18,887 results match your criteria Chronic Myeloid Leukemia and BCR-ABL


[Overexpression of miR-30a Promotes Apoptosis of Leukemia K562 Cells].

Zhongguo Shi Yan Xue Ye Xue Za Zhi 2019 Apr;27(2):396-402

Department of Immunology, College of Basic Medical Science ,Chongqing Medical University, Chongqing 400016, China,E-mail:

Objective: To investigate the pro-apoptotic effect and mechanism of miR-30a overexpression on chronic myeloid leukemia K562 cells.

Methods: The k562 cells were transfected with the recombinant plasmid pEGFP-pre-miR-30a, the real-time quantitative PCR was used to detect the level of miR-30a and BCR/ABL, and then the cell apoptosis was assessed by flow cytometry with AnnexinV-FITC/PI double staining. Western blot was used to detect the expression of BCR/ABL protein,apoptosis-related protein BCL-2 and BAX, PTEN, AKT and p-AKT. Read More

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http://dx.doi.org/10.19746/j.cnki.issn.1009-2137.2019.02.014DOI Listing
April 2019
2 Reads

A Case of Childhood Blastic Phase Chronic Myeloid Leukemia With Minor BCR-ABL.

J Pediatr Hematol Oncol 2019 Apr 15. Epub 2019 Apr 15.

Department of Pediatrics, National Center for Global Health and Medicine.

Chronic myeloid leukemia (CML) is commonly associated with major BCR-ABL transcript. We present a child with blastic phase CML associated with minor BCR-ABL transcript without prior CML diagnosis. Diagnosis was achieved by fluorescence in situ hybridization of peripheral blood neutrophils, which identified 90% as BCR-ABL positive. Read More

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http://dx.doi.org/10.1097/MPH.0000000000001488DOI Listing
April 2019
2 Reads

Predictive value of early molecular response for deep molecular response in chronic phase of chronic myeloid leukemia.

Medicine (Baltimore) 2019 Apr;98(15):e15222

Department of Hematology, The First Hospital of Jilin University.

To investigate the association of 3- and 6-month BCR-ABL transcript levels on the international scale (BCR-ABL) and other factors with deep molecular response (DMR) achievement in chronic myeloid leukemia (CML)-chronic phase (CP) patients receiving tyrosine kinase inhibitor (TKI) therapy.We retrospectively analyzed the clinical data of 206 patients enrolled in our hospital between January 2010 and July 2018. These patients were initially diagnosed with CML-CP and received imatinib or nilotinib therapy. Read More

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http://dx.doi.org/10.1097/MD.0000000000015222DOI Listing
April 2019
2 Reads

[The mechanisms of taxodione-induced apoptosis in BCR-ABL-positive leukemia cells].

Nihon Yakurigaku Zasshi 2019 ;153(4):147-154

Division of Hygienic Chemistry, Faculty of Pharmacy, Keio University.

Chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL) are caused by a fusion protein, BCR-ABL, which induces cellular transformation by activating the signaling molecules, STAT5 and Akt. The specific BCR-ABL inhibitors including imatinib, nilotinib, and dasatinib, are clinically utilized in the treatment with CML and ALL patients. Although these BCR-ABL inhibitors are initially successful in the treatment of leukemia, many patients develop drug resistance due to the appearance of the gatekeeper mutation of BCR-ABL, T315I. Read More

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http://dx.doi.org/10.1254/fpj.153.147DOI Listing
January 2019
1 Read

Addiction to DUSP1 protects JAK2V617F-driven polycythemia vera progenitors against inflammatory stress and DNA damage, allowing chronic proliferation.

Oncogene 2019 Apr 9. Epub 2019 Apr 9.

Department of Biology, Faculty of Medicine and Dentistry, Palacky University, Olomouc, Czech Republic.

