, et al. "Pro-Inflammatory and Pro-Oxidative Changes during Nilotinib Treatment in CML Patients: Results of a Prospective Multicenter Front-Line TKIs Study (KIARO Study)." Blood 138, Supplement 1 (2021): 1479. http://dx.doi.org/10.1182/blood-2021-152530.

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Abstract Background: Tyrosine kinase inhibitors (TKI) may offer a normal life expectancy to Chronic Myeloid Leukemia (CML) patients. However, during treatment with nilotinib, a higher than expected incidence of arterial occlusive events (AOEs) was observed. We retrospectively showed an "inflammatory status" during nilotinib treatment that may explain this increased incidence of AOEs. Here, we report results of a prospective multicenter (KIARO) study including 186 CML patients (89 imatinib, 59 nilotinib, 38 dasatinib) in which pro/anti-inflammatory cytokines were measured at diagnosis and durin

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2

Levy, Moshe Yair, Lin Xie, Yuexi Wang, et al. "Real-World Comparisons of Cardiovascular Events between Different Tyrosine Kinase Inhibitors Among Patients with Chronic Myeloid Leukemia." Blood 132, Supplement 1 (2018): 3567. http://dx.doi.org/10.1182/blood-2018-99-113490.

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Abstract INTRODUCTION: Chronic myeloid leukemia (CML) is a bone marrow and blood disorder accounting for 15% of adult leukemia. A shift in CML management has occurred over the past decade with the introduction of tyrosine kinase inhibitors (TKIs), changing CML status from fatal to a chronic, lifelong illness. However, an association between TKI use and cardiovascular events has been observed. This study aimed to compare major adverse cardiac events (MACE), arterial occlusive events (AOEs), and venous thrombotic events (VTEs) among CML patients in chronic phase (CP-CML) treated with different T

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Kantarjian, Hagop M., Javier Pinilla-Ibarz, Philipp D. Le Coutre, et al. "Five-year results of the ponatinib phase II PACE trial in heavily pretreated CP-CML patients (pts)." Journal of Clinical Oncology 35, no. 15_suppl (2017): 7012. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.7012.

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7012 Background: The tyrosine kinase inhibitor (TKI) ponatinib has potent activity against native and mutant BCR-ABL1 and is approved for use in pts with relapsed/intolerant CML or Ph+ ALL, or with BCR-ABL1/T315I. Methods: In the pivotal PACE study (NCT01207440), ponatinib (starting dose 45 mg/d) was assessed in pts with CML or Ph+ ALL resistant/intolerant to dasatinib or nilotinib, or with T315I. In Oct ’13, dose reductions were implemented due to observed arterial occlusive events (AOEs). Efficacy and safety at 5 yrs (data as of 3 Oct ’16) for CP-CML pts are reported. Results: Of 270 CP-CML

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Levy, Moshe Yair, Lin Xie, Yuexi Wang, et al. "Major Adverse Cardiac, Arterial Occlusive, and Venous Occlusive Events Among Chronic Myeloid Leukemia Patients Prescribed Ponatinib Vs Bosutinib." Blood 134, Supplement_1 (2019): 4751. http://dx.doi.org/10.1182/blood-2019-129053.

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INTRODUCTION: Chronic myeloid leukemia (CML) is a bone marrow and blood disorder accounting for 15% of adult leukemia. Tyrosine kinase inhibitors (TKIs) have been the standard of care for CML treatment. However, an association between TKI use and cardiovascular events has been observed. Ponatinib and bosutinib are introduced to provide more options for patients who failed their first-line treatment. The incidence of major adverse cardiac events (MACEs), arterial occlusive events (AOEs), and venous occlusive events (VOEs) were assessed among CML patients who were prescribed ponatinib vs bosutin

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5

Cortes, Jorge E., Jane Apperley, Elza Lomaia, et al. "OPTIC primary analysis: A dose-optimization study of 3 starting doses of ponatinib (PON)." Journal of Clinical Oncology 39, no. 15_suppl (2021): 7000. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.7000.

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7000 Background: PON, a third-generation tyrosine kinase inhibitor (TKI), demonstrated deep and long-lasting responses and survival in patients (pts) with chronic-phase chronic myeloid leukemia (CP-CML) resistant/intolerant to second-generation TKI therapy (PACE; NCT01207440); post hoc analysis suggested a relationship between dose and both adverse events and response. Here we present the primary analysis of OPTIC (NCT02467270), an ongoing, randomized, phase 2 trial with a novel response-based dosing regimen of PON in pts with resistant/intolerant CP-CML. Methods: Pts with CP-CML resistant/int

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Caocci, Giovanni, Olga Mulas, Elisabetta Abruzzese, et al. "Arterial Occlusive Events in Chronic Myeloid Leukemia Patients Treated with Ponatinib in the Real-Life Practice: Prophylaxis and Identification of Risk Factors." Blood 132, Supplement 1 (2018): 3006. http://dx.doi.org/10.1182/blood-2018-99-111502.

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Abstract Background . Arterial occlusive events (AOEs) represent emerging complications in chronic myeloid leukemia (CML) patients treated with ponatinib, with a cumulative incidence correlated with the higher dose of the drug and longer treatment duration. Current recommendations highlight the importance of a careful evaluation of cardiovascular (CV) risk factors at baseline.Moreover, a preventive strategy with primary prophylaxis based on aspirin still remains under discussion and no data have been reported on secondary prophylaxis. Methods. We investigated a consecutive series of adult CML

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7

Ito, Tomoki, Nobuhiko Uoshima, Yasuhiro Maeda, et al. "Evaluation Of Large Granular Lymphocytes and Endothelial-Cell-Related Biomarkers In Patients With Chronic Myeloblastic Leukemia: Comparison Among 3 TKIs." Blood 122, no. 21 (2013): 5167. http://dx.doi.org/10.1182/blood.v122.21.5167.5167.

