18,763 results match your criteria Chronic Myeloid Leukemia and BCR-ABL


High circ_100053 predicts a poor outcome for chronic myeloid leukemia and is involved in imatinib resistance.

Oncol Res 2019 Feb 14. Epub 2019 Feb 14.

Department of Hematology, Hunan Provincial People's Hospital, The First-Affiliated Hospital of Hunan Normal University, Changsha, Hunan Province, China, 410002.

Chronic myeloid leukemia (CML) is a rare clonal myeloproliferative malignancy, which is caused by a reciprocal translocation between chromosomes 9 and 22 t(9;22) (q34;q11). Altered circle RNAs (circRNAs) could contribute to leukemogenesis. In this study, we aimed to investigate the expression profiling of circRNAs in CML. Read More

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http://dx.doi.org/10.3727/096504018X15412701483326DOI Listing
February 2019

Current perspectives for the treatment of chronic myeloid leukemia

Turk J Med Sci 2019 Feb 11;49(1):1-10. Epub 2019 Feb 11.

With an annual incidence of 1-2 in a million, Ph*(+) chronic myeloid leukemia (CML) is a clonal hematopoietic stem cell disease that makes myeloid neoplastic cells breed out of control. This BCR-ABL(+) myeloproliferative disease makes up about 15%-20% of all leukemia cases in adults. CML is seen more in males than females, with a rate of three to two. Read More

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http://dx.doi.org/10.3906/sag-1810-81DOI Listing
February 2019

C/EBPβ is a critical mediator of IFN-α-induced exhaustion of chronic myeloid leukemia stem cells.

Blood Adv 2019 Feb;3(3):476-488

Department of Transfusion Medicine and Cell Therapy, Kyoto University Hospital, Kyoto, Japan.

Even in the era of ABL tyrosine kinase inhibitors, eradication of chronic myeloid leukemia (CML) stem cells is necessary for complete cure of the disease. Interferon-α (IFN-α) has long been used for the treatment of chronic-phase CML, but its mechanisms of action against CML stem cells remain unclear. We found that IFN-α upregulated CCAAT/enhancer binding protein β (C/EBPβ) in BCR-ABL-expressing mouse cells by activating STAT1 and STAT5, which were recruited to a newly identified 3' distal enhancer of that contains tandemly aligned IFN-γ-activated site elements. Read More

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http://dx.doi.org/10.1182/bloodadvances.2018020503DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6373744PMC
February 2019

Flow Cytometry Assessment of CD26 Leukemic Stem Cells in Peripheral Blood: A Simple and Rapid New Diagnostic Tool for Chronic Myeloid Leukemia.

Cytometry B Clin Cytom 2019 Feb 3. Epub 2019 Feb 3.

Hematology Unit, Azienda Ospedaliera Universitaria Senese, Siena, Italy.

Background: Recent investigations in chronic myeloid leukemia (CML) have focused on the identification and characterization of leukemic stem cells (LSCs). These cells reside within the CD34 /CD38 /Lin fraction and score positive for CD26 (dipeptidylpeptidase IV) a marker, expressed in both bone marrow (BM) and peripheral blood (PB) samples, that discriminates CML cells from normal hematopoietic stem cells (HSCs) or from LSCs of other myeloid neoplasms. CD26 evaluation could be a useful tool to improve the identification of CML LCSs by using flow-cytometry assay. Read More

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http://dx.doi.org/10.1002/cyto.b.21764DOI Listing
February 2019
1 Read

Effect of Imatinib on Bone Marrow Morphology and Angiogenesis in Chronic Myeloid Leukemia.

Adv Hematol 2019 1;2019:1835091. Epub 2019 Jan 1.

Department of Biostatistics & Health Informatics, Sanjay Gandhi Post Graduate of Medical Sciences, Raebareli Road, Lucknow, U.P. 226014, India.

Background And Objectives: Chronic myeloid leukemia (CML) is characterized by hyperproliferation of myeloid precursors, increased fibrosis, and neoangiogenesis in the bone marrow. Imatinib inhibits BCR-ABL tyrosine kinase produced due to reciprocal translocation t(9;22) in neoplastic CML cells. It reduces hyperproliferation of myeloid precursors and has been found to affect bone marrow fibrosis and angiogenesis. Read More

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https://www.hindawi.com/journals/ah/2019/1835091/
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http://dx.doi.org/10.1155/2019/1835091DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6332991PMC
January 2019
4 Reads

The e13a2 BCR-ABL transcript negatively affects sustained deep molecular response and the achievement of treatment-free remission in patients with chronic myeloid leukemia who receive tyrosine kinase inhibitors.

Cancer 2019 Feb 1. Epub 2019 Feb 1.

Department of Hematology, Local Social Health Authority (ASST) Spedali Civili Brescia, Brescia, Italy.

Background: Stopping tyrosine kinase inhibitor (TKI) treatment has become a realistic and safe objective for patients who have chronic myeloid leukemia (CML). Both a sustained deep molecular response (sDMR) and the lack of a molecular recurrence after TKI discontinuation are required to reach a durable treatment-free remission (TFR).

