Proteasome inhibition causes regression of leukemia and abrogates BCR-ABL-induced evasion of apoptosis in part through regulation of forkhead tumor suppressors.
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Recent advancements of bortezomib in acute lymphocytic leukemia treatmentHaematological complete remission by ponatinib and bortezomib in a patient with relapsed, Ph⁺ pre-B acute lymphoblastic leukaemia.Hypoxia selects bortezomib-resistant stem cells of chronic myeloid leukemia.Resveratrol protects leukemic cells against cytotoxicity induced by proteasome inhibitors via induction of FOXO1 and p27Kip1The Ph-positive and Ph-negative myeloproliferative neoplasms: some topical pre-clinical and clinical issues.Bortezomib treatment causes remission in a Ph+ALL patient and reveals FoxO as a theranostic marker.Combination of bortezomib and mitotic inhibitors down-modulate Bcr-Abl and efficiently eliminates tyrosine-kinase inhibitor sensitive and resistant Bcr-Abl-positive leukemic cells.Proteasome inhibitor MG-132 enhances histone deacetylase inhibitor SAHA-induced cell death of chronic myeloid leukemia cells by an ROS-mediated mechanism and downregulation of the Bcr-Abl fusion protein.PLK1 is a binding partner and a negative regulator of FOXO3 tumor suppressorCancer cell signaling pathways targeted by spice-derived nutraceuticals.Emerging therapeutic strategies for targeting chronic myeloid leukemia stem cellsLiposomal bortezomib is active against chronic myeloid leukemia by disrupting the Sp1-BCR/ABL axis.Growth arrest specific 2 is up-regulated in chronic myeloid leukemia cells and required for their growth.Gambogic acid induces apoptosis in imatinib-resistant chronic myeloid leukemia cells via inducing proteasome inhibition and caspase-dependent Bcr-Abl downregulation.Why doesn't imatinib cure chronic myeloid leukemia?IKK-dependent activation of NF-κB contributes to myeloid and lymphoid leukemogenesis by BCR-ABL1.Genetic events other than BCR-ABL1.Novel approaches to pediatric leukemia treatment.The Interface between BCR-ABL-Dependent and -Independent Resistance Signaling Pathways in Chronic Myeloid Leukemia.Bortezomib has little ex vivo activity in chronic myeloid leukemia: individual tumor response testing comparative study in acute and chronic myeloid leukemia.Analysis of altered proteins related to blast crisis in chronic myeloid leukemia by proteomic study.Anti-leukemic activity of bortezomib and carfilzomib on B-cell precursor ALL cell lines.Proteasome inhibitor MG132 induces thyroid cancer cell apoptosis by modulating the activity of transcription factor FOXO3a.DNA hypermethylation promotes the low expression of pro-apoptotic BCL2L11 associated with BCR-ABL1 fusion gene of chronic myeloid leukaemia.
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P2860
Proteasome inhibition causes regression of leukemia and abrogates BCR-ABL-induced evasion of apoptosis in part through regulation of forkhead tumor suppressors.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 04 August 2009
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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
Proteasome inhibition causes r ...... of forkhead tumor suppressors.
@en
Proteasome inhibition causes r ...... of forkhead tumor suppressors.
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type
label
Proteasome inhibition causes r ...... of forkhead tumor suppressors.
@en
Proteasome inhibition causes r ...... of forkhead tumor suppressors.
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prefLabel
Proteasome inhibition causes r ...... of forkhead tumor suppressors.
@en
Proteasome inhibition causes r ...... of forkhead tumor suppressors.
@nl
P2093
P2860
P1433
P1476
Proteasome inhibition causes r ...... of forkhead tumor suppressors.
@en
P2093
Alexandra Grassian
Armelle Melet
Catherine Wu
Heather Yeckes-Rodin
Jeffery L Kutok
Kenneth Miller
M Rajan Dewar
Roya Khosravi-Far
Ruibao Ren
P2860
P304
P356
10.1158/0008-5472.CAN-09-0605
P407
P577
2009-08-04T00:00:00Z