Inflammatory and oncogenic signaling converge in disease evolution of BCR-ABL-negative myeloproliferative neoplasms, clonal hematopoietic stem cell disorders characterized by gain-of-function mutation in JAK2 kinase (JAK2V617F), with highest prevalence in patients with polycythemia vera (PV). Despite the high risk, DNA-damaging inflammatory microenvironment, PV progenitors tend to preserve their genomic stability over decades until their progression to post-PV myelofibrosis/acute myeloid leukemia. Using induced pluripotent stem cells-derived CD34 progenitor-enriched cultures from JAK2V617F PV patient and from JAK2 wild-type healthy control, CRISPR-modified HEL cells and patients' bone marrow sections from different disease stages, we demonstrate that JAK2V617F induces an intrinsic IFNγ- and NF-κB-associated inflammatory program, while suppressing inflammation-evoked DNA damage both in vitro and in vivo. Read More

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http://www.nature.com/articles/s41388-019-0813-7
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http://dx.doi.org/10.1038/s41388-019-0813-7DOI Listing
April 2019
3 Reads

Results of the European survey on the assessment of deep molecular response in chronic phase CML patients during tyrosine kinase inhibitor therapy (EUREKA registry).

J Cancer Res Clin Oncol 2019 Apr 2. Epub 2019 Apr 2.

Abteilung Hämatologie und Internistische Onkologie, Klinik für Innere Medizin II, Universitätsklinikum Jena, Am Klinikum 1, 07740, Jena, Germany.

Purpose: The advent of tyrosine kinase inhibitor (TKI) therapies has revolutionized the treatment of chronic myeloid leukemia (CML). The European LeukemiaNet (ELN) recommends quantification of BCR-ABL1 transcripts by real-time quantitative PCR every 3 months during TKI treatment. Since a proportion of patients in deep molecular response (DMR: MR, MR, MR) maintain remission after treatment stop, assessment of DMR is crucial. Read More

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http://dx.doi.org/10.1007/s00432-019-02910-6DOI Listing
April 2019
1 Read

Differential roles of STAT1 and STAT2 in the sensitivity of JAK2V617F- vs. BCR-ABL-positive cells to interferon alpha.

J Hematol Oncol 2019 Apr 2;12(1):36. Epub 2019 Apr 2.

Department of Hematology, Oncology, Hemostaseology, and Stem Cell Transplantation, Faculty of Medicine, RWTH Aachen University, Pauwelsstr 30, 52074, Aachen, Germany.

Background: Interferon alpha (IFNa) monotherapy is recommended as the standard therapy in polycythemia vera (PV) but not in chronic myeloid leukemia (CML). Here, we investigated the mechanisms of IFNa efficacy in JAK2V617F- vs. BCR-ABL-positive cells. Read More

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http://dx.doi.org/10.1186/s13045-019-0722-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6444528PMC
April 2019
2 Reads

Fulminant blast crisis with de novo 11q23 rearrangement in a Philadelphia-positive CML patient undergoing treatment with dasatinib.

Tumori 2019 Apr 1:300891619839473. Epub 2019 Apr 1.

1 Department of Oncology and Hematology, BMT with Section of Pneumology, Hubertus Wad Tumorzentrum, University Cancer Center Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Background:: Progression of chronic myeloid leukemia (CML) is frequently accompanied by cytogenetic evolution, with an extra copy of the Philadelphia chromosome, trisomy 8 and 19, and isochromosome (17p) commonly detected. Translocations involving 11q23 chromosomal region have been rarely reported in CML. The few reported patients with blast crisis (BC) of CML carrying an 11q rearrangement have insufficient responses to tyrosine kinase inhibitors (TKIs) and possess a poor prognosis. Read More

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http://dx.doi.org/10.1177/0300891619839473DOI Listing
April 2019
3 Reads

GCA links TRAF6-ULK1-dependent autophagy activation in resistant chronic myeloid leukemia.

Autophagy 2019 Mar 30:1-15. Epub 2019 Mar 30.

c Leukemia Research Institute , The Catholic University of Korea , Seoul , Republic of Korea.