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Abstract Background Tyrosine kinase inhibitors (TKIs) currently represent the main therapy for chronic myeloblastic leukemia (CML). Although they are therapeutically effective, some TKI-related events such as pleural effusion and elevation of large granular lymphocytes (LGL) have been reported. In addition, these events itself may affect the therapeutic response to TKIs. In the present study, we measured the levels of some cytokines, chemokines, soluble factors and coagulation markers in patients with CML, and investigated the relationship between these markers and TKI-related events. Methods

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8

Takaku, Tomoiku, Yoshitsugu Kojima, and Yoshiaki Yanai. "Analysis of Arterial Occlusive Events (AOE) in CML Patients Using Real-World Data : A Large Cohort." Blood 144, Supplement 1 (2024): 4538. https://doi.org/10.1182/blood-2024-201854.

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Background While the prognosis of chronic myeloid leukemia (CML) has been significantly improved by the development of tyrosine kinase inhibitors (TKIs), the importance of managing various adverse events associated with long-term TKI treatment is increasing. In particular, arterial occlusive events (AOEs) can be fatal and potentially cause irreversible sequelae in patients, requiring the choice of TKIs according to individual patient risk and proactive therapeutic interventions for prevention. In this study, we conducted an analysis using data from the DPC database, MDV (Medical Data Vision Co

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9

Jedema, Inge, Linda van Dreunen, Roelof Willemze, and J. H. Frederik Falkenburg. "Treatment with Tyrosine Kinase Inhibitors May Impair the Potential Curative Effect of Allogeneic Stem Cell Transplantation." Blood 114, no. 22 (2009): 857. http://dx.doi.org/10.1182/blood.v114.22.857.857.

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Abstract Abstract 857 Tyrosine kinase inhibitors (TKI) like imatinib and dasatinib are the current treatment of choice for patients with chronic myeloid leukemia (CML). Although most patients enter a complete remission during treatment, cure of the disease is usually not achieved since recurrence of the disease is seen in the majority of patients upon discontinuation of the treatment, indicating that the leukemic stem cell is not efficiently targeted. Furthermore, in accelerated phase and blast crisis of CML TKI treatment only results in temporary control of the disease. In these situations al

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10

Yu, Lu, Huifang Wang, Xiaoli Liu, et al. "Ponatinib 2-Year Efficacy, Safety and Health-Related Quality of Life in Patients with Philadelphia Chromosome-Positive Leukemia: An Open-Label, Multicenter, Phase 2 Clinical Trial in China." Blood 144, Supplement 1 (2024): 6602. https://doi.org/10.1182/blood-2024-208258.

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Background: Ponatinib is a potent BCR::ABL1 tyrosine kinase inhibitor (TKI) effective against all single-mutation variants of BCR::ABL1, including the T315I mutation. The phase 2 clinical trial (NCT04233346) evaluated the efficacy and safety of ponatinib in Chinese patients with chronic myeloid leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) who were resistant or intolerant to dasatinib or nilotinib, or who had the BCR::ABL1 T315I mutation. Objective: The objective of this study was to assess the efficacy, safety, and health-related quality of life (HR

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Stemhagen, Annette, Deyaa Adib, Stephanie Lustgarten, Lisa McGarry, Ruth Du Moulin, and Sergio Santillana. "The OMNI patient registry: A prospective observational registry to assess vascular safety in patients with CML and Ph+ ALL treated with ponatinib." Journal of Clinical Oncology 35, no. 15_suppl (2017): TPS7073. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.tps7073.

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TPS7073 Background: Ponatinib is an oral TKI with potent activity against BCR-ABL1. The pivotal PACE study (NCT01207440) formed the basis for approval of ponatinib in the US for the treatment of patients with resistant/intolerant CML or Ph+ ALL, or those with the T315I mutation. Long-term follow-up of PACE showed a higher cumulative incidence of vascular occlusive events (VOEs) than reported at the time of approval — dose reductions were later implemented to mitigate VOEs. VOEs comprise arterial occlusive events (AOE) and venous thromboembolic events. The exposure-adjusted incidence of AOEs ha

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Truitt, Luke, Catherine Hutchinson, Karen Mochoruk, John F. DeCoteau, and C. Ronald Geyer. "Chaetocin Anti-Leukemia Activity Against Chronic Myelogenous Leukemia Stem Cells Is Potentiated By Bone Marrow Stromal Factors and Overcomes Innate Imatinib Resistance." Blood 124, no. 21 (2014): 4517. http://dx.doi.org/10.1182/blood.v124.21.4517.4517.

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Abstract Chronic myelogenous leukemia (CML) is maintained by a minor population of leukemic stem cells (LSCs) that exhibit innate resistance to tyrosine kinase inhibitors (TKIs) targeting BCR-ABL. Innate resistance can be induced by cytokines and growth factors secreted by bone marrow stromal cells (BMSFs) that protect CML-LSCs from TKIs, resulting in minimal residual disease. Developing therapies that can be combined with TKIs to eradicate TKI-insensitive CML-LSCs, is critical for disrupting innate TKI resistance and preventing disease relapse. Cancer cells balance reactive oxygen species (RO

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13

Jalkanen, Sari, Satu Mustjoki, Kimmo Porkka, and Jukka Vakkila. "Cytokine-Mediated Signaling Is Suppressed in Myeloid Cells and Enhanced in Lymphatic Cells in Patients with Chronic Myeloid Leukemia (CML) — Partial Normalization with Tyrosine Kinase Inhibitors." Blood 114, no. 22 (2009): 2180. http://dx.doi.org/10.1182/blood.v114.22.2180.2180.