Methods: The potential predictive role of BCR-ABL transcripts in attaining an sDMR and a TFR was analyzed in a strictly consecutive, unselected series of 194 patients who were diagnosed and treated with TKIs at the authors' center. Read More

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http://doi.wiley.com/10.1002/cncr.31977
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http://dx.doi.org/10.1002/cncr.31977DOI Listing
February 2019
2 Reads

NKG2A Down-Regulation by Dasatinib Enhances Natural Killer Cytotoxicity and Accelerates Effective Treatment Responses in Patients With Chronic Myeloid Leukemia.

Front Immunol 2018 17;9:3152. Epub 2019 Jan 17.

Department of Hematology, MacKay Memorial Hospital, Taipei, Taiwan.

Chronic myeloid leukemia (CML) is a hematological malignancy characterized by the presence of (9;22) chromosomal translocation that results in fusion gene. ABL tyrosine kinase inhibitors (TKIs), such as imatinib, nilotinib, and dasatinib, are currently the front-line treatment options for CML. Recently, natural killer (NK) cell activation and expansion have been shown to be associated with optimal treatment responses for CML. Read More

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http://dx.doi.org/10.3389/fimmu.2018.03152DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6344416PMC
January 2019
1 Read

Ponatinib: a novel multi-tyrosine kinase inhibitor against human malignancies.

Onco Targets Ther 2019 18;12:635-645. Epub 2019 Jan 18.

Department of Surgery, The University of Melbourne, The Royal Melbourne Hospital, Parkville, VIC 3050, Australia,

Human malignancies are often the result of overexpressed and constitutively active receptor and non-receptor tyrosine kinases, which ultimately lead to the mediation of key tumor-driven pathways. Several tyrosine kinases (ie, EGFR, FGFR, PDGFR, VEGFR), are aberrantly activated in most common tumors, including leukemia, glioblastoma, gastrointestinal stromal tumors, non-small-cell lung cancer, and head and neck cancers. Iclusig™ (ponatinib, previously known as AP24534) is an orally active multi-tyrosine kinase inhibitor and is currently approved by the US Food and Drug Administration for patients with chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia, specifically targeting the BCR-ABL gene mutation, T315I. Read More

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https://www.dovepress.com/ponatinib-a-novel-multi-tyrosine-k
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http://dx.doi.org/10.2147/OTT.S189391DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6343508PMC
January 2019
3 Reads

[A retrospective analysis of the efficacy and safety of imatinib in children with chronic myeloid leukemia during chronic phase].

Zhonghua Er Ke Za Zhi 2019 Feb;57(2):113-117

Hematology Oncology Center, Beijing Children's Hospital, Capital Medical University, Beijing 100045, China.

To evaluate the efficacy and safety of imatinib in the treatment of newly diagnosed chronic myeloid leukemia during chronic phase (CML-CP) in children and to analyze the difference of the efficacy and safety between imported original imatinib (Gleevec) and domestic generic imatinib (Xinwei). Clinical data of 35 children with newly diagnosed CML-CP in Beijing Children's Hospital from January 2014 to January 2018 were collected, among which 15 cases were treated with the imported original imatinib (original drug group) and 20 cases were treated with the domestic generic imatinib (generic drug group). The hematological, cytogenetic and molecular reactions and safety of the treatments were monitored at months 3, 6 and 12. Read More

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http://dx.doi.org/10.3760/cma.j.issn.0578-1310.2019.02.010DOI Listing
February 2019
1 Read

The proportion of different BCR-ABL1 transcript types in chronic myeloid leukemia. An international overview.

Leukemia 2019 Jan 23. Epub 2019 Jan 23.

Institut für Medizinische Informationsverarbeitung, Biometrie und Epidemiologie (IBE), Ludwig-Maximilians-Universität München, Munich, Germany.

There are different BCR-ABL1 fusion genes that are translated into proteins that are different from each other, yet all leukemogenic, causing chronic myeloid leukemia (CML) or acute lymphoblastic leukemia. Their frequency has never been systematically investigated. In a series of 45503 newly diagnosed CML patients reported from 45 countries, it was found that the proportion of e13a2 (also known as b2a2) and of e14a2 (also known as b3a2), including the cases co-expressing e14a2 and e13a2, was 37. Read More

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http://www.nature.com/articles/s41375-018-0341-4
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http://dx.doi.org/10.1038/s41375-018-0341-4DOI Listing
January 2019
4 Reads

Detection of fusion gene transcripts in the saliva of Nigerian patients with chronic myeloid leukemia.

Niger J Clin Pract 2019 Jan;22(1):51-55

Department of Medical Laboratory Sciences, Faculty of Health Sciences and Technology, University of Nigeria, Enugu, Nigeria.

Background: The presence of BCR-ABL1 fusion gene resulting from a t(9; 22) reciprocal chromosome translocation is the molecular hallmark of chronic myeloid leukemia (CML). In the diagnosis and treatment of CML, peripheral blood or bone marrow samples are usually taken for analysis. However, both methods are invasive sample collection methods, thus a noninvasive saliva sample method for the detection of the fusion gene transcripts (BCR-ABL) was investigated in some Nigerians with CML. Read More

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http://dx.doi.org/10.4103/njcp.njcp_225_18DOI Listing
January 2019
1 Read

Albumin binding and anticancer effect of magnesium oxide nanoparticles.

Int J Nanomedicine 2019 27;14:257-270. Epub 2018 Dec 27.