Imatinib is the first molecularly targeted compound for chronic myeloid leukemia (CML) capable to inhibit BCR-ABL kinase activity. However, recent clinical evidence indicates that a substantial proportion of CML patients exhibit BCR-ABL-dependent or independent resistance to imatinib. Despite the importance of imatinib resistance in CML, the underlying molecular mechanisms of this resistance are largely unknown. Read More

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http://dx.doi.org/10.1080/15548627.2019.1596492DOI Listing
March 2019
3 Reads
11.753 Impact Factor

[Prognosis of clonal chromosomal abnormalities in Philadelphia negative metaphases cells in chronic myeloid leukemia with tyrosine kinase inhibitor therapy].

Zhonghua Xue Ye Xue Za Zhi 2019 Mar;40(3):209-214

Department of Hematology, Henan Cancer Hospital, the Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou 450008, China.

To investigate the characteristics and prognosis of clonal chromosomal abnormalities appearing in Philadelphia negative metaphases (CCA/Ph(-)) cells in chronic myeloid leukemia (CML) with tyrosine kinase inhibitor (TKI) therapy. The clinical data of 30 cases with CCA/Ph(-) during TKI treatment in Henan Cancer Hospital from August 2007 to July 2017 were retrospectively analyzed. The univariate factor was analyzed by Kaplan-Meier method. Read More

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http://dx.doi.org/10.3760/cma.j.issn.0253-2727.2019.03.009DOI Listing
March 2019
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Molecular dynamics investigation on the Asciminib resistance mechanism of I502L and V468F mutations in BCR-ABL.

J Mol Graph Model 2019 Jun 21;89:242-249. Epub 2019 Mar 21.

International Joint Research Laboratory of Nano-Micro Architecture Chemistry, Laboratory of Theoretical and Computational Chemistry, Institute of Theoretical Chemistry, Jilin University, Changchun, 130023, People's Republic of China; Key Laboratory for Molecular Enzymology and Engineering of the Ministry of Education, Jilin University, Changchun, 130023, People's Republic of China. Electronic address:

Asciminib, a highly selective non-ATP competitive inhibitor of BCR-ABL, has demonstrated to be a promising drug for patients with chronic myeloid leukemia. It is a pity that two resistant mutations (I502L and V468F) have been found during the clinical trial, which is a challenge for the curative effect of Asciminib. In this study, molecular dynamics simulations and molecular mechanics generalized Born surface area (MM-GB/SA) calculations were performed to investigate the molecular mechanism of Asciminib resistance induced by the two mutants. Read More

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http://dx.doi.org/10.1016/j.jmgm.2019.03.018DOI Listing
June 2019
1 Read

Impact of Additional Cytogenetic Abnormalities on the Clinical Behavior of Patients With Chronic Myeloid Leukemia: Report on a Latin American Population.

Clin Lymphoma Myeloma Leuk 2019 Feb 21. Epub 2019 Feb 21.

Department of Hematology and Oncology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.

Introduction: Additional cytogenetic abnormalities (ACA) in patients with chronic myeloid leukemia (CML) are related to an increased risk of treatment failure, leukemic progression, and decreased survival. Currently, there are scarce data available for the Latin American population. The aim of this study was to outline the impact of ACA emergence in Mexican patients with CML. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S21522650193000
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http://dx.doi.org/10.1016/j.clml.2019.02.007DOI Listing
February 2019
3 Reads

Discovery and characterization of a novel highly potent and selective type II native and drug-resistant V299L mutant BCR-ABL inhibitor (CHMFL-ABL-039) for Chronic Myeloid Leukemia (CML).

Cancer Biol Ther 2019 Mar 20:1-9. Epub 2019 Mar 20.

a High Magnetic Field Laboratory , Chinese Academy of Sciences , Hefei , Anhui , P. R. China.

BCR fused ABL kinase is the critical driving oncogene for chronic myeloid leukemia (CML) and has been extensively studied as the drug discovery target in the past decade. The successful introduction of tyrosine kinase inhibitors (TKI) such as Imatinib, Dasatinib and Bosutinib has greatly improved the CML patient survival rate. However, upon the chronic treatment, a variety of TKI resistant mutants, such as the V299L mutant which has been found in more and more patients with the high-throughput sequencing technology, are observed, although the incidence is still considered rare compared to the more prevalent gatekeeper T315I mutant. Read More

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http://dx.doi.org/10.1080/15384047.2019.1579958DOI Listing
March 2019
1 Read
3.072 Impact Factor

Chronic myelogenous leukemia, a still unsolved problem: pitfalls and new therapeutic possibilities.