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Abstract Abstract 2180 Poster Board II-157 Introduction. Aberrant phosphorylation of the BCR-ABL1 tyrosine kinase (TK) is characteristic of chronic myeloid leukemia (CML). This oncoprotein interacts directly with intracellular signaling proteins, alters the responsiveness of cytokine receptors and regulates secretion of autocrine cytokines. Targeted inhibition of BCR-ABL1 with TK inhibitor (TKI) imatinib mesylate (IM) is the current standard treatment of CML. For overcoming IM resistance or intolerance, 2nd generation TKIs (nilotinib, dasatinib) with broader kinase inhibition profile have been

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Pulte, E. Dianne, Haiyan Chen, Lauren S. L. Price, et al. "FDA Approval Summary: Revised Indication and Dosing Regimen for Ponatinib Based on the Results of the OPTIC Trial." Oncologist 27, no. 2 (2022): 149–57. http://dx.doi.org/10.1093/oncolo/oyab040.

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Abstract On December 18, 2020, US Food and Drug Administration (FDA) approved a supplemental application for ponatinib extending the indication in patients with chronic-phase chronic myeloid leukemia (CP-CML) to patients with resistance or intolerance of at least 2 prior kinase inhibitors. Ponatinib was initially approved in December 2012 but was briefly voluntarily withdrawn due to serious safety concerns including the risk of arterial occlusive events (AOE). It returned to the market in December 2013 with an indication limited to patients with T315I mutation or for whom no other tyrosine kin

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Kantarjian, Hagop M., Michael W. Deininger, Elisabetta Abruzzese, et al. "Efficacy and Safety of Ponatinib (PON) in Patients with Chronic-Phase Chronic Myeloid Leukemia (CP-CML) Who Failed One or More Second-Generation (2G) Tyrosine Kinase Inhibitors (TKIs): Analyses Based on PACE and Optic." Blood 136, Supplement 1 (2020): 43–44. http://dx.doi.org/10.1182/blood-2020-133922.

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Introduction: The use of 2G TKIs in patients with CP-CML who have failed ≥1 2G TKIs is not associated with durable responses; there is limited clinical evidence to support that switching to alternate 2G TKI therapy improves long-term clinical outcomes for these patients. Patients with resistant and intolerant CP-CML with substantial prior 2G treatment demonstrated deep, lasting responses to PON in the pivotal PACE trial. A post hoc modeling analysis of the data from PACE suggested a relationship between dose and safety events (including arterial occlusive events [AOEs]). The OPTIC trial was de

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Hiwase, Devendra K., Deborah L. White, Jason A. Powell, et al. "Blocking of Cytokine Survival Signals along with Intense Bcr-Abl Kinase Inhibition May Eradicate CML Progenitor Cells." Blood 114, no. 22 (2009): 3250. http://dx.doi.org/10.1182/blood.v114.22.3250.3250.

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Abstract Abstract 3250 Poster Board III-1 Preclinical studies of imatinib set the paradigm of continuous Bcr-Abl kinase inhibition for optimal response in chronic myeloid leukemia (CML). However, the clinical success of once daily dasatinib, despite its short serum half life, implies that intermittent inhibition of Bcr-Abl kinase activity is sufficient for clinical response. In vitro studies also demonstrated that short-term intense (≥90%) Bcr-Abl kinase inhibition triggers cell death in BCR-ABL + cell lines, demonstrating their oncogene addiction. However, the effect of short-term intense kin

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Busch, Caroline, and Helen Wheadon. "Bone marrow niche crosses paths with BMPs: a road to protection and persistence in CML." Biochemical Society Transactions 47, no. 5 (2019): 1307–25. http://dx.doi.org/10.1042/bst20190221.

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Abstract Chronic myeloid leukaemia (CML) is a paradigm of precision medicine, being one of the first cancers to be treated with targeted therapy. This has revolutionised CML therapy and patient outcome, with high survival rates. However, this now means an ever-increasing number of patients are living with the disease on life-long tyrosine kinase inhibitor (TKI) therapy, with most patients anticipated to have near normal life expectancy. Unfortunately, in a significant number of patients, TKIs are not curative. This low-level disease persistence suggests that despite a molecularly targeted ther

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Zhao, Helong, Anthony D. Pomicter, Anna M. Eiring та ін. "MS4A3 promotes differentiation in chronic myeloid leukemia by enhancing common β-chain cytokine receptor endocytosis". Blood 139, № 5 (2022): 761–78. http://dx.doi.org/10.1182/blood.2021011802.

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Abstract The chronic phase of chronic myeloid leukemia (CP-CML) is characterized by the excessive production of maturating myeloid cells. As CML stem/progenitor cells (LSPCs) are poised to cycle and differentiate, LSPCs must balance conservation and differentiation to avoid exhaustion, similar to normal hematopoiesis under stress. Since BCR-ABL1 tyrosine kinase inhibitors (TKIs) eliminate differentiating cells but spare BCR-ABL1-independent LSPCs, understanding the mechanisms that regulate LSPC differentiation may inform strategies to eliminate LSPCs. Upon performing a meta-analysis of publish

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Rouhimoghadam, Milad, Anthony D. Pomicter, Alexandria Van Scoyk, et al. "Exploiting LY3009120 and Asciminib Combination to Target TKI-Resistant CML." Blood 138, Supplement 1 (2021): 3600. http://dx.doi.org/10.1182/blood-2021-153353.

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Abstract The oncogenic BCR-ABL1 tyrosine kinase is the driver of chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ALL). Tyrosine kinase inhibitors (TKIs) targeting ABL kinase are generally effective, but subsets of patients treated with single-agent TKIs develop resistance due to mutations in BCR-ABL1 that impair TKI binding. We have previously reported that BCR-ABL1 compound mutants (exhibiting two mutations within the same BCR-ABL molecule) that include the T315I gatekeeper mutation confer a high degree of resistance to all clinical ABL TKI

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Kuznetsova, Valeriya, Virginia Camacho, Sweta Patel, Victoria Matkins, and Robert S. Welner. "Perturbed function of natural killer cells by inflammatory cytokines in chronic myeloid leukemia." Journal of Immunology 206, no. 1_Supplement (2021): 57.06. http://dx.doi.org/10.4049/jimmunol.206.supp.57.06.

