• New forms of resistance can arise as: missense mutations within the Abl kinase domain, over-expression of Bcr-Abl, increased production of transmembrane plasma proteins, or the constitutive activation of downstream signaling molecules such as Src-family kinases. (wikipedia.org)
  • A significant minority of chronic myeloid leukaemia patients eventually develop resistance to imatinib, often as a result of point mutations within the BCR-ABL kinase domain. (bmj.com)
  • The binding of these inhibitors blocks the Bcr-Abl kinase in the inactive conformation and provides an advantage in overcoming drug resistance due to kinase mutations. (eurekaselect.com)
  • Mutations in the Bcr-Abl kinase domain may cause, or contribute to, resistance to tyrosine kinase inhibitors (TKIs) in chronic myeloid leukemia patients. (cml-foundation.org)
  • CHMFL-074 shows better inhibitory activity than Imatinib against indigenous BCR-ABL kinase and several mutations such as for example E255K, F317L, F317I, M351T, Q252H,Y253F and H369P. (molecularcircuit.com)
  • De Benedittis, Caterina (2015) Next-Generation Sequencing-Based Mutations Scanning Strategy of the BCR-ABL Kinase Domain in Patients with PhiladelPhia-Chromosome Positive Leukemias Treated with Tyrosine Kinase Inhibitors , [Dissertation thesis], Alma Mater Studiorum Università di Bologna. (unibo.it)
  • This study was conducted to evaluate the frequency of JAK2, CALR and MPL mutations in with BCR-ABL myeloproliferative neoplasms and their association with demographic data and hematologic parameters in a referral center, in the Middle East. (iranpath.org)
  • To develop a mouse model for CML-initiating GMP, we expressed p210(BCR-ABL) in an established line of E2A-knockout mouse BM cells that retain pluripotency in ex vivo culture. (ca.gov)
  • Differential signaling networks of Bcr-Abl p210 and p190 kinases in leukemia cells defined by functional proteomics. (cepheid.com)
  • The e13a2 and e14a2 transcripts encode P210 BCR-ABL1 proteins with slightly different sizes. (cmleukemia.com)
  • On the other hand about 30% of patients with Ph+ ALL harbor the M-BCR p210or p210[5,6,7]. (bios-mep.info)
  • To ensure highest sensitivity, the ipsogen BCR-ABL1 Mbcr Kit has been optimized to detect BCR-ABL Mbcr p210 b2a2 or b3a2 transcripts and the ABL control gene using prediluted plasmid standards and primers and probe mixes (see figures Accurate detection of BCR-ABL Mbcr standards. BCR-ABL Mbcr standards (F1–F5): 10 1 , 10 2 , 10 3 , 10 5 , and 10 6 copies/5 µl. "> Accurate detection of BCR-ABL Mbcr standards and Reliable detection of ABL plasmid standards. ABL standards (C1–C3): 10 3 ,10 4 , and 10 5 copies/5 µl. "> Reliable detection of ABL plasmid standards ). (qiagen.com)
  • The ipsogen BCR-ABL1 Mbcr Kit is a ready-to-use kit for the detection of BCR-ABL Mbcr p210 b2a2 or b3a2 fusion gene transcripts using real-time PCR. (qiagen.com)
  • The kit is based on the amplification and detection of specific BCR-ABL Mbcr p210 b2a2 or b3a2 transcripts, relative to ABL control gene expression, in total RNA. (qiagen.com)
  • Using the ipsogen BCR-ABL1 Mbcr Kit allows detection and quantification of BCR-ABL Mbcr p210 b2a2 or b3a2 fusion gene and ABL transcripts. (qiagen.com)
  • The ipsogen BCR-ABL1 Mbcr Kit enables sensitive and reliable detection and quantification of BCR-ABL Mbcr p210 b2a2 or b3a2 transcripts, relative to ABL control gene expression, for research use only. (qiagen.com)
  • BCR-ABL kinase domain mutation analysis in chronic myeloid leukemia patients treated with tyrosine kinase inhibitors: recommendations from an expert panel on behalf of European LeukemiaNet. (cml-foundation.org)
  • In chronic myeloid leukemia and Philadelphia-positive acute lymphoblastic leukemia patients resistant to tyrosine kinase inhibitors (TKIs), BCR-ABL kinase domain mutation status is an essential component of the therapeutic decision algorithm. (unibo.it)
  • Even though the first Bcr-Abl TK inhibitor was named "the magic bullet" to cure cancer by Time magazine, a second generation of Bcr-Abl TKI was subsequently developed to combat the initial resistance that emerged. (wikipedia.org)