Drug Des Devel Ther 2019 8;13:825-843. Epub 2019 Mar 8.

Department of Hematology, Military Institute of Medicine, 04-141 Warsaw, Poland,

Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder of hematopoietic stem cells. At the molecular level, the disorder results from t(9;22)(q34;q11) reciprocal translocation between chromosomes, which leads to the formation of an oncogenic gene fusion. Instead of progress in the understanding of the molecular etiology of CML and the development of novel therapeutic strategies, clinicians still face many challenges in the effective treatment of patients. Read More

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http://dx.doi.org/10.2147/DDDT.S191303DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6415732PMC
March 2019
1 Read

Outcomes of unplanned tyrosine kinase inhibitor discontinuation in patients with chronic myeloid leukemia: retrospective analysis of real-world experience in a single institution.

Hematology 2019 Dec;24(1):355-361

a Department of Hematology and Hematopoietic Stem Cell Transplantation , Yamanashi Prefectural Central Hospital , Kofu , Japan.

Objectives: To explore real-world prognoses for tyrosine kinase inhibitor (TKI) discontinuation in chronic myeloid leukemia (CML) patients and the associated reasons for TKI discontinuation.

Methods: We investigated, using the medical records of 85 consecutive CML patients who received TKIs between December 2001 and August 2016 at our hospital, reasons for discontinuation, duration of TKI treatment before discontinuation, molecular response (MR) status at TKI discontinuation, treatment-free remission (TFR) duration, and overall survival after TKI discontinuation.

Results: TKI therapy was discontinued in 21 patients. Read More

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http://dx.doi.org/10.1080/16078454.2019.1590964DOI Listing
December 2019
1 Read

Pre- and post-transplant ponatinib for a patient with acute megakaryoblastic blast phase chronic myeloid leukemia with T315I mutation who underwent allogeneic hematopoietic stem cell transplantation.

Int J Hematol 2019 Mar 16. Epub 2019 Mar 16.

Department of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-chou, Mizuho-ku, Nagoya, Aichi, 467-8601, Japan.

A 42-year-old female complaining of fever and night sweats was diagnosed with acute megakaryoblastic blast phase chronic myeloid leukemia (CML-BP). She had massive splenomegaly, left pleural effusion with leukemia infiltration, and moderate myelofibrosis. She received dasatinib monotherapy (140 mg/day) as for induction, after which her pleural effusion rapidly resolved and hematological remission was achieved. Read More

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http://dx.doi.org/10.1007/s12185-019-02628-8DOI Listing
March 2019
3 Reads

Neferine in the Lotus Plumule Potentiates the Antitumor Effect of Imatinib in Primary Chronic Myeloid Leukemia Cells In Vitro.

J Food Sci 2019 Apr 13;84(4):904-910. Epub 2019 Mar 13.

Xiangya Hospital, Central South Univ., Changsha, China.

Imatinib, the prototype BCR-ABL tyrosine kinase inhibitor (TKI), is the first-line treatment for Philadelphia chromosome-positive chronic myeloid leukemia (CML) in the chronic phase. However, a subgroup of patients exhibit poor response or experience relapse. This issue may be overcome by combination therapy using natural compounds. Read More

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http://dx.doi.org/10.1111/1750-3841.14484DOI Listing
April 2019
2 Reads

TOPK is regulated by PP2A and BCR/ABL in leukemia and enhances cell proliferation.

Int J Oncol 2019 May 5;54(5):1785-1796. Epub 2019 Mar 5.

Department of Hematology, Tokyo Medical and Dental University, Tokyo 113‑8519, Japan.