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Abstract Natural killer (NK) cells’ mature phenotype and counts positively correlate with prolonged treatment-free survival in chronic myeloid leukemia (CML), while dysfunctional NK cells are predictive of relapse in leukemic patients. However, the molecular drivers of NK cell alterations during leukemia remain unclear. Given an established role of inflammatory cytokines in CML progression, we define the leukemic environmental cues impacting NK maturation and function in a BCR-ABL chimeric mouse model of CML where NK cells do not carry the CML oncogene. Reflecting clinical observations, NK cel

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Nievergall, Eva, Deborah L. White, Agnes S. M. Yong та ін. "Effective Elimination of CML Progenitor and Stem Cells Through Combination of α-CD123 Antibody-Dependent Cell-Mediated Cytotoxicity and Tyrosine Kinase Inhibitor Treatment". Blood 120, № 21 (2012): 32. http://dx.doi.org/10.1182/blood.v120.21.32.32.

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Abstract Abstract 32 Since the introduction of tyrosine kinase inhibitor (TKI) therapy overall survival and complete molecular response rates in chronic phase chronic myeloid leukemia (CP-CML) patients have significantly improved. However, leukemic stem cells (LSCs) and progenitor cells persist and are thought to be responsible for disease progression, development of TKI resistance and disease recurrence after stopping TKI therapy. Protection by cytokines, such as IL-3 and GM-CSF, provides a potential mechanism of LSC resistance. While in acute myeloid leukemia (AML) monoclonal antibody (mAb)

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Guan, Xin, Chaoran Zhang, Peng Hu, et al. "Expression of Th1/2/17 Cytokines in CML with or without Pulmonary Bacterial and Fungal Coinfection." Journal of Oncology 2023 (April 18, 2023): 1–10. http://dx.doi.org/10.1155/2023/6318548.

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Background. Tyrosine kinase inhibitors (TKIs) are the standard therapy for patients with chronic myeloid leukemia (CML). While their use greatly increases patient survival rates and can lead to normal life expectancy, bacterial infections in the lungs continue to play a significant role in determining patient outcomes. Methods. In this study, the medical records of 272 CML and 53 healthy adults were analyzed. Information on age, sex, body temperature, procalcitonin (PCT), C-reactive protein (CRP), and cytokine levels were collected from patients. Since the data belonged to a nonstate distribut

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Jabbour, Elias J., Jorge E. Cortes, Moshe Talpaz, et al. "Long-Term Follow-up of the Efficacy and Safety of Ponatinib in Philadelphia Chromosome-Positive Leukemia Patients with the T315I Mutation." Blood 128, no. 22 (2016): 3067. http://dx.doi.org/10.1182/blood.v128.22.3067.3067.

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Abstract Background: Ponatinib is a tyrosine kinase inhibitor (TKI) approved for adult patients (pts) with relapsed/refractory CML or Ph+ ALL and those with the BCR-ABL T315I mutation, which is uniformly resistant to other TKIs approved for the treatment of CML and Ph+ ALL. Prior to the availability of ponatinib, resistant pts with the T315I mutation (T315I+) had worse outcomes than those without the mutation; in a matched pair analysis in chronic phase (CP)-CML pts, median overall survival (OS) was 48.4 mos after development of resistance in T315I+ pts versus not reached in those without the

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Cortes, Jorge E., Dong-Wook Kim, Javier Pinilla-Ibarz, et al. "Evaluation of the Benefit/Risk Profile of Ponatinib in CP-CML Patients over Time: 4-Year Follow-up of the Phase 2 PACE Study." Blood 126, no. 23 (2015): 5142. http://dx.doi.org/10.1182/blood.v126.23.5142.5142.

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Abstract Introduction: Ponatinib, a potent oral tyrosine kinase inhibitor (TKI), is approved for use in patients with refractory CML and Ph+ ALL, including patients with the BCR-ABLT315I mutation. This post hoc analysis was undertaken to assess the evolution of the efficacy and safety of ponatinib over time in CP-CML patients in the ongoing phase 2 PACE trial (NCT01207440). Updated data with 4 years of follow-up, including an analysis of the management of select adverse events (AEs), will be presented. Methods: Patients with CML/Ph+ ALL who were resistant or intolerant to dasatinib or nilotini

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Kinde, Samuel Birru, Ilias Doxiadis, Rawleigh Howe, et al. "Prognostic Role of Human Leukocyte Antigen Alleles and Cytokine Single-Nucleotide Polymorphisms in Patients with Chronic Myeloid Leukemia Treated with Tyrosine Kinase Inhibitor Drugs." Genes 15, no. 6 (2024): 732. http://dx.doi.org/10.3390/genes15060732.

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Tyrosine kinase inhibitor (TKI) drugs have significantly improved chronic myeloid leukemia (CML) outcomes. Neopeptides from CML cells may induce specific immune responses, which are crucial for deep molecular (DMR) and treatment-free remission (TFR). In this study of Ethiopian patients with CML (n = 162), the HLA alleles and single-nucleotide polymorphisms of five cytokines revealed significant associations with clinical outcomes. Clinically unfavorable outcomes correlated with HLA alleles A*03:01/02, A*23:17:01, B*57:01/02/03, and HLA-DRB4*01:01 (p-value = 0.0347, p-value = 0.0285, p-value =

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Hernesniemi, Sari, Jukka Vakkila, Kimmo Porkka, and Satu Mustjoki. "Single-Cell Profiling of Aberrant Cytokine Signaling in Patients with Chronic Myeloid Leukemia (CML) at Diagnosis and during Dasatinib Therapy." Blood 112, no. 11 (2008): 4214. http://dx.doi.org/10.1182/blood.v112.11.4214.4214.