Department of Nanotechnology, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran,

Background: Recently, nanomaterials have moved into biological and medicinal implementations like cancer therapy. Therefore, before clinical trials, their binding to plasma proteins like human serum albumin (HSA) and their cytotoxic effects against normal and cancer cell lines should be addressed.

Methods: Herein, the interaction of magnesium oxide nanoparticles (MgO NPs) with HSA was studied by means of fluorescence spectroscopy, circular dichroism (CD) spectroscopy, and docking studies. Read More

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https://www.dovepress.com/albumin-binding-and-anticancer-eff
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http://dx.doi.org/10.2147/IJN.S186428DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6312066PMC
February 2019
6 Reads

A rare BCR-ABL1 transcript in Philadelphia-positive acute myeloid leukemia: case report and literature review.

BMC Cancer 2019 Jan 10;19(1):50. Epub 2019 Jan 10.

Department of Clinical and Molecular Medicine, Hematology Sant'Andrea University Hospital, Sapienza University of Rome, Rome, Italy.

Background: Philadelphia (Ph) chromosome results from the reciprocal translocation t(9;22)(q34.1;q11.2) and is diagnostic for chronic myeloid leukemia (CML). Read More

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https://bmccancer.biomedcentral.com/articles/10.1186/s12885-
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http://dx.doi.org/10.1186/s12885-019-5265-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6329120PMC
January 2019
9 Reads

[Chronic myeloid leukemia presenting with marked eosinophilia].

Rinsho Ketsueki 2018 ;59(12):2594-2599

Department of Hematology, Tonan Hospital.

An 80-year-old female with fever, edema in the lower extremities, and marked eosinophilia was referred to our hospital. Based on the presence of the Philadelphia chromosome, she was diagnosed with chronic myeloid leukemia (CML). Although imatinib induced a complete cytogenetic response (CCyR), CML relapsed after 28 months of starting it. Read More

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https://www.jstage.jst.go.jp/article/rinketsu/59/12/59_2594/
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http://dx.doi.org/10.11406/rinketsu.59.2594DOI Listing
January 2018
4 Reads

Low-dose staurosporine selectively reverses BCR-ABL-independent IM resistance through PKC-α-mediated G2/M phase arrest in chronic myeloid leukaemia.

Artif Cells Nanomed Biotechnol 2019 Jan 8:1-9. Epub 2019 Jan 8.

a Department of Hematology, Key Laboratory of Hematological Disease Diagnostic & Treat Centre of Guizhou Province , Affiliated Hospital of Guizhou Medical University, Guizhou Province Institute of Hematology , Guiyang , China.

Imatinib (IM) resistance has become a critical problem for the treatment of patients with relapsed chronic myeloid leukaemia (CML), so novel therapies are in need. Various isotypes of protein kinases C (PKCs) are up-regulated in CML and related with BCR-ABL regulating several signalling pathways that are crucial to malignant cellular transformation. However, it is still unknown whether PKC isotypes play crucial roles in IM resistance. Read More

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http://dx.doi.org/10.1080/21691401.2018.1490310DOI Listing
January 2019
7 Reads

[Monitoring the chronic myeloid leukemia patients between 2008 and 2018; the experience of the Hematology and Bone Marrow Transplantation Unit Târgu-Mureș].

Orv Hetil 2019 Jan;160(2):67-72

Hematológiai és Csontvelő-átültetési Klinika, Marosvásárhelyi Orvosi és Gyógyszerészeti Egyetem Târgu Mureș, Str. Revoluției nr. 35, Jud. Mureș, cod 540042 Romania.

Introduction And Aim: Chronic myeloid leukemia is a clonal myeloproliferative disorder characterized by the BCR-ABL gene rearrangement with translocation between chromosomes 9 and 22. The constitutively active BCR-ABL tyrosine kinase inhibitor became the standard frontline therapy. The molecular monitoring is essential. Read More

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https://www.akademiai.com/doi/10.1556/650.2019.31250
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http://dx.doi.org/10.1556/650.2019.31250DOI Listing
January 2019
5 Reads

Estimation of the distribution of longitudinal biomarker trajectories prior to disease progression.

Stat Med 2019 Jan 6. Epub 2019 Jan 6.

Department of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Most studies characterize longitudinal biomarker trajectories by looking forward at them from a commonly used time origin, such as the initial treatment time. For a better understanding of the relationship between biomarkers and disease progression, we propose to align all subjects by using their disease progression time as the origin and then looking backward at the biomarker distributions prior to that event. We demonstrate that such backward-looking plots are much more informative than forward-looking plots when the research goal is to understand the shape of the trajectory leading up to the event of interest. Read More

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http://dx.doi.org/10.1002/sim.8085DOI Listing
January 2019
2 Reads
2.037 Impact Factor

A Case of Chronic Myelogenous Leukemia Occurring in a Patient Treated for Essential Thrombocythemia.

Am J Case Rep 2019 Jan 3;20:10-14. Epub 2019 Jan 3.

Department of Hematology and Medical Oncology, Emory University, Atlanta, GA, USA.

BACKGROUND Essential thrombocythemia (ET) is one of the BCR-ABL gene fusion negative chronic myeloproliferative disorders (MPDs), which also include polycythemia vera (PV), and myelofibrosis. Few clinical cases have reported the progression of ET to chronic myelogenous leukemia (CML) with the expression of the BCR-ABL gene. This report describes such a case and includes a review of other reported cases of CML co-occurring with BCR-ABL-negative chronic MPDs. Read More

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http://dx.doi.org/10.12659/AJCR.911854DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6325661PMC
January 2019
1 Read

Cytotoxic and pro-apoptotic action of MjTX-I, a phospholipase A2 isolated from snake venom, towards leukemic cells.

