Enhanced BCR-ABL kinase inhibition does not result in increased inhibition of downstream signaling pathways or increased growth suppression in CML progenitors.
about
Kinase-independent mechanisms of resistance of leukemia stem cells to tyrosine kinase inhibitorsOne more stem cell niche: how the sensitivity of chronic myeloid leukemia cells to imatinib mesylate is modulated within a "hypoxic" environment.Low expression of Abelson interactor-1 is linked to acquired drug resistance in Bcr-Abl-induced leukemia.Selective targeting of neuroblastoma tumour-initiating cells by compounds identified in stem cell-based small molecule screensERK2, but not ERK1, mediates acquired and "de novo" resistance to imatinib mesylate: implication for CML therapyImpact of additional chromosomal aberrations and BCR-ABL kinase domain mutations on the response to nilotinib in Philadelphia chromosome-positive chronic myeloid leukemia.Effective targeting of quiescent chronic myelogenous leukemia stem cells by histone deacetylase inhibitors in combination with imatinib mesylate.CBP/catenin antagonist safely eliminates drug-resistant leukemia-initiating cells.Inhibition of CXCR4 in CML cells disrupts their interaction with the bone marrow microenvironment and sensitizes them to nilotinibImproved outcome following allogeneic stem cell transplantation in chronic myeloid leukemia is associated with higher expression of BMI-1 and immune responses to BMI-1 protein.Persistence of leukemia stem cells in chronic myelogenous leukemia patients in prolonged remission with imatinib treatmentChronic myeloid leukemia stem cells are not dependent on Bcr-Abl kinase activity for their survivalCaMKII γ, a critical regulator of CML stem/progenitor cells, is a target of the natural product berbaminePotentiation of Nilotinib-mediated cell death in the context of the bone marrow microenvironment requires a promiscuous JAK inhibitor in CML.Alternative approaches to eradicating the malignant clone in chronic myeloid leukemia: tyrosine-kinase inhibitor combinations and beyond.A novel mouse model identifies cooperating mutations and therapeutic targets critical for chronic myeloid leukemia progression.The metabolically-modulated stem cell niche: a dynamic scenario regulating cancer cell phenotype and resistance to therapy.Tetrandrine citrate eliminates imatinib-resistant chronic myeloid leukemia cells in vitro and in vivo by inhibiting Bcr-Abl/β-catenin axis.Activation of tyrosine kinase c-Abl contributes to α-synuclein-induced neurodegenerationTargeting autophagy potentiates tyrosine kinase inhibitor-induced cell death in Philadelphia chromosome-positive cells, including primary CML stem cells.Roles of SIRT1 in leukemogenesis.Molecular biology of bcr-abl1-positive chronic myeloid leukemia.Effects of dasatinib on SRC kinase activity and downstream intracellular signaling in primitive chronic myelogenous leukemia hematopoietic cellsRefining targeted therapies in chronic myeloid leukemia: development and application of nilotinib, a step beyond imatinib.Inhibition of autophagy: a new strategy to enhance sensitivity of chronic myeloid leukemia stem cells to tyrosine kinase inhibitors.Mechanisms of resistance to BCR-ABL kinase inhibitors.Kinase-inhibitor-insensitive cancer stem cells in chronic myeloid leukemia.Concise review: cancer cells escape from oncogene addiction: understanding the mechanisms behind treatment failure for more effective targeting.Co-operating STAT5 and AKT signaling pathways in chronic myeloid leukemia and mastocytosis: possible new targets of therapy.Knowledge-guided gene prioritization reveals new insights into the mechanisms of chemoresistance.Indole-3-carbinol induces apoptosis of chronic myelogenous leukemia cells through suppression of STAT5 and Akt signaling pathways.Salarin C inhibits the maintenance of chronic myeloid leukemia progenitor cells.Induction of p53 suppresses chronic myeloid leukemia.Enhanced ABL-inhibitor-induced MAPK-activation in T315I-BCR-ABL-expressing cells: a potential mechanism of altered leukemogenicity.Knockdown of SOD1 sensitizes the CD34+ CML cells to imatinib therapy.Combination of simvastatin and imatinib sensitizes the CD34+ cells in K562 to cell death.Nilotinib for the treatment of chronic myeloid leukemia.Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activityBCR-ABL kinase is dead; long live the CML stem cell.Antitumoral effects of cyclin-dependent kinases inhibitors CR8 and MR4 on chronic myeloid leukemia cell lines
P2860
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P2860
Enhanced BCR-ABL kinase inhibition does not result in increased inhibition of downstream signaling pathways or increased growth suppression in CML progenitors.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
2008年學術文章
@zh
2008年學術文章
@zh-hant
name
Enhanced BCR-ABL kinase inhibi ...... uppression in CML progenitors.
@en
Enhanced BCR-ABL kinase inhibi ...... uppression in CML progenitors.
@nl
type
label
Enhanced BCR-ABL kinase inhibi ...... uppression in CML progenitors.
@en
Enhanced BCR-ABL kinase inhibi ...... uppression in CML progenitors.
@nl
prefLabel
Enhanced BCR-ABL kinase inhibi ...... uppression in CML progenitors.
@en
Enhanced BCR-ABL kinase inhibi ...... uppression in CML progenitors.
@nl
P2093
P2860
P356
P1433
P1476
Enhanced BCR-ABL kinase inhibi ...... uppression in CML progenitors.
@en
P2093
S J Forman
T L Holyoake
P2860
P2888
P304
P356
10.1038/SJ.LEU.2405086
P577
2008-02-14T00:00:00Z