Fusion Proteins, bcr-abl

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  Subject Areas on Research

  • A Nanopore Sequencing-Based Assay for Rapid Detection of Gene Fusions. 
  • A novel Bcr-Abl-mTOR-eIF4A axis regulates IRES-mediated translation of LEF-1. 
  • A novel mechanism for Bcr-Abl action: Bcr-Abl-mediated induction of the eIF4F translation initiation complex and mRNA translation. 
  • A requirement for NF-kappaB activation in Bcr-Abl-mediated transformation. 
  • Abl tyrosine kinases regulate cell-cell adhesion through Rho GTPases. 
  • Aerobic glycolysis suppresses p53 activity to provide selective protection from apoptosis upon loss of growth signals or inhibition of BCR-Abl. 
  • Analysis of the biologic properties of p230 Bcr-Abl reveals unique and overlapping properties with the oncogenic p185 and p210 Bcr-Abl tyrosine kinases. 
  • Antagonism of SET using OP449 enhances the efficacy of tyrosine kinase inhibitors and overcomes drug resistance in myeloid leukemia. 
  • Apoptosis in haematological malignancies. 
  • Assessment of Outcomes After Stopping Tyrosine Kinase Inhibitors Among Patients With Chronic Myeloid Leukemia: A Nonrandomized Clinical Trial. 
  • Association of the protein kinases c-Bcr and Bcr-Abl with proteins of the 14-3-3 family. 
  • BCR first exon sequences specifically activate the BCR/ABL tyrosine kinase oncogene of Philadelphia chromosome-positive human leukemias. 
  • BCR sequences essential for transformation by the BCR-ABL oncogene bind to the ABL SH2 regulatory domain in a non-phosphotyrosine-dependent manner. 
  • BCR-ABL-induced oncogenesis is mediated by direct interaction with the SH2 domain of the GRB-2 adaptor protein. 
  • Baculovirus expression of functional P210 BCR-ABL oncogene product. 
  • Bcr-Abl kinase modulates the translation regulators ribosomal protein S6 and 4E-BP1 in chronic myelogenous leukemia cells via the mammalian target of rapamycin. 
  • Bcr-Abl-mediated protection from apoptosis downstream of mitochondrial cytochrome c release. 
  • CD4(+) T cells contribute to the remodeling of the microenvironment required for sustained tumor regression upon oncogene inactivation. 
  • Chronic Myelogenous Leukemia, Version 1.2014. 
  • Chronic Myeloid Leukemia, Version 1.2019, NCCN Clinical Practice Guidelines in Oncology. 
  • Chronic Myeloid Leukemia, Version 2.2021, NCCN Clinical Practice Guidelines in Oncology. 
  • Crk is required for apoptosis in Xenopus egg extracts. 
  • Design and rationale for the life after stopping tyrosine kinase inhibitors (LAST) study, a prospective, single-group longitudinal study in patients with chronic myeloid leukemia. 
  • Down syndrome childhood acute lymphoblastic leukemia has a unique spectrum of sentinel cytogenetic lesions that influences treatment outcome: a report from the Children's Oncology Group. 
  • Efficient and rapid induction of a chronic myelogenous leukemia-like myeloproliferative disease in mice receiving P210 bcr/abl-transduced bone marrow. 
  • Elevated expression of a subset of interferon inducible genes in primary bone marrow cells expressing p185 Bcr-Abl versus p210 Bcr-Abl by DNA microarray analysis. 
  • Engineering a BCR-ABL-activated caspase for the selective elimination of leukemic cells. 
  • Expression of constitutively active Raf-1 in the mitochondria restores antiapoptotic and leukemogenic potential of a transformation-deficient BCR/ABL mutant. 
  • Finding the right BCR-ABL1 tyrosine kinase inhibitor: a case report of successful treatment of a patient with chronic myeloid leukemia and a V299L mutation using nilotinib. 
  • Improving frontline treatment for chronic myeloid leukemia: emerging evidence for use of nilotinib and dasatinib. 
  • Inhibition of apoptosome formation by suppression of Hsp90beta phosphorylation in tyrosine kinase-induced leukemias. 