J Venom Anim Toxins Incl Trop Dis 2018 20;24:40. Epub 2018 Dec 20.

Departamento de Análises Clínicas, Toxicológicas e Bromatológicas. Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP Brazil.

Background: Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm marked by increased myeloproliferation and presence of leukemic cells resistant to apoptosis. The current first-line therapy for CML is administration of the tyrosine kinase inhibitors imatinib mesylate, dasatinib or nilotinib. Although effective to treat CML, some patients have become resistant to this therapy, leading to disease progression and death. Read More

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http://dx.doi.org/10.1186/s40409-018-0180-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6300906PMC
December 2018
2 Reads

Vitamin Е activates expression of С/EBP alpha transcription factor and G-CSF receptor in leukemic K562 cells.

Exp Oncol 2018 Dec;40(4):328-331

Institute of Molecular Biology and Genetics, NAS of Ukraine, Kyiv 03680, Ukraine.

Background: Chronic myeloid leukemia (CML) is a clonal hematopoietic stem cell disorder associated with the activity of BCR-ABL fusion oncogene. Tyrosine kinase inhibitors are the current treatment of CML, but secondary mutations finally contribute to therapy resistance and blast crisis of the disease. The search for the novel compounds for the effective control of CML is now in the spotlight. Read More

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December 2018
7 Reads

B-ALL Relapses After Autologous Stem Cell Transplantation Associated With a Shift from e1a2 to e14a2 Transcripts: A Case Report.

Anticancer Res 2019 Jan;39(1):431-435

Department of Clinical and Experimental Medicine, University of Catania, Catania, Italy.

Background/aim: The Philadelphia chromosome is found in 30% of acute lymphoblastic leukemia (ALL) patients, a distinct ALL subgroup where the BCR-ABL fusion gene is associated with poor prognosis. Treatment with tyrosine kinase inhibitors (TKIs) often induces complete remission and these patients subsequently undergo an autologous stem cell transplantation (ASCT). However, 20% of subjects experience a relapse associated with the selection of point-mutations in the BCR-ABL kinase domain. Read More

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http://ar.iiarjournals.org/lookup/doi/10.21873/anticanres.13
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http://dx.doi.org/10.21873/anticanres.13130DOI Listing
January 2019
15 Reads

BCR-Abl Silencing by Short Interfering RNA: A Potent Approach to Sensitize Chronic Myeloid Leukemia Cells to Tyrosine Kinase Inhibitor Therapy.

Stem Cells Dev 2019 Jan 24. Epub 2019 Jan 24.

1 Department of Chemical & Materials Engineering, Faculty of Engineering, University of Alberta, Edmonton, Canada.

Nonviral gene therapy with specific short interfering RNAs (siRNAs) against BCR-Abl can be an alternative and/or supportive therapy of chronic myeloid leukemia (CML) with tyrosine kinase inhibitors (TKIs), given the often observed resistance to TKIs in clinical setting. In this study, we explored the feasibility of BCR-Abl siRNA therapy in CML K562 cells in vitro by employing a cationic polymer derived from cholesterol (Chol) grafted low-molecular weight polyethyleneimine (PEI). The first generation TKI imatinib upregulated the expression of BCR-Abl in K562 cells as expected. Read More

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http://dx.doi.org/10.1089/scd.2018.0196DOI Listing
January 2019
5 Reads

Prevalence of BCR-ABL T315I Mutation in Malaysian Patients with Imatinib-Resistant Chronic Myeloid Leukemia

Asian Pac J Cancer Prev 2018 Dec 25;19(12):3317-3320. Epub 2018 Dec 25.

Haematology Unit, Cancer Research Centre, Institute for Medical Research, Jalan Pahang, Wilayah Persekutuan Kuala Lumpur, Malaysia. Email:

Objective: Chronic Myeloid Leukemia (CML) is caused by a reciprocal translocation between chromosomes 9 and 22, t(9;22) (q34;q11) which encodes for the BCR-ABL fusion protein. Discovery of Imatinib Mesylate (IM) as first line therapy has brought tremendous improvement in the management of CML. However, emergence of point mutations within the BCR-ABL gene particularly T315I mutation, affects a common BCR-ABL kinase contact residue which impairs drug binding thus contribute to treatment resistance. Read More

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http://dx.doi.org/10.31557/APJCP.2018.19.12.3317DOI Listing
December 2018
3 Reads
1.500 Impact Factor

Predictive Models for Designing Potent Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia for Understanding its Molecular Mechanism of Resistance by Molecular Docking and Dynamics Simulations.

J Biomol Struct Dyn 2018 Dec 22:1-68. Epub 2018 Dec 22.

a Centre for Nanosciences and Molecular Medicine , Amrita Institute of Medical Sciences and Research Centre, Amrita Vishwa Vidyapeetham , Kochi Campus , Kerala State , 682 041 , INDIA.