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Abstract Aberrant cytokine and growth factor signaling is the hallmark of CML and results from constitutive oligomerization of the oncogenic BCR-ABL tyrosine kinase (TK). Inhibition of BCR-ABL by imatinib mesylate is the current standard of care of CML and results in durable responses in majority of patients. However, a proportion of patients shows primary or secondary resistance to imatinib, which can be attributed either to selection of clones harboring mutations in the kinase domain of BCR-ABL or activation of a BCR-ABL independent pathway. Dasatinib, a potent multikinase inhibitor, can res

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Aleksandrova, T. N., A. S. Lyamkina, E. S. Mikhailova, A. I. Autenshlus, and T. I. Pospelova. "Cytokine profile of patients with chronic myeloid leukemia." Journal of Siberian Medical Sciences 7, no. 1 (2023): 77–88. http://dx.doi.org/10.31549/2542-1174-2023-7-1-77-88.

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Introduction. Altered cytokine secretion has been described in many types of cancer. Being a key mediator of intercellular interactions, they can contribute to the development of resistance to targeted therapy and cytostatic drugs in chronic myeloid leukemia (CML). Aim. To evaluate the relationship between cytokine spectrum indicators in patients with CML and the effectiveness of targeted tyrosine kinase inhibitors (TKI) therapy. Materials and methods. Quantitative determination of the concentration of cytokines TNF-α, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-18, IFN-α in blood serum of patients wit

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Aleksandrova, T. N., I. I. Mulina, A. S. Lyamkina, et al. "The role of cytokines and cell cycle regulators in predicting of therapy response in patients with chronic myeloid leukemia." Journal of Siberian Medical Sciences 7, no. 2 (2023): 77–89. http://dx.doi.org/10.31549/2542-1174-2023-7-2-77-89.

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Introduction. Despite significant advances in therapy of patients with chronic myeloid leukemia (CML), improved survival rates, development of resistance to tyrosine kinase inhibitors (TKIs) remains an urgent problem. Aim. To study the correlation between the level of expression of regulatory proteins p53, c-myc, ki-67 and caspase-3 on the bone marrow cells and the concentration of certain pro- and anti-inflammatory cytokines in blood serum with the effectiveness of therapy in patients with CML. Materials and methods. Seventy-four CML patients with chronic phase of the disease receiving TKI th

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Okabe, Seiichi, Tetsuzo Tauchi, Yuko Tanaka, and Kazuma Ohyashiki. "Interleukin 1 Beta As a Promising Therapeutic Target in ABL Tyrosine Kinase Inhibitor Resistant Chronic Myeloid Leukemia Cells." Blood 132, Supplement 1 (2018): 4249. http://dx.doi.org/10.1182/blood-2018-99-114030.

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Abstract Introduction: Although ABL tyrosine kinase inhibitor (TKI), imatinib, nilotinib and dasatinib have demonstrated the potency against chronic myeloid leukemia (CML) and Philadelphia chromosome (Ph) positive acute lymphoblastic leukemia (Ph+ALL) patients, resistance to ABL TKI can develop in the many patients. It has already reported that ABL kinase domain mutations have been implicated in the pathogenesis of ABL TKI resistance, however, it is fully not known the molecular mechanism of drug resistance ABL TKIs. Therefore, new approach against ABL TKI resistant cells may improve the outco

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Held, Stefanie AE, Anita Bringmann, Annkristin Heine та ін. "Interferon Gamma (IFNγ) Interferes with the Effects of Tyrosine Kinase Inhibitors (TKI) In CML Cells." Blood 116, № 21 (2010): 3393. http://dx.doi.org/10.1182/blood.v116.21.3393.3393.

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Abstract Abstract 3393 Introduction: Chronic myeloid leukemia (CML) is a myeloproliferative disease which resolves in the constitutive activity of the BCR-ABL protein. Since the introduction of imatinib as first line therapy for CML, the overall survival of patients could be significantly extended. However, mutations of the BCR-ABL protein and environmental effects mediated by adhesion molecules, cytokines and growth factors were shown to induce resistance to TKIs. For the development of immunotherapeutic approaches that combine TKIs with vaccination strategies or donor lymphocyte infusions it

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Zhao, Helong, Anthony D. Pomicter, Anna M. Eiring та ін. "MS4A3 Promotes Differentiation in Chronic Myeloid Leukemia By Enhancing Common β Chain Cytokine Receptor Endocytosis". Blood 138, Supplement 1 (2021): 59. http://dx.doi.org/10.1182/blood-2021-151559.

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Abstract Background Chronic phase chronic myeloid leukemia (CP-CML) is characterized by overproduction of differentiating myeloid cells, while blast phase CML (BP-CML) cells exhibit a differentiation block. Tyrosine kinase inhibitors (TKIs) are effective in CP-CML, but resistance is common in BP-CML and can occur without explanatory BCR-ABL1 kinase mutations (BCR-ABL1-independent resistance). Similarly, CML stem/progenitor cells (LSPCs) are insensitive to TKIs, and residual leukemia persists in the majority of CML patients on TKI therapy. We previously reported overlap between the transcriptom

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32

Jabbour, Elias J., Michael W. Deininger, Elisabetta Abruzzese, et al. "Dose Modification Dynamics of Ponatinib in Patients with Chronic-Phase Chronic Myeloid Leukemia (CP-CML) from the PACE and Optic Trials." Blood 138, Supplement 1 (2021): 2550. http://dx.doi.org/10.1182/blood-2021-146175.

