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https://www.readbyqxmd.com/read/29033451/dasatinib-and-azacitidine-followed-by-haploidentical-stem-cell-transplant-for-chronic-myeloid-leukemia-with-evolving-myelodysplasia-a-case-report-and-review-of-treatment-options
#1
Fabian Lang, Lydia Wunderle, Heike Pfeifer, Susanne Schnittger, Gesine Bug, Oliver G Ottmann
BACKGROUND CML presenting with a variant Philadelphia translocation, atypical BCR-ABL transcript, additional chromosomal aberrations, and evolving MDS is uncommon and therapeutically challenging. The prognostic significance of these genetic findings is uncertain, even as singular aberrations, with nearly no data on management and outcome when they coexist. MDS evolving during the course of CML may be either treatment-associated or an independently coexisting disease, and is generally considered to have an inferior prognosis...
October 16, 2017: American Journal of Case Reports
https://www.readbyqxmd.com/read/29026321/characteristics-and-mutation-analysis-of-ph-positive-leukemia-patients-with-t315i-mutation-receiving-tyrosine-kinase-inhibitors
#2
Peipei Xu, Dan Guo, Xiaoyan Shao, Miaoxin Peng, Bing Chen
BACKGROUND: TKIs are the first-line treatment for patients with Ph-positive (Ph+) leukemia. However, drug resistance is frequently observed, mainly due to mutations within the breakpoint cluster region-Abelson leukemia virus (BCR-ABL) kinase domain. The T315I substitution confers complete resistance to TKIs. The aim of this study was to analyze the clinical characteristics of 17 patients with T315I mutation after TKI treatment and provide a basis for prognosis. PATIENTS AND METHODS: The clinical data of 17 TKI-resistant Ph+ leukemia patients who were found to have a ABL kinase domain mutation from September 2008 to January 2017 were collected...
2017: OncoTargets and Therapy
https://www.readbyqxmd.com/read/29020105/correction-mpt0b169-a-new-antitubulin-agent-inhibits-bcr-abl-expression-and-induces-mitochondrion-mediated-apoptosis-in-nonresistant-and-imatinib-resistant-chronic-myeloid-leukemia-cells
#3
Shuit-Mun Wong, Fu-Hwa Liu, Yueh-Lun Lee, Huei-Mei Huang
[This corrects the article DOI: 10.1371/journal.pone.0148093.].
2017: PloS One
https://www.readbyqxmd.com/read/28990077/inhibitory-effect-of-the-anthelmintic-drug-pyrvinium-pamoate-on-t315i-bcr%C3%A2-abl%C3%A2-positive-cml-cells
#4
Jing Zhang, Yanli Jin, Jingxuan Pan
Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder characterized by a chromosome translocation that generates the BCR‑ABL oncogene, which encodes a constitutively activated tyrosine kinase. Despite progress in controlling CML at the chronic phase by first and second generations of BCR‑ABL tyrosine kinase inhibitors (TKIs), effective drugs with good safety are not available for CML patients harboring T315I BCR‑ABL and those in advanced stages of CML. Therefore, there is an urgent requirement for the development of effective therapies against T315I BCR‑ABL...
October 2, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28986256/microrna-7-inhibits-cell-proliferation-of-chronic-myeloid-leukemia-and-sensitizes-it-to-imatinib-in-vitro
#5
Ming-Jie Jiang, Juan-Juan Dai, Dian-Na Gu, Qian Huang, Ling Tian
MicroRNA is a large class of noncoding small RNA that exerts critical roles in many physiological processes including cell proliferation. MicroRNA-7 (miR-7) has been considered as a tumor suppressor in most malignant tumors versus a tumor promoter in some other ones. However, its role in chronic myeloid leukemia remains unknown. Herein, we found that K562 cell proliferation was largely suppressed when it was stably transfected with miR-7. In accordance with that, apoptosis was also significantly upregulated in miR-7 stably-transfected K562 cells...
October 3, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28978850/recent-topics-in-imids-and-cereblon
#6
Takumi Ito, Hiroshi Handa
Immunomodulatory drugs (IMiDs) are a new class of anticancer compounds that are derived from thalidomide. Lenalidomide and pomalidomide are well-known IMiDs, and they have already been approved by FDA for the treatment of several diseases, including multiple myeloma. Cereblon (CRBN) is a common primary target for IMiDs. It works as a substrate receptor of CRL4. Accumulating evidence has shown that the substrate specificity of CRL4(CRBN) is altered by ligands such as IMiDs. Recently, novel CRBN-binding compounds have been developed and are called "cereblon modulators"...