  • Imatinib (Gleevec) was discovered in 1992 and is regarded as first generation drug since it is the first Bcr-Abl tyrosine kinase inhibitor to be used in the treatment of CML. (wikipedia.org)
  • T315I mutated BCR-ABL is the main cause of the resistance mediated by imatinib and second generation BCR-ABL inhibitor. (jcancer.org)
  • Using cell lines derived from conditional MYC, RAS, and BCR-ABL transgenic murine models, we demonstrate shared responses to inhibition of lipogenesis by the acetyl-coA carboxylase inhibitor 5-(tetradecloxy)-2-furic acid (TOFA), and other lipogenesis inhibitors. (biomedcentral.com)
  • MK-0457, an Aurora kinase and BCR-ABL inhibitor, was studied on a Phase I/II study in 77 patients with refractory hematologic malignancies. (northwestern.edu)
  • In particular, BCR‐ABL inhibitor‐induced impaired glucose metabolism remains controversial. (tokushima-u.ac.jp)
  • Therefore, we conducted signal detection analyses for BCR‐ABL inhibitor‐induced impaired glucose metabolism by using the FDA Adverse Event Reporting System (FAERS) and Japanese Adverse Drug Event Report (JADER) database. (tokushima-u.ac.jp)
  • Imatinib mesylate (IM), a potent inhibitor of the BCR/ABL tyrosine kinase, has become standard first-line therapy for patients with chronic myeloid leukemia (CML), but the frequency of resistance increases in advancing stages of disease. (lu.se)
  • This abnormality was discovered by Peter Nowell in 1960 and is a consequence of fusion between the Abelson (Abl) tyrosine kinase gene at chromosome 9 and the break point cluster (Bcr) gene at chromosome 22, resulting in a chimeric oncogene (Bcr-Abl) and a constitutively active Bcr-Abl tyrosine kinase that has been implicated in the pathogenesis of CML. (wikipedia.org)
  • Bcr-Abl was regarded as highly attractive target for drug intervention since the Bcr-Abl fusion gene encodes a constitutively activated kinase. (wikipedia.org)
  • An abnormal chromosomal translocation known as t(9;22) results in the establishment of the Philadelphia chromosome, which contains the BCR-ABL gene, culminating in the development of this syndrome ( 1 ). (spandidos-publications.com)
  • Translation products of a fusion gene derived from CHROMOSOMAL TRANSLOCATION of C-ABL GENES to the genetic locus of the breakpoint cluster region gene on chromosome 22. (jefferson.edu)
  • The fusion gene on the derivative chromosome 22q11 produces a chimeric BCR-ABL1 mRNA transcript and corresponding translated oncoprotein. (blallab.com)
  • Chronic myeloid leukemia (CML) is characterized by the presence of BCR-ABL1 fusion gene. (cmleukemia.com)
  • Human chronic myelogenous leukemia (CML) is characterized by a translocation between chromosomes 9 and 22 that results in a BCR-ABL fusion gene coding for chimeric proteins. (pasteur.fr)
  • Using in vitro cell lines derived in from conditional MYC, RAS, and BCR-ABL transgenic murine models and oncogene-driven human cell lines, we determined gene regulation, metabolic profiles, and sensitivity to inhibition of lipogenesis in lymphoid malignancies. (biomedcentral.com)
  • Site of breakage in chromosome 22 (BCR gene) can occur in different regions within a 5.8kb region known as the major breakpoint cluster region (M-bcr), spanning 5 exons previously known as b1 to b5 but now as exon 12 to 16 [1]. (aku.edu)
  • In CML, the breakpoint in the BCR gene mostly (95%) falls within the major break point cluster region with b2a2 at 40 % and b3a2 at 55% [1]. (aku.edu)
  • BCR gene fused ABL kinase may be the critical traveling pressure for the Philadelphia Chromosome positive (Ph+) Chronic Myeloid Leukemia (CML) and continues to be extensively explored like a medication target. (molecularcircuit.com)
  • The various other important level of resistance mechanism is because of the amplification from the BCR-ABL gene [10]. (molecularcircuit.com)