Although treatment of chronic myeloid leukemia (CML) has improved with the development of tyrosine kinase inhibitors (TKIs), patients develop fatal blast crisis (BC) whilst receiving TKI treatment. Alternative treatments for cases resistant to TKIs are required. A serine/threonine protein kinase, T‑lymphokine‑activated killer cell‑originated protein kinase (TOPK), is highly expressed in various malignant tumors. Read More

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http://www.spandidos-publications.com/10.3892/ijo.2019.4740
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http://dx.doi.org/10.3892/ijo.2019.4740DOI Listing
May 2019
9 Reads

A tetrameric protein scaffold as a nano-carrier of antitumor peptides for cancer therapy.

Biomaterials 2019 Jun 6;204:1-12. Epub 2019 Mar 6.

Institute of Human Virology and Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD, 21201, USA. Electronic address:

A major pharmacological barrier to peptide therapeutics is their susceptibility to proteolytic degradation and poor membrane permeability, which, in principle, can be overcome by nanoparticle-based delivery technologies. Proteins, by definition, are nano materials and have been clinically proven as an efficient delivery vehicle for small molecule drugs. Here we describe the design of a protein-based peptide drug carrier derived from the tetramerization domain of the chimeric oncogenic protein Bcr/Abl of chronic myeloid leukemia. Read More

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http://dx.doi.org/10.1016/j.biomaterials.2019.03.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6441627PMC
June 2019
3 Reads

Can increased immunogenicity in chronic myeloid leukemia improve outcomes?

Expert Rev Hematol 2019 Mar 11:1-9. Epub 2019 Mar 11.

b Division of Malignant Hematology , Moffitt Cancer Center , Tampa , FL , USA.

Introduction: Chronic myeloid leukemia (CML) has long been thought to be the model disease for immunotherapy with its characteristic BCR-ABL fusion protein. Although targeted therapy using tyrosine kinase inhibitors (TKIs) is highly effective at inducing remission, most patients require life-long TKI to decrease the risk of relapse. In recent years, much effort has been devoted to finding ways to eliminate CML stem cells (LSCs); the source of disease persistence. Read More

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https://www.tandfonline.com/doi/full/10.1080/17474086.2019.1
Publisher Site
http://dx.doi.org/10.1080/17474086.2019.1588105DOI Listing
March 2019
4 Reads

Bioactive Compounds from Seaweed with Anti-Leukemic Activity: A Mini-Review on Carotenoids and Phlorotannins.

Mini Rev Med Chem 2019 Mar 10. Epub 2019 Mar 10.

Team of Histomorphology, Physiopathology and Applied Toxicology, CIIMAR/CIMAR - Interdisciplinary Center for Marine and Environmental Research, U.Porto - University of Porto, Avenida General Norton de Matos s/n, 4450-208 Matosinhos. Portugal.

Chronic myeloid leukemia (CML) represents 15 - 20% of all new cases of leukemia and is characterized by an uncontrolled proliferation of abnormal myeloid cells. Currently, the first-line of treatment involves tyrosine kinase inhibitors (TKIs), which specifically inhibits the activity of the fusion protein BCR-ABL. However, resistance, mainly due to mutations, can occur. Read More

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http://dx.doi.org/10.2174/1389557519666190311095655DOI Listing
March 2019
2 Reads

[Efficacy and safety of domestic dasatinib as second-line treatment for chronic myeloid leukemia patients in the chronic phase].

Zhonghua Xue Ye Xue Za Zhi 2019 Feb;40(2):98-104

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

To investigate the efficiency and safety of domestic tyrosine kinase inhibitor (TKI) dasatinib (Yinishu) as second-line treatment for patients with chronic myeloid leukemia in chronic phase (CML-CP). A retrospective analysis of clinical data of CML-CP patients who received domestic dasatinib as second-line treatment in the CML collaborative group hospitals of Hubei province from March 2016 to July 2018 was performed. The optimal response rate, the cumulative complete cytogenetic response (CCyR), the cumulative major molecular responses (MMR), progression free survival (PFS), event free survival (EFS) and adverse effects (AEs) of the patients were assessed at 3, 6 and 12 months of treatment. Read More

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http://dx.doi.org/10.3760/cma.j.issn.0253-2727.2019.02.002DOI Listing
February 2019
1 Read

Development of a Potent Protein Degrader against Oncogenic BCR-ABL Protein.