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Abstract Introduction: Ponatinib is a potent, oral, third-generation tyrosine kinase inhibitor (TKI) that is FDA approved for treatment of patients with relapsed/refractory CML. Patients with resistant or intolerant CP-CML demonstrated deep, lasting responses to ponatinib 45 mg once daily in the pivotal phase 2 PACE trial (Ponatinib Ph+ ALL and CML Evaluation, NCT01207440; completed). The phase 2 OPTIC trial (Optimizing Ponatinib Treatment in CP-CML, NCT02467270; ongoing) prospectively evaluated a response-based dose-reduction strategy in an attempt to optimize the dose schedule of ponatinib i

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Langhammer, Melanie, Julia Schöpf, Timo Jaquet, et al. "Abstract 7469: Inflammation plays an important role in the progression of chronic myeloid leukemia." Cancer Research 84, no. 6_Supplement (2024): 7469. http://dx.doi.org/10.1158/1538-7445.am2024-7469.

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Abstract The development of Tyrosine Kinase Inhibitors (TKIs) resulted in a significant increase in the life expectancy of patients with chronic myeloid leukemia (CML). Nevertheless, TKIs still fail in a significant proportion of therapy-naïve patients, or their effectiveness is hampered by secondary resistance. It is therefore urgent to explore the underlying mechanisms in order to develop new therapeutic approaches to cure CML instead of controlling the disease with a lifelong TKI therapy. Using the ScltTA/TRE-BCR::ABL1 mouse model for chronic phase CML we show that BCR::ABL1 leads to the el

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Zhang, Bin, Yin Wei Ho, Tessa L. Holyoake, and Ravi Bhatia. "Inhibition Of Microenvironmental Interleukin-1 Signaling Enhances TKI-Mediated Targeting Of Chronic Myelogenous Leukemia Stem Cells." Blood 122, no. 21 (2013): 512. http://dx.doi.org/10.1182/blood.v122.21.512.512.

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Abstract BCR-ABL tyrosine kinase inhibitors (TKI), although highly effective in inducing remission and improving survival in chronic myelogenous leukemia (CML) patients, fail to eliminate leukemia stem cells (LSC), which remain a potential source of relapse. Most CML patients need continued TKI treatment to prevent disease relapse, and new strategies to eliminate residual leukemia stem cells are required to enhance possibility of achieving treatment-free remission. In previous studies we have shown that increased several cytokines expressed by leukemia cells may provide a selective growth adva

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Zhang, Bin, YinWei Ho, Tinisha McDonald, et al. "Role of Enhanced Microenvironmental Interleukin-1 (IL-1) Expression and Increased IL-1 Responsiveness in Persistence of Leukemia Stem Cells in TKI Treated CML Patients." Blood 124, no. 21 (2014): 4357. http://dx.doi.org/10.1182/blood.v124.21.4357.4357.

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Abstract BCR-ABL tyrosine kinase inhibitors (TKI), although highly effective in the treatment of chronic myelogenous leukemia (CML) patients, fail to eliminate leukemia stem cells (LSC), which remain a potential source of relapse. In previous studies we have shown that altered expression of inflammatory cytokines in the CML bone marrow (BM) microenvironment provides a selective growth advantage to CML compared with normal long term hematopoietic stem cells (LTHSC) (Cancer Cell 2012, 21:577). Our studies suggest an important role for the pivotal pro-inflammatory cytokine Interleukin-1α/β (IL-1α

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Cortes, Jorge E., Delphine Rea, Michael J. Mauro, et al. "Asciminib Provides Long-Term, Durable Molecular Responses in Patients with T315I-Mutated CML-CP: Final Analysis from a Phase 1 Trial." Blood 144, Supplement 1 (2024): 1765. https://doi.org/10.1182/blood-2024-209537.

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Background: T315I-mutated CML-CP is resistant to ATP-competitive tyrosine kinase inhibitors (TKIs), except ponatinib, which may be associated with safety concerns. A follow-up analysis of a phase 1 trial (NCT02081378) previously demonstrated durable efficacy and favorable safety of asciminib, the first BCR::ABL1 inhibitor to Specifically Target the ABL Myristoyl Pocket (STAMP), in patients with T315I-mutated CML-CP after ≥1 prior TKI. We provide final safety and efficacy data for patients with T315I-mutated CML-CP treated with asciminib monotherapy. Methods: This analysis includespatients with

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Mustjoki, Satu, Peter Rohon, Katrin Rapakko, et al. "Low or Undetectable Numbers of Philadelphia Chromosome Positive (Ph+) Leukemia Cells in the Primitive (CD34posCD38neg) Stem Cell Fraction in Chronic Myeloid Leukemia (CML) Patients during Tyrosine Kinase Inhibitor Therapy." Blood 112, no. 11 (2008): 1079. http://dx.doi.org/10.1182/blood.v112.11.1079.1079.

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Abstract Targeted tyrosine kinase inhibitors (TKIs) efficiently induce rapid hematologic and cytogenetic remission in most chronic myeloid leukemia (CML) patients. However, in vitro experiments have suggested that the most primitive CML stem cells residing in the CD34posCD38neg fraction are relatively resistant to TKIs. The prevalence of these stem cells in vivo in patients under TKI therapy is unclear. The aim of this project was to analyze the effect of TKI therapy on Ph+ leukemia stem cell pool in patients and to analyze the proportion of Ph+ cells in different stem cell fractions. A total

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Janowski, Michał, Karolina Łuczkowska, Michał Gniot, et al. "The Depth of the Molecular Response in Patients with Chronic Myeloid Leukemia Correlates with Changes in Humoral Immunity." Journal of Clinical Medicine 13, no. 8 (2024): 2353. http://dx.doi.org/10.3390/jcm13082353.