  • Two principal breaks occur in the (breakpoint cluster region) gene locus on chromosome 22: the (major) M-BCR, between exons 12 and 16, and the (minor) m-BCR, in the first intron of and m-BCR to that of p185(Abelson tyrosin protein kinase 1) gene on chromosome 9 falls within the intron between the exons 1 and 2. (bios-mep.info)
  • The fusion gene on der9 differs between m-BCR-p185and M-BCR-p210gene encodes a small ABL/BCR with an approximate molecular mass of 40 kDa (p40transcript is detectable in 65% of the CML patients [15] and the p96transcript is present in 100% of examined patients with m-BCR Ph+ ALL [16]. (bios-mep.info)
  • It carries a new gene called bcr-abl, which sets off a process that creates abnormal white blood cells. (webmd.com)
  • They kill off CML blood cells by blocking the protein made by the abnormal gene bcr-abl. (webmd.com)
  • The kit provides reagents optimized for reliable and sensitive detection and quantification of BCR-ABL Mbcr b2a2 or b3a2 transcripts, relative to ABL control gene expression, in total RNA. (qiagen.com)
  • Specific primers and probe mixes and standard serial dilutions of control and fusion DNA are provided for the quantification of the BCR-ABL1 Mbcr genes and the ABL control gene according to Europe Against Cancer (EAC) recommendations (see figures BCR-ABL Mbcr fusion gene transcript. BCR-ABL Mbcr fusion gene transcript. "> BCR-ABL Mbcr fusion gene transcript and ABL control gene transcript. ABL control gene transcript. "> ABL control gene transcript ). (qiagen.com)
  • BCR-ABL Mbcr fusion gene transcript. (qiagen.com)
  • BCR-ABL-transformed GMP as myeloid leukemic stem cells. (ca.gov)
  • Expression of BCR-ABL in these cells reproducibly stimulated myeloid expansion in culture and generated leukemia-initiating cells specifically in the GMP compartment. (ca.gov)
  • The data show that Scorpions PCR enables rapid screening for BCR-ABL T315I in chronic myeloid leukaemia patients and is appropriate for use in a clinical setting. (bmj.com)
  • Chronic myeloid leukemia (CML) results from BCR-ABL oncogene, which blocks CML cells differentiation and protects these cells from apoptosis. (jcancer.org)
  • Chronic myeloid leukemia (CML) is a clonal expansion of the progenitor hematopoietic stem cells arising from the existence of the fusion BCR-ABL oncogene, that represents 15%-20% of the newly diagnosed cases of leukemia patients [ 1 - 2 ]. (jcancer.org)
  • BCR-ABL1 mediated miR-150 downregulation through MYC contributed to myeloid differentiation block and drug resistance in chronic myeloid leukemia. (jefferson.edu)
  • Recommendations aimed to rationalize the use of BCR-ABL mutation testing in chronic myeloid leukemia have been compiled by a panel of experts appointed by the European LeukemiaNet (ELN) and European Treatment and Outcome Study and are here reported. (cml-foundation.org)
  • The BCR-ABL1 minor breakpoint (e1a2) constitutes a rare but distinct leukemic variant and accurate detection and quantitation of these fusion transcripts are paramount to improving outcomes for all chronic myeloid leukemia (CML) patients. (asuragen.com)
  • Chronic myeloid leukemia (CML) with p190 BCR-ABL: analysis and characteristics, outcomes and prognostic significance. (cepheid.com)
  • Guidelines for the measurement of BCR-ABL transcripts in chronic myeloid leukaemia. (cepheid.com)
  • The proportion of different BCR-ABL1 transcript types in chronic myeloid leukemia. (cmleukemia.com)
  • The MPDs (which include polycythemia vera (PV), essential thrombocythemia (ET), chronic eosinophilic leukemia (CEL), primary myelofibrosis (PMF), chronic myelomono- cytic leukemia (CMML), and systemic mast cell disease (SMCD)) exclude chronic myeloid leukemia (CML) because of the pathognomic importance of the BCR-ABL translocation for the diagnosis and treatment of this disorder with imatinib mesylate. (elsevierpure.com)
  • In fact M-BCR p210is associated with primarily myeloid leukemia. (bios-mep.info)
  • Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm caused by an acquired 9;22-chromosomal translocation in a hematopoietic stem cell (HSC) resulting in the expression of the BCR-ABL1 fusion protein. (haematologica.org)