Chem Pharm Bull (Tokyo) 2019 ;67(3):165-172

Divisions of Molecular Target and Gene Therapy Products, National Institute of Health Sciences.

Chromosomal translocation occurs in some cancer cells, resulting in the expression of aberrant oncogenic fusion proteins that include BCR-ABL in chronic myelogenous leukemia (CML). Inhibitors of ABL tyrosine kinase, such as imatinib and dasatinib, exhibit remarkable therapeutic effects, although emergence of drug resistance hampers the therapy during long-term treatment. An alternative approach to treat CML is to downregulate expression of the BCR-ABL protein. Read More

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http://dx.doi.org/10.1248/cpb.c18-00703DOI Listing
April 2019
1 Read

Andrographolide and its potent derivative exhibit anticancer effects against imatinib-resistant chronic myeloid leukemia cells by downregulating the Bcr-Abl oncoprotein.

Biochem Pharmacol 2019 May 26;163:308-320. Epub 2019 Feb 26.

Institute of Traditional Medicine, National Yang-Ming University, Taipei 11221, Taiwan; Program in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei 11221, Taiwan. Electronic address:

Chronic myelogenous leukemia (CML) is clinically treated with imatinib, which inhibits the kinase activity of the Bcr-Abl oncoprotein. However, imatinib resistance remains a common clinical issue. Andrographolide, the major compound of the medicinal plant Andrographis paniculata, was reported to exhibit anticancer activity. Read More

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http://dx.doi.org/10.1016/j.bcp.2019.02.028DOI Listing
May 2019
14 Reads

Network meta-analysis: a new analysis tool of the experimental evidence.

Minerva Med 2019 Apr;110(2):173-175

Department of Geriatrics, "Casa Sollievo della Sofferenza" Hospital, San Giovanni Rotondo, Foggia, Italy.

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http://dx.doi.org/10.23736/S0026-4806.18.05768-3DOI Listing
April 2019
2 Reads

Imatinib-induced irreversible interstitial lung disease: A case report.

Medicine (Baltimore) 2019 Feb;98(8):e14402

Department of Hematology.

Rationale: Imatinib mesylate (imatinib) is a classic tyrosine kinase inhibitor used to treat chronic myeloid leukemia. Although it is well tolerated by most patients and helps in the achievement of complete remission, a few rare imatinib-associated adverse effects such as pulmonary interstitial fibrosis have been reported. Because of its rareity, the clinical features of imatinib-induced interstitial lung disease (ILD) remain unclear. Read More

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http://dx.doi.org/10.1097/MD.0000000000014402DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6407980PMC
February 2019
1 Read

Concurrent JAK2-Positive Myeloproliferative Disorder and Chronic Myelogenous Leukemia: A Novel Entity? A Case Report With Review of the Literature.

J Investig Med High Impact Case Rep 2019 Jan-Dec;7:2324709619832322

2 GV Montgomery VA Medical Center, Jackson, MS, USA.

JAK2 V617F mutation and BCR-ABL translocation have been considered to be mutually exclusive. However, many cases where both hits coexisted have been reported. We have personally managed a case too. Read More

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http://dx.doi.org/10.1177/2324709619832322DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6393948PMC
February 2019
1 Read

Everolimus in combination with Imatinib overcomes resistance in Chronic myeloid leukaemia.

Med Oncol 2019 Feb 22;36(3):30. Epub 2019 Feb 22.

Laboratory of Oncobiology and Hematology and University Clinic of Hematology, Faculty of Medicine, University of Coimbra, FMUC, Azinhaga de Santa Comba-Celas, 3000-548, Coimbra, Portugal.

Although Imatinib and other tyrosine kinase inhibitors (TKIs) have excellent results, the appearance of resistance is a problem in chronic myeloid leukaemia (CML). PI3K/AKT/mTOR pathway is activated by BCR-ABL playing a crucial rule in CML. This study aimed to evaluate the therapeutic potential of Everolimus, in CML models sensitive and resistant to Imatinib. Read More

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http://dx.doi.org/10.1007/s12032-019-1253-5DOI Listing
February 2019
2 Reads

Novel mutations in the kinase domain of BCR-ABL gene causing imatinib resistance in chronic myeloid leukemia patients.