2017: [Rinshō Ketsueki] the Japanese Journal of Clinical Hematology
https://www.readbyqxmd.com/read/28974549/modulation-of-navitoclax-sensitivity-by-dihydroartemisinin-mediated-mcl-1-repression-in-bcr-abl-b-lineage-acute-lymphoblastic-leukemia
#7
Amit Budhraja, Meghan E Turnis, Michelle L Churchman, Anisha Kothari, Xue Yang, Haiyan Xu, Ewa Kaminska, John C Panetta, David Finkelstein, Charles G Mullighan, Joseph T Opferman
PURPOSE: BCR-ABL+ B-ALL leukemic cells are highly dependent on the expression of endogenous anti-apoptotic MCL-1 to promote viability and are resistant to BH3-mimetic agents such as navitoclax (ABT-263) that targets BCL-2, BCL-XL, and BCL-W. However, the survival of most normal blood cells and other cell types are also dependent on Mcl-1. Despite the requirement for MCL-1 in these cell types, initial reports of MCL-1-specific BH3-mimetics have not described any overt toxicities associated with single-agent use, but these agents are still early in clinical development...
October 3, 2017: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/28971501/current-paradigms-in-the-management-of-philadelphia-chromosome-positive-acute-lymphoblastic-leukemia-in-adults
#8
REVIEW
Riad El Fakih, Elias Jabbour, Farhad Ravandi, Mona Hassanein, Farhan Anjum, Syed Ahmed, Hagop Kantarjian
Philadelphia chromosome-positive (Ph-positive) acute lymphoblastic leukemia (ALL) is a biologically, clinically, and genetically distinct subtype of precursor-B ALL. The Ph chromosome, results from a reciprocal translocation of the ABL1 kinase gene on chromosome 9 to the breakpoint cluster region (BCR) gene on chromosome 22. Depending on the translocation breakpoint, typically a p210 BCR-ABL1 or a p190 BCR- ABL onc protein are generated; both are constitutively active tyrosine kinases that play a central role to alter signaling pathways of cell proliferation, survival, and self-renewal, leading to leukemogenesis...
October 3, 2017: American Journal of Hematology
https://www.readbyqxmd.com/read/28962554/propofol-enhances-bcr-abl-tkis-inhibitory-effects-in-chronic-myeloid-leukemia-through-akt-mtor-suppression
#9
Zhimin Tan, Aixia Peng, Jingwen Xu, Mingwen Ouyang
BACKGROUND: The anti-cancer activities of intravenous anesthetic drug propofol have been demonstrated in various types of cancers but not in chronic myeloid leukemia (CML). METHODS: We systematically examined the effect of propofol and its combination with BCR-ABL tyrosine kinase inhibitors (TKIs) in CML cell lines, patient progenitor cells and mouse xenograft model. We analyzed propofol's underlying mechanism focusing on survival pathway in CML cells. RESULTS: We show that propofol alone is active in inhibiting proliferation and inducing apoptosis in KBM-7, KU812 and K562 cells, and acts synergistically with imatinib or dasatinib, in in vitro cell culture system and in vivo xenograft model...
September 29, 2017: BMC Anesthesiology
https://www.readbyqxmd.com/read/28949401/kronisk-myeloisk-leukemi-f%C3%A3-rebild-f%C3%A3-r-m%C3%A3-lstyrd-terapi-revolutionerande-%C3%A3-verlevnadsvinster-med-definitiv-bot-i-sikte-och-kraftigt-f%C3%A3-rb%C3%A3-ttrad-h%C3%A3-lsoekonomi
#10
Johan Richter, Leif Stenke
Chronic myeloid leukemia - a model disease for targeted therapy Chronic myeloid leukemia (CML) pioneered as the first human malignancy linked to a specific cytogenetic aberration (the Philadelphia chromosome), which led the way to specific targeted therapies with imatinib (Glivec) and later tyrosine kinase inhibitors (TKI). Continuous TKI administration, blocking the oncogenic fusion protein Bcr-Abl, has revolutionized the outcome of CML, transforming an almost uniformly deadly disease into a chronic disorder with a near to normal life expectancy for many patients...
September 21, 2017: Läkartidningen
https://www.readbyqxmd.com/read/28943239/how-to-effectively-treat-acute-leukemia-patients-bearing-mll-rearrangements
#11
REVIEW
Dieter Steinhilber, Rolf Marschalek
Chromosomal translocations - leading to the expression of fusion genes - are well-studied genetic abberrations associated with the development of leukemias. Most of them represent altered transcription factors that affect transcription or epigenetics, while others - like BCR-ABL - are enhancing signaling. BCR-ABL has become the prototype for rational drug design, and drugs like Imatinib and subsequently improved drugs have a great impact on cancer treatments. By contrast, MLL-translocations in acute leukemia patients are hard to treat, display a high relapse rate and the overall survival rate is still very poor...