BCR-ABL fusion protein drives chronic myeloid leukaemia (CML) which constitutively activates tyrosine kinase involved in the initiation and maintenance of CML phenotype. Ponatinib, an oral drug was discovered as an efficient BCR-ABL inhibitor by addressing imatinib drug resistance arising due to the point mutations at its active sites. In this study, 44 BCR-ABL kinase inhibitors, which are derivatives of ponatinib were used to develop a robust 2D-QSAR and 3D-Pharmacophore models by dividing dataset into 32 training set and 12 test set molecules. Read More

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http://dx.doi.org/10.1080/07391102.2018.1559765DOI Listing
December 2018
1 Read

[Types of bcr-abl and their correlations with the blood count in chronic myeloid leukemia (CML) in Togo].

Pan Afr Med J 2018 20;30:221. Epub 2018 Jul 20.

Service d'Hématologie, CHU Tokoin, Université de Lomé, Togo.

This study aims to describe the different bcr-abl gene transcript variants in order to determine their frequency and to study their influence on CBC diagnostic test. We conducted a cross-sectional study of 34 patients with chronic myeloid leukemia in Togo. The search for fusion transcripts was performed in the laboratory of biological haematology at the Henri Mondor Hospital, Créteil (France). Read More

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http://dx.doi.org/10.11604/pamj.2018.30.221.9821DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6295301PMC
January 2019
1 Read

Pharmacovigilance evaluation of the relationship between impaired glucose metabolism and BCR-ABL inhibitor use by using an adverse drug event reporting database.

Cancer Med 2019 Jan 18;8(1):174-181. Epub 2018 Dec 18.

Department of Pharmacy, Tokushima University Hospital, Tokushima, Japan.

Breakpoint cluster region-Abelson murine leukemia (BCR-ABL) inhibitors markedly improve the prognosis of chronic myeloid leukemia. However, high treatment adherence is necessary for successful treatment with BCR-ABL inhibitors. Therefore, an adequate understanding of the adverse event profiles of BCR-ABL inhibitors is essential. Read More

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http://dx.doi.org/10.1002/cam4.1920DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6346261PMC
January 2019
1 Read

Overexpression of Hes1 is involved in sensitization of K562 cells to Imatinib.

J Cell Biochem 2018 Dec 11. Epub 2018 Dec 11.

Institute of Biochemistry and Biophysics, University of Tehran, Tehran, Iran.

Tyrosine kinase inhibitor (TKI)-based therapy has created promising results among much chronic myeloid leukemia (CML) patients. Imatinib as a relatively specific inhibitor of Bcr-Abl is at present one of the undisputed therapeutic agent for newlydiagnosed patients with CML. However, the occurrence of imatinib-resistance enlightens the urgent need to identify other therapeutic agents against CML. Read More

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https://onlinelibrary.wiley.com/doi/abs/10.1002/jcb.28296
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http://dx.doi.org/10.1002/jcb.28296DOI Listing
December 2018
5 Reads

Nilotinib in the treatment of chronic myeloid leukemia.

Future Oncol 2018 Dec 14. Epub 2018 Dec 14.

Division of Hematology & Internal Medicine, Department of Clinical & Biological Sciences of the University of Turin, 'San Luigi Gonzaga' University Hospital, 10043 Orbassano-Turin, Italy.

Nilotinib, a second-generation tyrosine kinase inhibitor, was designed to overcome resistance of a wide range of BCR-ABL mutants to imatinib. When used in the first-line treatment in newly diagnosed  chronic myeloid leukemia (CML), it induces faster and deeper molecular responses in higher than imatinib percentage of patients. Treatment-free remission after achievement of sustained deep molecular response represents an emerging treatment goal for a proportion of patients with CML in chronic phase. Read More

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https://www.futuremedicine.com/doi/10.2217/fon-2018-0468
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http://dx.doi.org/10.2217/fon-2018-0468DOI Listing
December 2018
6 Reads

Induction of apoptosis and erythroid differentiation of human chronic myelogenous leukemia K562 cells by low concentrations of lidamycin.

Oncol Rep 2019 Jan 2;41(1):475-482. Epub 2018 Nov 2.

College of Life Sciences, North China University of Science and Technology, Tangshan, Hebei 063210, P.R. China.

Apoptosis induction and differentiation of promyelocytic leukemic cells into mature cells are major strategies for the drug-based treatment of leukemia. Lidamycin (LDM) which is a member of the enediyne antibiotic family exhibits extreme cytotoxicity. In the present study, the induction of apoptosis and differentiation in human chronic myeloid leukemia K562 cells by low concentrations of lidamycin were investigated. Read More

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http://dx.doi.org/10.3892/or.2018.6849DOI Listing
January 2019
2 Reads

Towards rapid prediction of drug-resistant cancer cell phenotypes: single cell mass spectrometry combined with machine learning.

Chem Commun (Camb) 2019 Jan;55(5):616-619

Department of Chemistry and Biochemistry, University of Oklahoma, Norman, Oklahoma 73019, USA.

Combined single cell mass spectrometry and machine learning methods is demonstrated for the first time to achieve rapid and reliable prediction of the phenotype of unknown single cells based on their metabolomic profiles, with experimental validation. This approach can be potentially applied towards prediction of drug-resistant phenotypes prior to chemotherapy. Read More

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http://dx.doi.org/10.1039/c8cc08296kDOI Listing
January 2019

Efficacy and Safety of Generic Dasatinib as a Second-line Treatment for Patients with Chronic Myeloid Leukemia: a Multicenter Retrospective Study in Hubei Province, China.

