Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity - Wikidata - wikimedia - TriplyDB

Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity

Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity

http://www.wikidata.org/entity/Q41356541

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The Philadelphia chromosome in leukemogenesis The concept of treatment-free remission in chronic myeloid leukemia Chronic myeloid leukemia: reminiscences and dreams Management of Chronic Myeloid Leukemia Patients Resistant to Tyrosine Kinase Inhibitors Treatment Protein Kinase CK2: A Targetable BCR-ABL Partner in Philadelphia Positive Leukemias Acute Myeloid Leukemia and Other Types of Disease Progression in Myeloproliferative Neoplasms Molecular mechanisms for survival regulation of chronic myeloid leukemia stem cells Kinase-independent mechanisms of resistance of leukemia stem cells to tyrosine kinase inhibitors Concise review: Leukemia stem cells in personalized medicine Inhibition of STAT5: a therapeutic option in BCR-ABL1-driven leukemia Signal transduction in the chronic leukemias: implications for targeted therapies Resistance to tyrosine kinase inhibition therapy for chronic myelogenous leukemia: a clinical perspective and emerging treatment options Low doses of imatinib induce myelopoiesis and enhance host anti-microbial immunity One more stem cell niche: how the sensitivity of chronic myeloid leukemia cells to imatinib mesylate is modulated within a "hypoxic" environment.Cancer stem cells in basic science and in translational oncology: can we translate into clinical application?Dual targeting of p53 and c-MYC selectively eliminates leukaemic stem cells Personalized synthetic lethality induced by targeting RAD52 in leukemias identified by gene mutation and expression profile.Aclacinomycin A sensitizes K562 chronic myeloid leukemia cells to imatinib through p38MAPK-mediated erythroid differentiation Knockout Serum Replacement Promotes Cell Survival by Preventing BIM from Inducing Mitochondrial Cytochrome C Release Tumour heterogeneity and cancer cell plasticity A novel AHI-1-BCR-ABL-DNM2 complex regulates leukemic properties of primitive CML cells through enhanced cellular endocytosis and ROS-mediated autophagy.LASP1 is a novel BCR-ABL substrate and a phosphorylation-dependent binding partner of CRKL in chronic myeloid leukemia Abl kinase constructs expressed in bacteria: facilitation of structural and functional studies including segmental labeling by expressed protein ligation Low expression of Abelson interactor-1 is linked to acquired drug resistance in Bcr-Abl-induced leukemia.Pre-leukemic evolution of hematopoietic stem cells: the importance of early mutations in leukemogenesis Dasatinib: a review of its use in the treatment of chronic myeloid leukaemia and Philadelphia chromosome-positive acute lymphoblastic leukaemia.Combination of the ABL kinase inhibitor imatinib with the Janus kinase 2 inhibitor TG101348 for targeting residual BCR-ABL-positive cells.Growth of tyrosine kinase inhibitor-resistant Philadelphia-positive acute lymphoblastic leukemia: Role of bone marrow stromal cells Hypoxia-inducible microRNA-210 regulates the DIMT1-IRF4 oncogenic axis in multiple myeloma Differentiation status of primary chronic myeloid leukemia cells affects sensitivity to BCR-ABL1 inhibitors.Single-cell molecular analysis defines therapy response and immunophenotype of stem cell subpopulations in CML.Advances in the treatment of chronic myeloid leukemia.Inhibition of calcineurin combined with dasatinib has direct and indirect anti-leukemia effects against BCR-ABL1(+) leukemia.SL-401 and SL-501, targeted therapeutics directed at the interleukin-3 receptor, inhibit the growth of leukaemic cells and stem cells in advanced phase chronic myeloid leukaemia.JAK2/STAT5 inhibition by nilotinib with ruxolitinib contributes to the elimination of CML CD34+ cells in vitro and in vivo.A therapeutically targetable mechanism of BCR-ABL-independent imatinib resistance in chronic myeloid leukemia.An update on dual Src/Abl inhibitors.Tyrosine kinase inhibition: a therapeutic target for the management of chronic-phase chronic myeloid leukemia.Using functional genomics to overcome therapeutic resistance in hematological malignancies.Cancer stem cell plasticity and tumor hierarchy.

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P2860

Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity

http://www.wikidata.org/entity/Q41356541

description

2010 nî lūn-bûn

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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2010年论文

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2010年论文

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name

Human chronic myeloid leukemia ...... inhibition of BCR-ABL activity

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type

label

Human chronic myeloid leukemia ...... inhibition of BCR-ABL activity

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prefLabel

Human chronic myeloid leukemia ...... inhibition of BCR-ABL activity

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P1433

Journal of Clinical Investigation

P1476

Human chronic myeloid leukemia ...... inhibition of BCR-ABL activity

@en

P2093

Amie S Corbin

http://www.w3.org/2001/XMLSchema#string

Anupriya Agarwal

http://www.w3.org/2001/XMLSchema#string

Marc Loriaux

http://www.w3.org/2001/XMLSchema#string

Michael W Deininger

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P2860

AC133, a novel marker for human hematopoietic stem and progenitor cells

The Ki-67 protein: from the known and the unknown

Expression and activity of P-glycoprotein, a multidrug efflux pump, in human hematopoietic stem cells

Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia

The ABC transporter Bcrp1/ABCG2 is expressed in a wide variety of stem cells and is a molecular determinant of the side-population phenotype

Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification

Overriding imatinib resistance with a novel ABL kinase inhibitor

Phase III, randomized, open-label study of daily imatinib mesylate 400 mg versus 800 mg in patients with newly diagnosed, previously untreated chronic myeloid leukemia in chronic phase using molecular end points: tyrosine kinase inhibitor optimizati

Isolation of a highly quiescent subpopulation of primitive leukemic cells in chronic myeloid leukemia.

Imatinib mesylate (STI571) is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump.

P304

396-409

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scholarly article

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10.1172/JCI35721

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1

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P478

121

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Brian J. Druker

Jorge Eduardo Cortes

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2010-12-13T00:00:00Z

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P698

21157039

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P921

chronic myeloid leukemia

P932

3007128

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