  • Breakpoint cluster region‐Abelson murine leukemia (BCR‐ABL) inhibitors markedly improve the prognosis of chronic myeloid leukemia. (tokushima-u.ac.jp)
  • We have shown here that IM induces autophagy in CML blast crisis cell lines, CML primary cells, and p210BCR/ABL-expressing myeloid precursor cells. (lu.se)
  • BCR-ABL oncogene encodes a BCR-ABL tyrosine kinase (TK), which triggers different downstream targets including c-Myc, STAT5 and CrkL, which participated in the control of cell differentiation, proliferation, migration and other cellular behaviors [ 3 - 5 ]. (jcancer.org)
  • Hence, BCR-ABL oncogene has been the target for the treatment of patients with CML. (jcancer.org)
  • Bcr-Abl tyrosine-kinase inhibitors (TKI) are the first-line therapy for most patients with chronic myelogenous leukemia (CML). (wikipedia.org)
  • The t(9;22)/BCR-ABL1 abnormality is associated with chronic myelogenous leukemia (CML) and Philadelphia-positive acute lymphoblastic leukemia of B-cell lineage (Ph+ ALL). (blallab.com)
  • Eight of 18 patients with BCR-ABL T315I-mutated chronic myelogenous leukemia (44%) had hematologic responses and one of three patients (33%) with Philadelphia chromosome-positive acute lymphoblastic leukemia obtained complete remission. (northwestern.edu)
  • Bcr-Abl oncoprotein is aberrantly expressed in chronic myelogenous leukaemia (CML). (mun.ca)
  • JOA displayed the activity of inhibiting the BCR-ABL and promoted differentiation of not only imatinib -sensitive but also imatinib -resistant cells with BCR-ABL mutation, which could become a potent lead compound to overcome the imatinib -resistant induced by inhibitors of BCR-ABL tyrosine kinase in CML therapy. (jcancer.org)
  • For most patients with CML, BCR-ABL tyrosine kinase inhibitors (TKIs) have turned the an inevitably fatal disease into a manageable condition. (jcancer.org)
  • Another interesting family of allosteric inhibitors is represented by those compounds targeting the myristate-pocket of Bcr-Abl (myristate-pocket binders). (eurekaselect.com)
  • However, high treatment adherence is necessary for successful treatment with BCR‐ABL inhibitors. (tokushima-u.ac.jp)
  • Therefore, an adequate understanding of the adverse event profiles of BCR‐ABL inhibitors is essential. (tokushima-u.ac.jp)
  • Signals for an increased reporting rate of impaired glucose metabolism were detected only for nilotinib use, whereas these signals were not detected for other BCR‐ABL inhibitors. (tokushima-u.ac.jp)
  • Although FAERS‐ and JADER‐based signal detection analyses cannot determine causality perfectly, our study suggests the effects on glucose metabolism are different between BCR‐ABL inhibitors and provides useful information for the selection of appropriate BCR‐ABL inhibitors. (tokushima-u.ac.jp)
  • Second-generation BCR-ABL kinase inhibitors in CML. (bvsalud.org)
  • This review reports the last findings in the development of novel myristate-pocket binders of Bcr-Abl as promising anti-leukemia agents. (eurekaselect.com)
  • The junctional region of the BCR-ABLb3a2 molecule represents a potential leukemia-specific antigen which could be recognized by cytotoxic T lymphocytes (CTL). (pasteur.fr)
  • The hallmark of Philadelphia chromosome positive (Ph+) leukemia is the BCR/ABL kinase, which is successfully targeted by selective ATP competitors. (bios-mep.info)
  • The presence of ABL/BCR changed the phenotype of the leukemia most likely due to its capacity CR2 to influence the stem cell population as shown by our data. (bios-mep.info)
  • ABL)-negative B lineage acute lymphoblastic leukemia. (clinicaltrialsgps.com)
  • I. To compare the overall survival (OS) of blinatumomab in conjunction with chemotherapy to chemotherapy alone in patients with BCR-ABL-negative B cell precursor acute lymphoblastic leukemia (ALL) who are minimal residual disease (MRD) positive after induction and intensification chemotherapy, based on multiparameter flow cytometric (MFC) assessment of residual blasts. (clinicaltrialsgps.com)
