Imatinib mesylate (STI571) inhibits growth of primitive malignant progenitors in chronic myelogenous leukemia through reversal of abnormally increased proliferation.
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Enhanced phosphorylation of Nbs1, a member of DNA repair/checkpoint complex Mre11-RAD50-Nbs1, can be targeted to increase the efficacy of imatinib mesylate against BCR/ABL-positive leukemia cellsA stochastic model of oncogene expression and the relevance of this model to cancer therapy.Regulation of mitochondrial functions by protein phosphorylation and dephosphorylationKinase-independent mechanisms of resistance of leukemia stem cells to tyrosine kinase inhibitorsImatinib treatment induces CD5+ B lymphocytes and IgM natural antibodies with anti-leukemic reactivity in patients with chronic myelogenous leukemiaImatinib and nilotinib inhibit hematopoietic progenitor cell growth, but do not prevent adhesion, migration and engraftment of human cord blood CD34+ cellsEmerging Roles of SIRT1 in Cancer Drug ResistanceCancer stem cell-directed therapies: recent data from the laboratory and clinic.Differentiation status of primary chronic myeloid leukemia cells affects sensitivity to BCR-ABL1 inhibitors.Effective targeting of quiescent chronic myelogenous leukemia stem cells by histone deacetylase inhibitors in combination with imatinib mesylate.Mechanisms of primary and secondary resistance to imatinib in chronic myeloid leukemia.The elusive chronic myeloid leukemia stem cell: does it matter and how do we eliminate it?The paradox of response and survival in cancer therapeuticsInhibition of Grb2 expression demonstrates an important role in BCR-ABL-mediated MAPK activation and transformation of primary human hematopoietic cellsImatinib plus Granulocyte Colony-Stimulating Factor in Chronic Myeloid Leukemia Patients Who Have Achieved Partial or Complete Cytogenetic Response while on Imatinib.IL1RAP as a surface marker for leukemia stem cells is related to clinical phase of chronic myeloid leukemia patients.Inhibition of the Bcr-Abl tyrosine kinase as a therapeutic strategy for CML.BCR/ABL: from molecular mechanisms of leukemia induction to treatment of chronic myelogenous leukemia.Immune modulation of minimal residual disease in early chronic phase chronic myelogenous leukemia: a randomized trial of frontline high-dose imatinib mesylate with or without pegylated interferon alpha-2b and granulocyte-macrophage colony-stimulatinTargeting multiple kinase pathways in leukemic progenitors and stem cells is essential for improved treatment of Ph+ leukemia in mice.Right on target: eradicating leukemic stem cells.Imatinib mesylate in the treatment of chronic myeloid leukaemia.Chronic myelogenous leukemia as a paradigm of early cancer and possible curative strategies.Stem cell and kinase activity-independent pathway in resistance of leukaemia to BCR-ABL kinase inhibitorsPersistence of leukemia stem cells in chronic myelogenous leukemia patients in prolonged remission with imatinib treatmentLeukemia stem cells: the root of chronic myeloid leukemiaRetroviral insertional mutagenesis identifies RUNX genes involved in chronic myeloid leukemia disease persistence under imatinib treatmentConsiderations for targeting malignant stem cells in leukemia.Cancer stem cells: are we missing the target?Effect of imatinib mesylate on chronic myelogenous leukemia hematopoietic progenitor cells.Cancer Stem Cells: From Bench to BedsideActivation of stress response gene SIRT1 by BCR-ABL promotes leukemogenesis.Role of BCR/ABL gene-expression levels in determining the phenotype and imatinib sensitivity of transformed human hematopoietic cellsPD166326, a novel tyrosine kinase inhibitor, has greater antileukemic activity than imatinib mesylate in a murine model of chronic myeloid leukemia.Cancer stem cells: impact, heterogeneity, and uncertaintyPotentiation of Nilotinib-mediated cell death in the context of the bone marrow microenvironment requires a promiscuous JAK inhibitor in CML.Altered microenvironmental regulation of leukemic and normal stem cells in chronic myelogenous leukemiaInterferon alpha and T-cell responses in chronic myeloid leukemia.Imatinib mesylate can help to direct natural immunity toward an anti-leukemic reactivity by acting on the bone marrow microenvironment.Chronic myelogenous leukemia stem and progenitor cells demonstrate chromosomal instability related to repeated breakage-fusion-bridge cycles mediated by increased nonhomologous end joining
P2860
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P2860
Imatinib mesylate (STI571) inhibits growth of primitive malignant progenitors in chronic myelogenous leukemia through reversal of abnormally increased proliferation.
description
2002 nî lūn-bûn
@nan
2002年の論文
@ja
2002年学术文章
@wuu
2002年学术文章
@zh
2002年学术文章
@zh-cn
2002年学术文章
@zh-hans
2002年学术文章
@zh-my
2002年学术文章
@zh-sg
2002年學術文章
@yue
2002年學術文章
@zh-hant
name
Imatinib mesylate (STI571) inh ...... mally increased proliferation.
@en
type
label
Imatinib mesylate (STI571) inh ...... mally increased proliferation.
@en
prefLabel
Imatinib mesylate (STI571) inh ...... mally increased proliferation.
@en
P2093
P1433
P1476
Imatinib mesylate (STI571) inh ...... mally increased proliferation.
@en
P2093
Charles L Sawyers
Feiyu Zhang
Marilyn L Slovak
Melissa S Holtz
Ravi Bhatia
Stephen J Forman
P304
P356
10.1182/BLOOD.V99.10.3792
P407
P577
2002-05-01T00:00:00Z