Curr Med Sci 2018 Dec 7;38(6):1005-1011. Epub 2018 Dec 7.

Department of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.

Dasatinib is a second-generation tyrosine kinase inhibitor (TKI) and it could be used as a second-line treatment for patients with chronic myeloid leukemia (CML). Yinishu, a generic dasatinib made in China, was approved by the China Food and Drug Administration in 2013 and it costs much less than the patented dasatinib SPRYCEL. The present study aimed to examine the efficacy and safety of Yinishu as a second-line treatment for CML by comparing the baseline clinical characteristics, rates of adverse events and efficacy between Yinishu and SPRYCEL groups. Read More

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http://dx.doi.org/10.1007/s11596-018-1976-0DOI Listing
December 2018
1 Read

The HLA ligandome landscape of chronic myeloid leukemia delineates novel T-cell epitopes for immunotherapy.

Blood 2019 Feb 10;133(6):550-565. Epub 2018 Dec 10.

Department of Hematology and Oncology, University Hospital Tübingen, Tübingen, Germany.

Antileukemia immunity plays an important role in disease control and maintenance of tyrosine kinase inhibitor (TKI)-free remission in chronic myeloid leukemia (CML). Thus, antigen-specific immunotherapy holds promise for strengthening immune control in CML but requires the identification of CML-associated targets. In this study, we used a mass spectrometry-based approach to identify naturally presented HLA class I- and class II-restricted peptides in primary CML samples. Read More

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http://www.bloodjournal.org/lookup/doi/10.1182/blood-2018-07
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http://dx.doi.org/10.1182/blood-2018-07-866830DOI Listing
February 2019
8 Reads
10.452 Impact Factor

Feasibility of treatment discontinuation in chronic myeloid leukemia in clinical practice: results from a nationwide series of 236 patients.

Blood Cancer J 2018 Dec 2;8(10):91. Epub 2018 Dec 2.

Hematology Department, Hospital Universitario La Princesa, Madrid, Spain.

Over half of chronic myeloid leukemia (CML) patients in deep molecular response do not lose the major molecular response (MMR) after stopping treatment with tyrosine kinase inhibitors (TKI). This strategy is safe in clinical trials, but its applicability in the real-life setting remains unsettled. We describe the outcomes after TKI discontinuation in a nationwide series of 236 CML patients. Read More

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http://www.nature.com/articles/s41408-018-0125-0
Publisher Site
http://dx.doi.org/10.1038/s41408-018-0125-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6275158PMC
December 2018
15 Reads

[MET/ERK and MET/JNK Pathway Activation Is Involved in BCR-ABL Inhibitor-resistance in Chronic Myeloid Leukemia].

Authors:
Masanobu Tsubaki

Yakugaku Zasshi 2018 ;138(12):1461-1466

Division of Pharmacotherapy, Faculty of Pharmacy, Kindai University.

Resistance to the breakpoint cluster region-abelson (BCR-ABL) tyrosine kinase inhibitor (TKI), imatinib, poses a major problem in the treatment of chronic myeloid leukemia (CML). Imatinib resistance often results from a secondary mutation in BCR-ABL1. However, the basis of this BCR-ABL1-independent resistance in the absence of such mutation remains to be elucidated. Read More

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http://dx.doi.org/10.1248/yakushi.18-00142DOI Listing
February 2019
1 Read

We do still transplant CML, don't we?

Hematology Am Soc Hematol Educ Program 2018 11;2018(1):177-184

Centre for Clinical Haematology, Queen Elizabeth Hospital, Birmingham, United Kingdom.

The remarkable clinical activity of tyrosine kinase inhibitors (TKIs) in chronic myeloid leukemia (CML) has transformed patient outcome. Consequently, allogeneic stem cell transplantation (allo-SCT) is no longer the only treatment modality with the ability to deliver long-term survival. In contrast to the central position it held in the treatment algorithm 20 years ago, allografting is now largely reserved for patients with either chronic-phase disease resistant to TKI therapy or advanced-phase disease. Read More

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http://dx.doi.org/10.1182/asheducation-2018.1.177DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6246013PMC
November 2018
5 Reads

Molecular monitoring in CML: how deep? How often? How should it influence therapy?

Hematology Am Soc Hematol Educ Program 2018 11;2018(1):168-176

Cancer Theme, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia.

With the advent of tyrosine kinase inhibitors (TKIs), the goals of therapy in chronic myeloid leukemia (CML) are steadily shifting. Long-term disease control on TKI therapy has been the goal and expectation for most patients. More recently, treatment-free remission (TFR) has entered mainstream practice and is increasingly being adopted as the main goal of therapy. Read More

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http://dx.doi.org/10.1182/asheducation-2018.1.168DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6246017PMC
November 2018
6 Reads

The argument for using imatinib in CML.

Hematology Am Soc Hematol Educ Program 2018 11;2018(1):161-167

Department of Clinical Haematology, Hammersmith Hospital, Imperial College Healthcare NHS Trust, London, United Kingdom; and.