  • The World Health Organization (WHO) provides diagnostic criteria for BCR-ABL negative MPNs, including polycythemia vera (PV), essential thrombocythemia (ET), primary myelofibrosis (PMF), chronic eosinophilic leukemia (CEL), chronic neutrophilic leukemia (CNL), and myeloproliferative neoplasms, unclassifiable (MPN-U) (1). (iranpath.org)
  • however, the T315I BCR-ABL mutant has proved resistant to all available TKIs. (bmj.com)
  • MK-0457 has important activity in patients with leukemias expressing the highly resistant T315I BCR-ABL mutation. (northwestern.edu)
  • Targeting BCR/ABL by selective ATP competitors, such as imatinib or nilotinib, is a well validated therapeutic concept, but unable to definitively eradicate the disease. (bios-mep.info)
  • It is thus concluded that AVM inhibits the activity of BCR/ABL and their subsequent molecular signals, including AKT and MAPK, resulting in cytotoxicity via apoptosis. (spandidos-publications.com)
  • Therefore, imatinib was a paradigm of targeted therapies, which due to that imatinib inhibits the phosphorylation of BCR-ABL then suppress the activation of BCR-ABL tyrosine kinase [ 6 ]. (jcancer.org)
  • Dialogue Imatinib, the initial launched focus on therapy, which potently inhibits BCR-ABL, c-KIT and PDGFRs provides achieved remarkable achievement in the center [5]. (molecularcircuit.com)
  • Fusion Proteins, bcr-abl" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (jefferson.edu)
  • Several different variants of the bcr-abl fusion proteins occur depending upon the precise location of the chromosomal breakpoint. (jefferson.edu)
  • This graph shows the total number of publications written about "Fusion Proteins, bcr-abl" by people in this website by year, and whether "Fusion Proteins, bcr-abl" was a major or minor topic of these publications. (jefferson.edu)
  • Below are the most recent publications written about "Fusion Proteins, bcr-abl" by people in Profiles. (jefferson.edu)
  • 1 Different subtypes of BCR-ABL1 transcripts encode fusion proteins with different sizes that may lead to different disease phenotypes. (cmleukemia.com)
  • Therefore the ABL-part of the t(9;22) fusion proteins is constant [1]. (bios-mep.info)
  • The fusion proteins p185and p210are mutant ABL kinases. (bios-mep.info)
  • The inhibitory effect of BCR/ABL on the B-cell signaling is counteracted by the ABL/BCRs, the reciprocal t(9;22) fusion proteins [13]. (bios-mep.info)
  • Juozaitytė, E 2017-06-01 00:00:00 AbstractThe most important complications of Philadelphianegagive (non BCR-ABL) myeloproliferative neoplasms (MPNs) are vascular events. (sagepub.com)
  • Seventy-one patients with BCR-ABL negative myeloproliferative neoplasms were evaluated for JAK2 V617F, CALR type 1, type 2, and MPL by allele-specific PCR and conventional PCR from 2018 to 2019. (iranpath.org)
  • Seventy-one patients with BCR-ABL negative myeloproliferative neoplasms whose information was registered in the molecular pathology department of Shiraz Medical School, the southwest of Iran, were included in this study from 2018 to 2019. (iranpath.org)
  • In the presence of TKI the binding of ATP is blocked, phosphorylation is prevented and Bcr-Abl expressing cells either have a selective growth disadvantage or undergo apoptotic cell death. (wikipedia.org)
  • The results revealed that AVM inhibited the phosphorylation of BCR/ABL and their subsequent molecular signals including AKT and MAPK activation. (spandidos-publications.com)
  • Despite substantial breakpoint heterogeneity at the DNA level, a consistent set of BCR-ABL1 mRNA transcripts are produced that can be readily and sensitively detected by reverse transcription-PCR (RT-PCR) technique. (blallab.com)
  • Little is known about the role of the fusion protein encoded by the reciprocal derivative chromosome 9, the ABL/BCR. (bios-mep.info)
  • The QuantideX qPCR BCR-ABL minor Kit marries improved efficiency with unprecedented sensitivity, empowering labs to assess the deepest molecular responses in patients harboring the minor breakpoint with the ease-of-use they've come to expect from Asuragen. (asuragen.com)