September 21, 2017: Biochemical Pharmacology
https://www.readbyqxmd.com/read/28942039/comparative-effect-of-imatinib-and-ponatinib-on-autophagy-and-mirnome-in-chronic-myeloid-leukemia
#12
Cagla Kayabasi, Tugce Balci Okcanoglu, Besra Ozmen Yelken, Aycan Asik, Sunde Yilmaz Susluer, Cigir Biray Avci, Guray Saydam, Cumhur Gunduz
BCR-ABL tyrosine kinase inhibitors (TKIs) are selective therapies for the patients with Chronic Myeloid Leukemia (CML). Imatinib and ponatinib have remarkable long-term efficacy on a major molecular response. Although TKI related induction of cytotoxicity and apoptosis have been clearly investigated in molecular levels, their comparative effect on autophagy and miRNome are largely unknown. This study aimed to investigate the involvement of alterations of miRNA expressions in CML progression, and how imatinib and ponatinib affect this process, by comparing CML, imatinib-resistant CML and leukemia stem cells (LSC)...
December 30, 2017: Gene
https://www.readbyqxmd.com/read/28936999/non-adherence-to-cml-therapy-and-its-clinical-implications-in-india
#13
REVIEW
Hari Menon
Clinical trials have shown that early and deeper cytogenetic/ molecular responses to tyrosine kinase inhibitors (TKIs) help in achieving improved long-term outcomes including lower rates of disease progression in chronic myeloid leukaemia (CML). However, the level of molecular responses achieved with TKI therapy in patients with CML is variable and this could be explained by differences in adherence to CML therapy. A systematic literature review of CML studies reporting adherence to BCR-ABL inhibitors from the USA, Asia and Europe (19 articles: 9 retrospective, 4 prospective, rest cross-sectional) showed that average adherence varies from 19% to 100% of the proportion of prescribed drug taken...
May 2017: National Medical Journal of India
https://www.readbyqxmd.com/read/28928866/ct-721-a-potent-bcr-abl-inhibitor-exhibits-excellent-in-vitro-and-in-vivo-efficacy-in-the-treatment-of-chronic-myeloid-leukemia
#14
Yinghui Sun, Na Zhao, Huan Wang, Qiong Wu, Yunqi Han, Qichao Liu, Mangang Wu, Yuliang Liu, Fansheng Kong, He Wang, Ying Sun, Deguang Sun, Lutao Jing, Guojing Tang, Yuandong Hu, Dengming Xiao, Hong Luo, Yongxin Han, Yong Peng
Kinase inhibitors that target Bcr-Abl are highly effective in the treatment of chronic myeloid leukemia (CML). However, these inhibitors are often invalidated due to the drug resistance. Therefore, the discovery and development of novel Bcr-Abl inhibitors is required to overwhelm the drug resistance in the treatment of CML resistant to the currently used first-line Bcr-Abl inhibitors. Herein we have described a newly developed Bcr-Abl inhibitor CT-721, which displayed potent inhibitory effects on wild-type and T315I mutant Bcr-Abl...
2017: Journal of Cancer
https://www.readbyqxmd.com/read/28928163/high-bcr-abl-gusis-levels-at-diagnosis-of-chronic-phase-cml-are-associated-with-unfavorable-responses-to-standard-dose-imatinib
#15
Paolo Vigneri, Fabio Stagno, Stefania Stella, Alessandra Cupri, Stefano Forte, Michele Massimino, Agostino Antolino, Sergio Siragusa, Donato Mannina, Stefana S Impera, Caterina Musolino, Alessandra Malato, Giuseppe Mineo, Carmela Tomaselli, Pamela Murgano, Maurizio Musso, Fortunato Morabito, Stefano Molica, Bruno Martino, Livia Manzella, Martin C Müller, Andreas Hochhaus, Francesco Di Raimondo
PURPOSE: The approval of second-generation tyrosine kinase inhibitors (TKIs) for the first line treatment of chronic myeloid leukemia (CML) has generated an unmet need for baseline molecular parameters associated with inadequate Imatinib responses. EXPERIMENTAL DESIGN: We correlated BCR-ABL/GUSIS and BCR-ABL/ABLIS transcripts at diagnosis with the outcome - defined by the 2013 European LeukemiaNet recommendations - of 272 newly diagnosed CML patients receiving Imatinib 400 mg/daily...
September 19, 2017: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/28927158/regulation-of-htra2-on-wt1-gene-expression-under-imatinib-stimulation-and-its-effects-on-the-cell-biology-of-k562-cells
#16
Lixia Zhang, Yan Li, Xiaoyan Li, Qing Zhang, Shaowei Qiu, Qi Zhang, Min Wang, Haiyan Xing, Qing Rao, Zheng Tian, Kejing Tang, Jianxiang Wang, Yingchang Mi
The aim of the present study was to investigate the regulation of Wilms Tumor 1 (WT1) by serine protease high-temperature requirement protein A2 (HtrA2), a member of the Htr family, in K562 cells. In addition, the study aimed to observe the effect of this regulation on cell biological functions and its associated mechanisms. Expression of WT1 and HtrA2 mRNA, and proteins following imatinib and the HtrA2 inhibitor 5-[5-(2-nitrophenyl) furfuryl iodine]-1, 3-diphenyl-2-thiobarbituric acid (UCF-101) treatment was detected with reverse transcription-quantitative polymerase chain reaction and western blot analysis...
