NF-kappaB as a therapeutic target in chronic lymphocytic leukemia.
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The splicing modulator sudemycin induces a specific antitumor response and cooperates with ibrutinib in chronic lymphocytic leukemia.Post-formulation peptide drug loading of nanostructures for metered control of NF-κB signalingSTAT-3 activates NF-kappaB in chronic lymphocytic leukemia cells.NF-κB addiction and its role in cancer: 'one size does not fit all'.Constitutive activation of NF-κB signaling by NOTCH1 mutations in chronic lymphocytic leukemia.The novel NF-κB inhibitor IMD-0354 induces apoptosis in chronic lymphocytic leukemiaCpG oligodeoxynucleotide CpG-685 upregulates functional interleukin-21 receptor on chronic lymphocytic leukemia B cells through an NF-κB mediated pathwayBone marrow stroma-induced resistance of chronic lymphocytic leukemia cells to arsenic trioxide involves Mcl-1 upregulation and is overcome by inhibiting the PI3Kδ or PKCβ signaling pathwaysHigh expression of ID family and IGJ genes signature as predictor of low induction treatment response and worst survival in adult Hispanic patients with B-acute lymphoblastic leukemia.TAM receptors in leukemia: expression, signaling, and therapeutic implications.The Bruton tyrosine kinase (BTK) inhibitor PCI-32765 synergistically increases proteasome inhibitor activity in diffuse large-B cell lymphoma (DLBCL) and mantle cell lymphoma (MCL) cells sensitive or resistant to bortezomib.Hsp90 inhibition increases SOCS3 transcript and regulates migration and cell death in chronic lymphocytic leukemia.Global DNA methylation profiling reveals new insights into epigenetically deregulated protein coding and long noncoding RNAs in CLL.New drug discovery approaches targeting recurrent mutations in chronic lymphocytic leukemia.CD79B limits response of diffuse large B cell lymphoma to ibrutinib.Aberrant splicing of the tumor suppressor CYLD promotes the development of chronic lymphocytic leukemia via sustained NF-κB signaling.Vitamin K3 and vitamin C alone or in combination induced apoptosis in leukemia cells by a similar oxidative stress signalling mechanism.RelB, together with RelA, sustains cell survival and confers proteasome inhibitor sensitivity of chronic lymphocytic leukemia cells from bone marrow.Activation of the B-cell receptor successively activates NF-κB and STAT3 in chronic lymphocytic leukemia cells.Expression of ZAP70 in chronic lymphocytic leukaemia activates NF-κB signalling.NOTCH1 mutations identify a genetic subgroup of chronic lymphocytic leukemia patients with high risk of transformation and poor outcome.cAMP/PKA Signaling Pathway Induces Apoptosis by Inhibited NF-κB in Aluminum Chloride-Treated Lymphocytes In Vitro.STAT3 is constitutively acetylated on lysine 685 residues in chronic lymphocytic leukemia cells
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NF-kappaB as a therapeutic target in chronic lymphocytic leukemia.
description
article científic
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article scientifique
@fr
articolo scientifico
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artigo científico
@pt
bilimsel makale
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scientific article published on March 2010
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
NF-kappaB as a therapeutic target in chronic lymphocytic leukemia.
@en
NF-kappaB as a therapeutic target in chronic lymphocytic leukemia.
@nl
type
label
NF-kappaB as a therapeutic target in chronic lymphocytic leukemia.
@en
NF-kappaB as a therapeutic target in chronic lymphocytic leukemia.
@nl
prefLabel
NF-kappaB as a therapeutic target in chronic lymphocytic leukemia.
@en
NF-kappaB as a therapeutic target in chronic lymphocytic leukemia.
@nl
P2860
P921
P1476
NF-kappaB as a therapeutic target in chronic lymphocytic leukemia.
@en
P2093
Monica Lopez-Guerra
P2860
P304
P356
10.1517/14728221003598930
P407
P577
2010-03-01T00:00:00Z