  • Inhibition of isoprenylcysteine carboxylmethyltransferase augments BCR-ABL1 tyrosine kinase inhibition-induced apoptosis in chronic myeloid leukemia. 
  • Loss of beta-catenin impairs the renewal of normal and CML stem cells in vivo. 
  • Molecular monitoring to improve outcomes in patients with chronic myeloid leukemia in chronic phase: importance of achieving treatment-free remission. 
  • Mutant forms of growth factor-binding protein-2 reverse BCR-ABL-induced transformation. 
  • Oncogenic Abl and Src tyrosine kinases elicit the ubiquitin-dependent degradation of target proteins through a Ras-independent pathway. 
  • Physiologic hypoxia promotes maintenance of CML stem cells despite effective BCR-ABL1 inhibition. 
  • Polymerase chain reaction detection of the BCR-ABL fusion transcript after allogeneic marrow transplantation for chronic myeloid leukemia: results and implications in 346 patients. 
  • Preleukemic phase of chronic myelogenous leukemia: morphologic and immunohistochemical characterization of 7 cases. 
  • Protein tyrosine phosphatase 1B antagonizes signalling by oncoprotein tyrosine kinase p210 bcr-abl in vivo. 
  • Regulation of apoptosis in Xenopus egg extracts. 
  • Regulation of myeloid leukaemia by the cell-fate determinant Musashi. 
  • SH1 domain autophosphorylation of P210 BCR/ABL is required for transformation but not growth factor independence. 
  • Sequential Development of JAK2V617F Mutation and BCR-ABL1 Fusion in Individual Patients With Myeloproliferative Neoplasms. 
  • Stress and death: breaking up the c-Abl/14-3-3 complex in apoptosis. 
  • Structural and signaling requirements for BCR-ABL-mediated transformation and inhibition of apoptosis. 
  • Structure-Activity Relationship Studies of Mitogen Activated Protein Kinase Interacting Kinase (MNK) 1 and 2 and BCR-ABL1 Inhibitors Targeting Chronic Myeloid Leukemic Cells. 
  • Successful treatment using omacetaxine for a patient with CML and BCR-ABL1 [corrected] 35INS. 
  • TNK1 is a ubiquitin-binding and 14-3-3-regulated kinase that can be targeted to block tumor growth. 
  • The 5' non-coding region of the BCR/ABL oncogene augments its ability to stimulate the growth of immature lymphoid cells. 
  • The BCR-ABL tyrosine kinase inhibits apoptosis by activating a Ras-dependent signaling pathway. 
  • The BCR/ABL oncogene alters the chemotactic response to stromal-derived factor-1alpha. 
  • The BIM deletion polymorphism: A paradigm of a permissive interaction between germline and acquired TKI resistance factors in chronic myeloid leukemia. 
  • The Bcr-Abl tyrosine kinase activates mitogenic signaling pathways and stimulates G1-to-S phase transition in hematopoietic cells. 
  • The HDAC inhibitor SB939 overcomes resistance to BCR-ABL kinase Inhibitors conferred by the BIM deletion polymorphism in chronic myeloid leukemia. 
  • The coiled-coil domain and Tyr177 of bcr are required to induce a murine chronic myelogenous leukemia-like disease by bcr/abl. 
  • The role of protein phosphorylation in therapy resistance and disease progression in chronic myelogenous leukemia. 
  • Therapy Resistance and Disease Progression in CML: Mechanistic Links and Therapeutic Strategies. 
  • Transcriptional regulation of survivin by c-Myc in BCR/ABL-transformed cells: implications in anti-leukaemic strategy. 
  • Using Bcr-Abl to examine mechanisms by which abl kinase regulates morphogenesis in Drosophila. 
  • Utility of peripheral blood dual color, double fusion fluorescent in situ hybridization for BCR/ABL fusion to assess cytogenetic remission status in chronic myeloid leukemia. 
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  Keywords of People

  • Lagoo, Anand Shreeram, Professor of Pathology, Pathology