June 2018 was the 20th anniversary of the clinical use of the first tyrosine kinase inhibitor (TKI), imatinib, for chronic myeloid leukemia. Since then, the change in prognosis for patients with this disease is one of the major success stories of modern cancer medicine. The dilemmas that face physicians and patients are no longer only those concerned with delaying inevitable progression to the terminal blastic phase or selecting the individuals most likely to benefit from allogeneic stem-cell transplantation; rather, they are now focused also on the choice of TKI, the management of comorbidities and adverse effects, strategies to improve quality of life, and the appropriateness of a trial of therapy discontinuation. Read More

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http://dx.doi.org/10.1182/asheducation-2018.1.161DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6246007PMC
November 2018
14 Reads

Imatinib dose reduction in major molecular response of chronic myeloid leukemia: results from the German Chronic Myeloid Leukemia-Study IV.

Haematologica 2018 Dec 4. Epub 2018 Dec 4.

Institut für Medizinische Informationsverarbeitung, Biometrie und Epidemiologie, Munich.

Standard first-line therapy of chronic myeloid leukemia is treatment with imatinib. In the randomized German Chronic Myeloid Leukemia-Study IV, more potent BCR-ABL inhibition with 800mg (high-dose) imatinib accelerated achievement of a deep molecular remission. However, whether and when a de-escalation of the dose intensity under high-dose imatinib can be safely performed without increasing the risk of losing deep molecular response is unknown. Read More

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http://dx.doi.org/10.3324/haematol.2018.206797DOI Listing
December 2018
5 Reads

Potential Leukemic Cells Engraftment After Hematopoietic Stem Cell Transplantation From Unrelated Donors With Undiagnosed Chronic Leukemia.

Transplant Proc 2018 Dec 18;50(10):3789-3796. Epub 2018 Apr 18.

Department of General Pathology, Pomeranian Medical University, Szczecin, Poland. Electronic address:

Background: Donor-related neoplasms are a potential complication of treatment strategies involving stem cell transplantation. Although mechanisms for detection of short-term complications after these procedures are well developed, complications with delayed onset, notably transmission of chronic diseases such as chronic myeloid leukemia (CML), have been difficult to assess. Consequently, we studied the potential of human CML cells to engraft hematopoietic tissues after intravenous implantation in mice. Read More

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http://dx.doi.org/10.1016/j.transproceed.2018.04.036DOI Listing
December 2018
1 Read

Targeting P-Glycoprotein: Nelfinavir Reverses Adriamycin Resistance in K562/ADR Cells.

Cell Physiol Biochem 2018 29;51(4):1616-1631. Epub 2018 Nov 29.

Department of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, Dalian, China.

Background/aims: The emergence of multidrug resistance (MDR) caused by P-glycoprotein (P-gp) overexpression is a serious obstacle to the treatment of chronic myelocytic leukemia. In recent years, some clinical trials have shown that nelfinavir (NFV), a traditional anti-HIV drug, has anti-cancer effects. Some researchers have also shown NFV might be a potential P-gp inhibitor. Read More

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http://dx.doi.org/10.1159/000495650DOI Listing
January 2019
6 Reads

Priapism as a rare presentation of chronic myeloid leukemia.

J Cancer Res Ther 2018 Oct-Dec;14(6):1442-1443

Department of Hematology, SGPGI, Lucknow, Uttar Pradesh, India.

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http://dx.doi.org/10.4103/0973-1482.199388DOI Listing
February 2019
1 Read

Development of plasma cell leukemia in a patient with chronic myeloid leukemia while on treatment with imatinib mesylate.

J Cancer Res Ther 2018 Oct-Dec;14(6):1431-1433

Department of Hematology, Yildirim Beyazit University, Ankara, Turkey.

Plasma cell leukemia (PCL) is a rare and an aggressive form of plasma cell dyscrasias. We report a 67-year-old male with PCL which developed while on imatinib mesylate (IM) therapy 38 months after diagnosis of chronic myeloid leukemia (CML). The patient has been treated successfully with bortezomib, melphalan and prednisolone. Read More

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http://www.cancerjournal.net/preprintarticle.asp?id=192762
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http://dx.doi.org/10.4103/0973-1482.192762DOI Listing
February 2019
6 Reads

Effect of Age on NK Cell Compartment in Chronic Myeloid Leukemia Patients Treated With Tyrosine Kinase Inhibitors.

Front Immunol 2018 8;9:2587. Epub 2018 Nov 8.

Faculty of Medicine, Institute of Immunology, University of Coimbra, Coimbra, Portugal.

Natural killer (NK) cells are a very important component of the innate immune response involved in the lysis of virus infected and tumor cells. Aging has a profound impact in the frequency, phenotype and function of NK cells. Chronic Myeloid Leukemia (CML) is caused by the BCR-ABL gene formation encoding aberrant oncoprotein tyrosine kinase. Read More

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http://dx.doi.org/10.3389/fimmu.2018.02587DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6246921PMC
November 2018
3 Reads

Dasatinib: A Review in Pediatric Chronic Myeloid Leukemia.

Paediatr Drugs 2018 Dec;20(6):593-600

, Springer, Private Bag 65901, Mairangi Bay, Auckland, 0754, New Zealand.