Sci Rep 2019 Feb 20;9(1):2412. Epub 2019 Feb 20.

Department of Biotechnology, Sri Venkateswara Institute of Medical Sciences, Tirupati, 517507, Andhra Pradesh, India.

Mutations in the drug binding region of BCR-ABL lead to imatinib resistance during the management of chronic myeloid leukemia (CML). In our study, 62 Philadelphia positive (Ph) CML patients showing conspicuous expression of BCR-ABL gene were treated with imatinib. At the end of 3 months, 21/62 (33. Read More

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http://dx.doi.org/10.1038/s41598-019-38672-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6382822PMC
February 2019
1 Read
5.078 Impact Factor

Feasibility of Qualitative Testing of BCR-ABL and JAK2 V617F in Suspected Myeloproliperative Neoplasm (MPN) Using RT-PCR Reversed Dot Blot Hybridization (RT-PCR RDB).

Clin Lymphoma Myeloma Leuk 2019 Jan 19. Epub 2019 Jan 19.

Stem Cell and Cancer Institute, Jakarta, Indonesia; Kalbe Genomics Laboratory, Jakarta, Indonesia.

Background: Defining the presence of BCR-ABL transcript in suspected myeloproliferative neoplasm is essential in establishing chronic myeloid leukemia. In the absence of BCR-ABL, the conventional diagnostic algorithm recommends JAK2 V617F mutation testing to support diagnosis of other MPN diseases such as polycythemia vera, essential thrombocythemia, and primary myelofibrosis. In certain cases of thrombocythemia, simultaneous upfront testing of both BCR-ABL and JAK2 may be desirable. Read More

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http://dx.doi.org/10.1016/j.clml.2019.01.005DOI Listing
January 2019
2 Reads

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
1 Read

Efficacy and safety of tyrosine kinase inhibitors for newly diagnosed chronic-phase chronic myeloid leukemia over a 5-year period: results from the Japanese registry obtained by the New TARGET system.

Int J Hematol 2019 Apr 14;109(4):426-439. Epub 2019 Feb 14.

National Hospital Organization Nagoya Medical Center, Nagoya, Japan.

We report the results of a multicenter observational study using the New TARGET system, in which the effectiveness and safety of tyrosine kinase inhibitors (TKIs) were evaluated in newly diagnosed chronic-phase chronic myeloid leukemia (CML) patients. A total of 506 patients were enrolled between April 2010 and March 2013. Median age was 56 (range 18-92) years; 35% of patients were females. Read More

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http://dx.doi.org/10.1007/s12185-019-02613-1DOI Listing

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
1 Read
0.841 Impact Factor

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
1 Read

Single nucleotide polymorphism in PTEN-Long gene: A risk factor in chronic myeloid leukemia.

Gene 2019 Apr 7;694:71-75. Epub 2019 Feb 7.

Laboratorio de Genética Hematológica, IMEX, CONICET-Academia Nacional de Medicina, Buenos Aires, Argentina.

The BCR-ABL1 oncogene is associated with chronic myeloid leukemia (CML) pathogenesis, but the molecular mechanisms that initiate leukemogenesis are still unclear. Cancer pathogenesis has been associated with genetic alterations that may lead to inactivation of tumor suppressor genes. Phosphatase and tensin homolog (PTEN) is frequently deleted or inactivated in various tumors. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S03781119193009
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http://dx.doi.org/10.1016/j.gene.2019.01.038DOI Listing
April 2019
7 Reads

[Research Progress of C-Myc in Chronic Myelogenous Leukemia --Review].