  • Xpert BCR-ABL Ultra p190 is a quantitative test for the BCR-ABL minor breakpoint (p190) transcripts that provide high test sensitivity, standardization, and on-demand molecular results in ≤2.5 hours. (cepheid.com)
  • These results provide further evidence that BCR-ABL-transformed GMP with abnormal beta-catenin activity can function as leukemic stem cells. (ca.gov)
  • Building on the simple workflow and best-in-class sensitivity established with the FDA-cleared QuantideX ® qPCR BCR-ABL IS Kit, the minor Kit allows labs and clinical researchers to examine the biology of disease for this very rare but distinct leukemic variant with unprecedented ease. (asuragen.com)
  • Such CTL recognize HLA-matched, BCR-ABL-positive leukemic cells, implying efficient natural processing and presentation of these junctional peptides. (pasteur.fr)
  • In models of Ph+ ALL we show that the functional interplay between ABL/BCR and BCR/ABL not only increases the transformation potential of BCR/ABL but is also indispensable for the growth and survival of Ph+ ALL leukemic cells. (bios-mep.info)
  • 1 The BCR-ABL1 fusion protein is a constitutively active tyrosine kinase and triggers a cascade of aberrant downstream signaling pathways leading to clonal outgrowth of CML cells and subsequent disease manifestation. (haematologica.org)
  • Here, we determined the effect of Jiyuan oridonin A (JOA), an ent -kaurene diterpenoid compound, on the differentiation blockade in imatinib-sensitive, particularly, imatinib-resistant CML cells with BCR-ABL-T315I mutation by cell proliferation assay, apoptosis analysis, cell differentiation analysis, cell cycle analysis and colony formation assay. (jcancer.org)
  • Elimination of BCR/ABL-dependent intracellular signals triggers apoptosis, but it is unclear whether this activates additional cell survival and/or death pathways. (lu.se)
  • IM-induced autophagy did not involve c-Abl or Bcl-2 activity but was associated with ER stress and was suppressed by depletion of intracellular Ca2+, suggesting it is mechanistically nonoverlapping with IM-induced apoptosis. (lu.se)
  • The QuantideX ® qPCR BCR-ABL minor Kit (RUO) is a clinical research tool enabling ultra-sensitive and precise detection of BCR-ABL1 minor fusion transcripts (e1a2) from whole blood specimens. (asuragen.com)
  • The QuantideX qPCR BCR-ABL minor Kit (RUO) delivers high performance through unmatched sensitivity and optimized laboratory efficiency. (asuragen.com)
  • The QuantideX ® qPCR BCR-ABL minor Kit, an in vitro diagnostic (IVD) assay, enables ultra-sensitive detection of BCR-ABL1 minor fusion transcripts from whole blood specimens. (asuragen.com)
  • Characteristics of BCR-ABL rearrangement variants in Pakistani patient" by Zeeshan Ansar Ahmed, Amna Nasir et al. (aku.edu)
  • 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. (sagepub.com)
  • Hughes and Ross observe that the small number of patients with atypical BCR-ABL1 transcripts, or whose BCR-ABL transcript type at diagnosis is unknown, and whose MR endpoints cannot be reliably determined, are not suitable candidates for TFR. (news-medical.net)
  • Due to increasing resistance and intolerance to imatinib efforts were made to develop new drugs that could inhibit the Bcr-Abl tyrosine kinase. (wikipedia.org)
  • Additionally, several resistance mechanisms, such as BCR-ABL genomic amplification, are considered ( 4 ). (spandidos-publications.com)
  • We utilize preclinical murine models and transgenic primary model of T-ALL to determine the effect of lipogenesis blockade across BCR-ABL-, RAS-, and c-MYC-driven lymphoid malignancies. (biomedcentral.com)
  • Established international organizations recommend definitive timepoints for monitoring BCR-ABL p190 in ALL and CML patients. (cepheid.com)
  • Xpert BCR-ABL Ultra p190 is an automated test for quantifying the amount of BCR-ABLp190 transcript as a ratio of BCR-ABL p190/ABLwith high sensitivity. (cepheid.com)