Chronic myeloid leukemia (CML) is a rare hematopoietic stem cell disease that is typically characterized by the abnormal BCR-ABL1 fusion gene on the Philadelphia (Ph) chromosome in neoplastic cells. Dasatinib (Sprycel) is an orally administered, small molecule tyrosine kinase inhibitor indicated for the treatment of certain hematological malignancies, including Ph-positive CML in the chronic phase (Ph+ CML-CP) in adult and pediatric patients. In open-label phase 1 and phase 2 clinical trials, dasatinib produced early and durable target responses (i. Read More

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http://dx.doi.org/10.1007/s40272-018-0319-8DOI Listing
December 2018
10 Reads

Unique Case of Myeloproliferative Neoplasm with Two Rare Clonal Abnormalities: Rare JAK2 Exon 12 Mutation and Rare e14a3 (b3a3) BCR/ABL Fusion Transcript.

Acta Haematol 2019 21;141(1):23-27. Epub 2018 Nov 21.

Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas,

Myeloproliferative neoplasms (MPNs) are clonal disorders divided into Philadelphia (Ph) chromosome-positive chronic myeloid leukemia (CML) or Ph chromosome-negative MPNs. Co-occurrence of these disease entities is very rare and typically involves presence of common p190 or p210 BCR/ABL fusion transcript (responsible for CML) along with JAK2V617F mutation (most common driver mutation in Ph-negative MPNs). Because of the rarity of such cases, it is not clear if the outcomes are any different in these patients. Read More

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http://dx.doi.org/10.1159/000494427DOI Listing
November 2018
2 Reads

A chronic myeloid leukemia case with a variant translocation t(11;22) (q23;q11.2): masked Philadelphia or simple variant translocation?

Authors:
Kadir Acar Burak Uz

Pan Afr Med J 2018 22;30:161. Epub 2018 Jun 22.

Gazi University Faculty of Medicine, Department of Internal Medicine, Division of Hematology, Turkey.

Chronic myeloid leukemia (CML) is characterized by the presence of the Philadelphia chromosome (Ph), usually due to a reciprocal translocation, t(9;22)(q34;q11.2). The remaining cases (2-10%) have variant translocation, and more rarely (~1%) a cryptic rearrangement is present which can be detected by fluorescence in situ hybridization analysis in a CML patient with a Ph-negative karyotype (Masked Ph). Read More

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http://dx.doi.org/10.11604/pamj.2018.30.161.9318DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6235488PMC
December 2018
10 Reads

Leukostasis retinopathy: An uncommon visual threatening complication of chronic myeloid leukemia with severe hyperleukocytosis - A case report and review of the literature.

Indian J Ophthalmol 2018 Dec;66(12):1871-1874

Department of Ophthalmology, Tongji Medical College, Tongji Hospital, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China.

To describe a rare case of an unusual visual threatening complication of chronic myeloid leukemia (CML). A 21-year-old male visited the hospital complaining of 1-week painless binocular acute visual loss without any other symptoms. The patient was diagnosed with CML. Read More

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http://dx.doi.org/10.4103/ijo.IJO_627_18DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6256890PMC
December 2018
1 Read

Safety and efficacy of bosutinib in fourth-line therapy of chronic myeloid leukemia patients.

Ann Hematol 2019 Feb 16;98(2):321-330. Epub 2018 Nov 16.

Instituto de Investigación Sanitaria, Hospital Universitario de la Princesa, Madrid, Spain.

Bosutinib is a second-generation tyrosine kinase inhibitor (2GTKI) approved at 400 mg once daily (QD) as first-line therapy in patients with chronic myeloid leukemia (CML) patients and at 500 mg QD in patients who are resistant to or intolerant of prior therapy. In clinical practice, bosutinib is often given to patients who have failed imatinib, nilotinib, and dasatinib (i.e. Read More

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http://link.springer.com/10.1007/s00277-018-3507-2
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http://dx.doi.org/10.1007/s00277-018-3507-2DOI Listing
February 2019
15 Reads

Recent Studies on Ponatinib in Cancers Other Than Chronic Myeloid Leukemia.

Cancers (Basel) 2018 Nov 9;10(11). Epub 2018 Nov 9.

Department of Pharmacy, University of Genova, Viale Benedetto XV 3, 16132 Genova, Italy.

Ponatinib is a third line drug for the treatment of chronic myeloid leukemia patients, especially those that develop the gatekeeper mutation T315I, which is resistant to the first and the second line drugs imatinib, nilotinib, dasatinib and bosutinib. The compound was first identified as a pan Bcr-Abl and Src kinase inhibitor. Further studies have indicated that it is a multitargeted inhibitor that is active on FGFRs, RET, AKT, ERK1/2, KIT, MEKK2 and other kinases. Read More

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http://dx.doi.org/10.3390/cancers10110430DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6267038PMC
November 2018
2 Reads

A modified DAW-22 compound F-B1 inhibits Bcr/Abl and induces apoptosis in chronic myelogenous leukemia cells.

Anticancer Drugs 2019 Feb;30(2):159-166

Key laboratory for Rare Disease of Shandong Province, Department of Pharmacology, Institute of Materia Medica, Shandong Academy of Medical Sciences, Jinan.

The Bcr/Abl kinase is an oncogenic fusion protein that plays a central role in the pathogenesis of chronic myeloid leukemia (CML). Some small-molecule kinase inhibitors such as imatinib were developed in the treatment of CML; however, resistant to imatinib is an emerging problem of CML therapy. Hence, additional approaches or compounds targeting leukemogenic cells are required. Read More

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http://Insights.ovid.com/crossref?an=00001813-900000000-9875
Publisher Site
http://dx.doi.org/10.1097/CAD.0000000000000712DOI Listing
February 2019
8 Reads