Zhongguo Shi Yan Xue Ye Xue Za Zhi 2019 Feb;27(1):297-300

Department of Hematology, The First People's Hospital of Huaian Affiliated to Nanjing Medical University, Huaian, 223300, Jiangsu Province, China.E-mail:

As a potential target for cancer treatment, the C-Myc high expresses abnormally in a variety of solid tumors and hematological malignancies in humans. In hematologic malignancies, the increasing expression of C-Myc is associated with poor prognosis of patients diffuse large B-cell lymphoma. However, some studies have shown that high expression of C-Myc might be one of the mechanisms of disease progression and abrupt change, therefore, it can promote the transformation of chronic myeloid leukemia. Read More

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http://dx.doi.org/10.7534/j.issn.1009-2137.2019.01.049DOI Listing
February 2019
2 Reads

[Effects of Tyrosine Kinase Inhibitors on the Th1 and Treg Cells of CML Patients].

Zhongguo Shi Yan Xue Ye Xue Za Zhi 2019 Feb;27(1):25-32

Department of Hematology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 611731, China.Department of Hematology, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu 610072, China.Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu 610072, China.E-mail:

Objective: To compare the immunomodulatory effects of the 2nd generation of tyrosine kinase inhibitors (TKIs)-dasatinib and nilotinib as well as the 1st generation of TKI-imatinib on chronic myeloid leukemia (CML) patients.

Method: To evaluate the T cell subtypes by flow cytometry on the CML patients of our center who received the treatment with dasatinib (n=10), nilotinib (n=26) or imatinib (n=44) for more than 3 months, and to analyze and correlate these data with the clinical remission situations and prognosis.

Results: 80. Read More

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http://dx.doi.org/10.7534/j.issn.1009-2137.2019.01.005DOI Listing
February 2019
10 Reads

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
9 Reads

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
28 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
7 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
3 Reads

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
16 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
2 Reads

Novel Application of Radotinib for the Treatment of Solid Tumors via Natural Killer Cell Activation.

J Immunol Res 2018 31;2018:9580561. Epub 2018 Dec 31.

Institute of Convergence Science, Korea University, Anam-ro 145, Seongbuk-ku, Seoul 02841, Republic of Korea.

Radotinib (Supect™) was developed to treat chronic myeloid leukemia (CML) as a BCR-ABL1 tyrosine kinase inhibitor (TKI). Other TKIs, including imatinib and nilotinib, were also developed for treatment of CML, and recent studies were increasing about the therapeutic effects of other TKIs on solid tumors. However, the effect of radotinib on solid tumors has not yet been investigated. Read More

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http://dx.doi.org/10.1155/2018/9580561DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6330826PMC
April 2019
1 Read

Renal dysfunction and anemia associated with long-term imatinib treatment in patients with chronic myelogenous leukemia.

Int J Hematol 2019 Mar 24;109(3):292-298. Epub 2019 Jan 24.

Division of Hematology, Department of Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.

Knowledge of the toxicity profile of long-term treatment with imatinib is limited. In the present study, we sought to evaluate renal function and hemoglobin levels during long-term imatinib treatment. Eighty-two patients with chronic myelogenous leukemia in chronic phase who had been on imatinib for over 5 years were retrospectively analyzed. Read More

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http://dx.doi.org/10.1007/s12185-019-02596-zDOI Listing
March 2019
21 Reads

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
19 Reads

Acute ischemic intestinal necrosis as a rare side effect of nilotinib.

Authors:
L Li W Liu Z Zeng S Chen

Niger J Clin Pract 2019 Jan;22(1):131-133

Collaborative Innovation Center of Hematology, Jiangsu Institute of Hematology, Key Laboratory of Thrombosis and Hemostasis of Ministry of Health, The First Affiliated Hospital of Soochow University, Suzhou, China.

Tyrosine kinase inhibitors (TKIs) are highly effective therapies for chronic myeloid leukemia (CML). However, continuous administration of TKIs could lead to toxicity that could induce serious vascular disorders. Nilotinib, a second-generation TKI, has been approved for patients with CML in the chronic phase or accelerated phase, after resistance to imatinib has been identified, or as a first-line treatment. Read More

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http://dx.doi.org/10.4103/njcp.njcp_33_18DOI Listing
January 2019
2 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
2 Reads

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
12 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-
Publisher Site
http://dx.doi.org/10.1186/s12885-019-5265-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6329120PMC
January 2019
18 Reads