  • Based on the innovative GeneXpert ® technology, Xpert BCR-ABL Ultra p190 automates the testing procedure, including RNA isolation, reverse transcriptionLeveraging Cepheid's lab in a cartridge™ technology, the Xpert BCR-ABL p190 test decreases workflow complexity and hands-on time by automating the entire testing process, delivering faster results. (cepheid.com)
  • Novel BCR-ABL1 fusion identified by targeted next-generation sequencing in a patient with an atypical myeloproliferative neoplasm. (jefferson.edu)
  • This product is a MHC pentamer of peptide composed BCR-ABL 210 kD fusion protein-derived peptide of ATGFKQSSK sequence covering 259-269 and A*03:01, A*11:01 molecule. (peptides.de)
  • We performed in silico threedimensional modeling of apoptin, molecular docking experiments between apoptin model and the known structure of Bcr- Abl, and the 3D structures of SH2 domains of CrkL and Bcr-Abl. (mun.ca)
  • Major developments in technology and analytical performance are integrated into the ipsogen BCR-ABL1 Mbcr IS-MMR Kit, to provide sensitive and accurate results aligned with the International Scale, and allow assessment of Major Molecular Response (MMR). (qiagen.com)
  • But newer treatments that target bcr-abl can also help many people get into remission. (webmd.com)
  • Empiric use of imatinib mesylate against the spectrum of BCR-ABL negative MPDs has had mixed results. (elsevierpure.com)
  • Mesa, RA 2007, ' Imatinib and tyrosine kinase inhibition, in the management of BCR-ABL negative myeloproliferative disorders ', Biologics: Targets and Therapy , vol. 1, no. 2, pp. 129-138. (elsevierpure.com)
  • Mesa, Ruben A. / Imatinib and tyrosine kinase inhibition, in the management of BCR-ABL negative myeloproliferative disorders . (elsevierpure.com)
  • Native BCR acts as a negative regulator of proliferation and oncogenic transformation by a down-regulation of RAS-mediated signaling [18]. (bios-mep.info)
  • Furthermore, imatinib mesylate significantly enhanced antitumor immune responses to dendritic cell-based immunization against an imatinib-resistant BCR-ABL negative lymphoma. (arizona.edu)
  • In CML, breakpoints in BCR result in either exons 13 or 14 (e13, e14) joined to exon 2 of ABL1 (a2). (blallab.com)
  • As a result, cells expressing different forms of BCR/ABL were recruited for the present study, including K562 (human wild‑type) or TCCY‑T315I (human imatinib‑resistant) and the Ba/F3‑(T315I/E279K/Y253H) (mouse BCR/ABL point mutation‑transfected cells). (spandidos-publications.com)
  • Interestingly, AVM appeared to be more sensitive to imatinib‑resistant (T315I, Y253H, and E279K) than wild‑type BCR/ABL cells, indicating its potential to overcome imatinib‑resistant severe issues in CML. (spandidos-publications.com)
  • Thus, cells expressing different forms of BCR/ABL were recruited for the present study, including K562 [human wild-type (WT)] or TCCY-T315I [human imatinib-resistant (IR)] and the Ba/F3-(T315I/E279K/Y253H) (mouse BCR/ABL point mutation-tranfected cells). (spandidos-publications.com)
  • We found that JOA at lower concentration significantly inhibited the proliferation of CML cells expressing mutant BCR-ABL (T315I mutation included) and wild-type BCR-ABL, which was due to that JOA induced the cell differentiation and the cell cycle arrest at G0/G1 phase. (jcancer.org)
  • Mechanistically, the cell differentiation mediated by JOA may be originated from the inhibition of BCR-ABL/c-MYC signaling in CML cells expressing wild-type BCR-ABL and BCR-ABL-T315I. (jcancer.org)
  • We examined cells from mouse models of MYC-, RAS-, and BCR-ABL-driven lymphoid malignancies and find a convergence on de novo lipogenesis. (biomedcentral.com)
  • In conclusion, the data shown here demonstrated that CHMFL-074 was impressive against both unchanged CML cell lines and BCR-ABL positive individual major hematopoietic cells. (molecularcircuit.com)
  • In this study we have calculated a 3D structure of apoptin and through modeling and docking approaches, we show its interaction with Bcr-Abl oncoprotein and its downstream signaling components, following which we confirm some of the newly-found interactions by biochemical methods. (mun.ca)