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Background and Objectives: The effective treatment of chronic myeloid leukemia leads to the restoration of proper immune system function. We aimed to investigate fluctuations in circulating cytokines, angiogenic factors and complement components in patients with CML during the first year of treatment with TKI and correlate them with the degree of achieved molecular response. Material and Methods: We recruited 31 patients with newly diagnosed CML. Peripheral blood and bone marrow samples were obtained, and concentrations of serum proteins were measured using an immunology multiplex assay. Resul

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Kuznetsova, Valeriya, Sweta Patel, Francesca Luca, Virginia Camacho, Victoria Matkins, and Robert S. Welner. "Perturbed function of natural killer cells by inflammatory cytokines in acute (AML) and chronic (CML) myeloid leukemias." Journal of Immunology 208, no. 1_Supplement (2022): 62.04. http://dx.doi.org/10.4049/jimmunol.208.supp.62.04.

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Abstract Natural killer (NK) cells have the capacity to eliminate malignant cells by releasing cytotoxic granules. Indeed, mature NK cell counts are associated with favorable prognosis in AML and prolonged TKI-free remission in CML. However, NK cell maturation and anti-leukemic activity are suppressed during the disease, and the environmental drivers of this impairment remain unclear. Given an established role of inflammatory cytokines (particularly IL-1β, IL-6, and TNFα) in the progression of myeloid malignancies, we define their impact on NK cell function in chimeric mouse models of leukemia

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Kok, Chung Hoow, Verity A. Saunders, Naranie Shanmuganathan, et al. "Increased Inflammatory Cytokines in Plasma Are Associated with Sustained Treatment-Free Remission in Chronic Myeloid Leukaemia." Blood 144, Supplement 1 (2024): 993. https://doi.org/10.1182/blood-2024-201881.

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Background: The immune status at the time of tyrosine kinase inhibitor (TKI) cessation may play a critical role in achieving sustained treatment-free remission (TFR) in chronic myeloid leukaemia (CML). Cytokine profiles may provide a measure of host immune activation against residual leukaemia. Aim: To investigate the expression of plasma cytokines at the time of TKI cessation (TOC) and assess their predictive significance for sustained TFR in two TFR cohorts from Australia (AU) and US. Methods: Blood was collected from 113 CML patients (pts) at TOC from an AU discovery cohort, 72 pts in the L

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de Lavallade, Hugues, David Marin, Melanie Hart, et al. "Chronic Myeloid Leukemia Patients on Tyrosine Kinase Inhibitor Have Normal T Cell Responses to Vaccination but An Impaired IgM Humoral Response Associated with Loss of Discrete Memory B Cell Subsets,." Blood 118, no. 21 (2011): 3753. http://dx.doi.org/10.1182/blood.v118.21.3753.3753.

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Abstract Abstract 3753 The tyrosine kinase inhibitors (TKIs) imatinib (IM), nilotinib (NIL) and dasatinib (DAS) are remarkably effective as single-agent therapy for chronic myeloid leukemia (CML) in chronic phase (CP). However little is known of their potential impact on the immune response. No human in vivo studies to assess how these molecular-targeted drugs affect immune function in patients are available and data from in vitro and animal studies with imatinib have been contradictory, ranging from impaired antigen-specific T-cell response to enhanced stimulation of tolerant T cells. Further

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Hochhaus, Andreas, Jorge E. Cortes, Dong-Wook Kim, et al. "Efficacy and Safety of Ponatinib in CP-CML Patients By Number of Prior Tyrosine Kinase Inhibitors: 4-Year Follow-up of the Phase 2 PACE Trial." Blood 126, no. 23 (2015): 4025. http://dx.doi.org/10.1182/blood.v126.23.4025.4025.

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Abstract Introduction: Ponatinib is a potent oral tyrosine kinase inhibitor (TKI) approved for use in patients with refractory CML and Ph+ ALL, including patients with the resistant BCR-ABLT315I mutation. To evaluate whether patient characteristics and outcomes with ponatinib differed by extent of pretreatment with other TKIs, this post hoc analysis examines results among CP-CML patients enrolled in the phase 2 PACE trial (NCT01207440) according to the number of TKIs received prior to study entry. Updated data with 4 years of follow-up will be presented. Methods: Patients with CML or Ph+ ALL w

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Thiant, Stephanie, Moutuaata M.Moutuou, Philippe Laflamme, et al. "Disruption of the Peripheral Lymphoid Niche Contributes to Lymphopenia in CML Patients Undergoing Imatinib Treatments." Blood 126, no. 23 (2015): 5165. http://dx.doi.org/10.1182/blood.v126.23.5165.5165.

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Abstract PURPOSE: Chronic myelogenous leukemia (CML) is a disorder affecting early hematopoietic stem cells (HSC) and is characterized by excessive proliferation and accumulation of myeloid progenitors and progeny in the periphery. During the chronic phase of the disease, CML patients are normally at low risk of developing infections but such complications tend to rise during the progression of the disease. Gleevec (imatinib mesylate) is currently administered as first line therapy for patients with Philadelphia chromosome-positive CML. Despite the relative high specificity of tyrosine kinase

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Kalota, Anna, and Alan M. Gewirtz. "Computationally Designed, Small Molecule Inhibitors of Tubulin Inhibit the Growth of Gleevec Resistant Chronic Myelogenous Leukemia Cells." Blood 108, no. 11 (2006): 2173. http://dx.doi.org/10.1182/blood.v108.11.2173.2173.