September 2017: Oncology Letters
https://www.readbyqxmd.com/read/28924539/genetic-polymorphisms-of-hemostatic-factors-and-thrombotic-risk-in-non-bcr-abl-myeloproliferative-neoplasms-a-pilot-study
#17
R Dambrauskienė, R Gerbutavičius, R Ugenskienė, R Jankauskaitė, A Savukaitytė, R Šimoliūnienė, M Rudžianskienė, R Gerbutavičienė, E Juozaitytė
The most important complications of Philadelphianegagive (non BCR-ABL) myeloproliferative neoplasms (MPNs) are vascular events. Our aim was to evaluate the effects of single nucleotide polymorphisms (SNPs), platelet glycoproteins (GPs) (Ia/IIa, Ibα, IIb/IIIa and VI), von Willebrand factor (vWF), coagulation factor VII (FVII), β-fibrinogen, and the risk of thrombosis in patients with non BCR-ABL MPNs at the Lithuanian University of Health Sciences. Kaunas, Lithuania. Genotyping was done for 108 patients. The TT genotype of the GP Ia/IIa c...
June 30, 2017: Balkan Journal of Medical Genetics: BJMG
https://www.readbyqxmd.com/read/28923853/adaptation-to-tki-treatment-reactivates-erk-signaling-in-tyrosine-kinase-driven-leukemias-and-other-malignancies
#18
J Kyle Bruner, Hayley S Ma, Li Li, Alice Can Ran Qin, Michelle A Rudek, Richard J Jones, Mark J Levis, Keith W Pratz, Christine A Pratilas, Donald Small
FMS-like tyrosine kinase-3 (FLT3) tyrosine kinase inhibitors (TKI) have been tested extensively to limited benefit in acute myeloid leukemia (AML). We hypothesized that FLT3/internal tandem duplication (ITD) leukemia cells exhibit mechanisms of intrinsic signaling adaptation to TKI treatment that are associated with an incomplete response. Here, we identified reactivation of ERK signaling within hours following treatment of FLT3/ITD AML cells with selective inhibitors of FLT3. When these cells were treated with inhibitors of both FLT3 and MEK in combination, ERK reactivation was abrogated and anti-leukemia effects were more pronounced compared with either drug alone...
October 15, 2017: Cancer Research
https://www.readbyqxmd.com/read/28914569/mutations-in-myeloproliferative-neoplasms-their-significance-and-clinical-use
#19
Fiorella Schischlik, Robert Kralovics
Clonal hematologic diseases of the blood such as polycythemia vera, essential thrombocythemia and primary myelofibrosis belong to the BCR-ABL negative Myeloproliferative Neoplasms (MPN). These diseases are characterized by clonal expansion of hematopoietic precursor cells followed by increased production of differentiated cells of the myeloid lineage. Initiation of clonal hematopoiesis, formation of a clinical phenotype as well as disease progression form part of MPN disease evolution. The disease is driven by acquired somatic mutations in critical pathways such as cytokine signaling, epigenetic regulation, RNA splicing, and transcription factor signaling...
September 25, 2017: Expert Review of Hematology
https://www.readbyqxmd.com/read/28903325/cxcl12-cxcr4-pathway-is-activated-by-oncogenic-jak2-in-a-pi3k-dependent-manner
#20
Hadjer Abdelouahab, Yanyan Zhang, Monika Wittner, Shinya Oishi, Nobutaka Fujii, Rodolphe Besancenot, Isabelle Plo, Vincent Ribrag, Eric Solary, William Vainchenker, Giovanni Barosi, Fawzia Louache
JAK2 activation is the driver mechanism in BCR-ABL-negative myeloproliferative neoplasms (MPN). These diseases are characterized by an abnormal retention of hematopoietic stem cells within the bone marrow microenvironment and their increased trafficking to extramedullary sites. The CXCL12/CXCR4 axis plays a central role in hematopoietic stem cell/ progenitor trafficking and retention in hematopoietic sites. The present study explores the crosstalk between JAK2 and CXCL12/CXCR4 signaling pathways in MPN. We show that JAK2, activated by either MPL-W515L expression or cytokine stimulation, cooperates with CXCL12/CXCR4 signaling to increase the chemotactic response of human cell lines and primary CD34(+) cells through an increased phosphatidylinositol-3-kinase (PI3K) signaling...
August 15, 2017: Oncotarget
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