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Abstract The abl tyrosine kinase inhibitor (TKI) imatinib mesylate has revolutionized treatment of Chronic Myelogenous Leukemia (CML). Nonetheless, for the small percentage of chronic phase patients in whom resistance to imatinib develops, and for patients in accelerated phase/blast crisis, disease management is problematic. Second generation TKI may address the resistance issue, but serious cardiotoxicity might be a concern for all TKIs. We are therefore investigating other candidates for rationally directed CML therapy. Herein we report that targeting tubulin with computationally designed sm

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Gutknecht, Michael, Lisa Güttler, Mark-Alexander Schwarzbich, et al. "Upregulation of Osteoactivin Upon Exposure to Tyrosine Kinase Inhibitors Impairs the T Cell Stimulatory Capacity of Monocyte-Derived Dendritic Cells." Blood 118, no. 21 (2011): 1112. http://dx.doi.org/10.1182/blood.v118.21.1112.1112.

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Abstract Abstract 1112 Targeted therapies using tyrosine kinase (TK) inhibitors have significantly improved the treatment of cancer patients. Imatinib (Glivec, Gleevec, STI 571) was the first TK inhibitor (TKI) established for the treatment of cancer and efficiently blocks the activity of c-ABL, a non-receptor TK which is pathologically activated in philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML). Nilotinib (Tasigna) and dasatinib (Sprycel) are second-generation TKI that have shown efficacy in the treatment of Ph+ CML resistant or intolerant to imatinib. However, mole

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Ågerstam, Helena, Nils Hansen, Sofia Von Palffy, et al. "IL1RAP Antibodies Block IL1-Induced Expansion of Primitive CML Cells and Display Therapeutic Effects in Xenograft Models." Blood 128, no. 22 (2016): 1118. http://dx.doi.org/10.1182/blood.v128.22.1118.1118.

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Abstract Chronic myeloid leukemia (CML) is currently treated with tyrosine kinase inhibitors (TKIs) but these do not effectively eliminate the CML stem cells. As a consequence, CML stem cells persist and cause relapse in most patients upon drug discontinuation. Furthermore, no effective therapy exists for the advanced stages of the disease. Thus, there is still a need for novel treatment strategies in CML. We have previously shown that Interleukin 1 receptor accessory protein (IL1RAP), a co-receptor of IL1R1, is highly expressed on primitive CML cells and that a polyclonal IL1RAP antibody can

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Rein, Lindsay A. M., and David A. Rizzieri. "A Phase I Trial of Incorporating Natural Killer (K-NK) Cells for Patients with Chronic Myeloid Leukemia (CML) and Molecular Residual Disease after Tyrosine Kinase Inhibitor (TKI) Therapy." Blood 136, Supplement 1 (2020): 5. http://dx.doi.org/10.1182/blood-2020-142062.

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Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment of patients with chronic myeloid leukemia (CML) ushering in an era where, in select patient populations, treatment planning goals have shifted towards the achievement of treatment free remission (TFR) after TKI cessation. Both duration and depth of response to TKI therapy are predictors of future success in achieving a lasting TFR and with improved outcomes independent of TKI cessation. Unfortunately, molecular residual disease (MRD) persists in many patients despite optimal therapy and predicts for worse outcomes over time an

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Ilander, Mette Matilda, Ulla Olsson-Strömberg, Hanna Lähteenmäki, et al. "Disease Relapse After TKI Discontinuation In CML Is Related Both To Low Number and Impaired Function Of NK-Cells:Data From Euro-SKI." Blood 122, no. 21 (2013): 379. http://dx.doi.org/10.1182/blood.v122.21.379.379.

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Abstract Background The inhibition of oncogenic BCR-ABL1 kinase with tyrosine kinase inhibitors (TKIs) has significantly improved the prognosis of CML. Recent reports suggest that approximately 40 % of CML patients who have achieved optimal therapy response (complete molecular remission, CMR) can stop imatinib treatment without recurrence of detectable BCR-ABL1 transcripts. However, no predictive prognostic factors for successful therapy discontinuation have yet been identified. We therefore set up an immunological substudy in the ongoing pan-European EURO-SKI stopping study. We aimed to ident

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Sweet, Kendra, Ehab L. Atallah, Jerry P. Radich, et al. "Second Treatment Free Remission after Combination Therapy with Ruxolitinib Plus Tyrosine Kinase Inhibitors in Chronic Phase Chronic Myeloid Leukemia (CML)." Blood 138, Supplement 1 (2021): 2555. http://dx.doi.org/10.1182/blood-2021-147954.

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Abstract Background: Discontinuation of tyrosine kinase inhibitors (TKIs) is feasible in a subset of CML patients who have maintained a deep molecular response for at least two years. Numerous discontinuation trials have been performed and consistently show approximately 50% of patients relapse after stopping TKIs. A recent study examining rates of treatment free remission (TFR) after a second attempt at stopping TKIs found, with a median follow up time of 38.3 months, 64.3% of patients had a molecular relapse (defined as a loss of major molecular response (MMR)). At 12, 24 and 36 months, TFR

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Abrishami, Mahsa, Landon Pastushok, Karen Mochoruk, John F. DeCoteau, and C. Ronald Geyer. "Synthetic Anti-IL3 Receptor Antibodies As Therapeutics to Block Innate Imatinib Resistance in Chronic Myelogenous Leukemia." Blood 124, no. 21 (2014): 4519. http://dx.doi.org/10.1182/blood.v124.21.4519.4519.

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Abstract Chronic myelogenous leukemia (CML) is maintained by a minor population of leukemic stem cells (LSCs) that exhibit innate resistance to tyrosine kinase inhibitors (TKIs) targeting BCR-ABL. Innate resistance can be induced by cytokines and growth factors secreted by bone marrow stromal cells that protect CML-LSCs from TKIs, resulting in minimal residual disease. Developing therapies that can be combined with TKIs to eradicate TKI-insensitive CML-LSCs, is critical for disrupting innate TKI resistance and preventing disease relapse. We previously showed that interleukin-3 (IL-3) reduces t

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