Essential requirement for PP2A inhibition by the oncogenic receptor c-KIT suggests PP2A reactivation as a strategy to treat c-KIT+ cancers
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The emerging role of FTY720 (Fingolimod) in cancer treatmentProtein Phosphatase 2A as a Therapeutic Target in Acute Myeloid LeukemiaRegulation of PP2A by Sphingolipid Metabolism and SignalingThe Basic Biology of PP2A in Hematologic Cells and MalignanciesPP2A: The Wolf in Sheep's Clothing?Disparate in vivo efficacy of FTY720 in xenograft models of Philadelphia positive and negative B-lineage acute lymphoblastic leukemiaPP2A inhibition from LB100 therapy enhances daunorubicin cytotoxicity in secondary acute myeloid leukemia via miR-181b-1 upregulation.From the Biology of PP2A to the PADs for Therapy of Hematologic MalignanciesTargeting the sphingosine-1-phosphate axis in cancer, inflammation and beyond.Essential role of protein phosphatase 2A in metaphase II arrest and activation of mouse eggs shown by okadaic acid, dominant negative protein phosphatase 2A, and FTY720.Antitumor effects of OSU-2S, a nonimmunosuppressive analogue of FTY720, in hepatocellular carcinoma.Therapeutic Re-Activation of Protein Phosphatase 2A in Acute Myeloid LeukemiaFingolimod (FTY720) stimulates Ca(2+)/calcineurin signaling in fission yeast.Association of PPP2CA polymorphisms with systemic lupus erythematosus susceptibility in multiple ethnic groups.Basal protein phosphatase 2A activity restrains cytokine expression: role for MAPKs and tristetraprolinSphingolipid signaling and hematopoietic malignancies: to the rheostat and beyond.Induction of brain tumor stem cell apoptosis by FTY720: a potential therapeutic agent for glioblastomaMouse model for probing tumor suppressor activity of protein phosphatase 2A in diverse signaling pathways.A systematic evaluation of the safety and toxicity of fingolimod for its potential use in the treatment of acute myeloid leukaemia.Targeting sphingosine-1-phosphate in hematologic malignanciesSuppression of PP2A is critical for protection of melanoma cells upon endoplasmic reticulum stress.Sphingosine analogue drug FTY720 targets I2PP2A/SET and mediates lung tumour suppression via activation of PP2A-RIPK1-dependent necroptosis.Upregulation of PP2Ac predicts poor prognosis and contributes to aggressiveness in hepatocellular carcinomaSphingosine-1-phosphate, FTY720, and sphingosine-1-phosphate receptors in the pathobiology of acute lung injury.PP2A-activating drugs selectively eradicate TKI-resistant chronic myeloid leukemic stem cells.The phosphorylated form of FTY720 activates PP2A, represses inflammation and is devoid of S1P agonism in A549 lung epithelial cells.Novel B55α-PP2A mutations in AML promote AKT T308 phosphorylation and sensitivity to AKT inhibitor-induced growth arrest.Antagonism of SET using OP449 enhances the efficacy of tyrosine kinase inhibitors and overcomes drug resistance in myeloid leukemia.Combined targeting of SET and tyrosine kinases provides an effective therapeutic approach in human T-cell acute lymphoblastic leukemia.Therapeutic targeting of c-KIT in cancer.Oncogenic properties of sphingosine kinases in haematological malignancies.Protein phosphatase 2A: a target for anticancer therapy.Relevance of leukemic stem cells in acute myeloid leukemia: heterogeneity and influence on disease monitoring, prognosis and treatment design.The antineoplastic properties of FTY720: evidence for the repurposing of fingolimod.All roads lead to PP2A: exploiting the therapeutic potential of this phosphatase.Reprogramming the oncogenic response: SET protein as a potential therapeutic target in cancer.Involvement of vacuolar H(+)-ATPase in killing of human melanoma cells by the sphingosine kinase analogue FTY720.Multiple variants in 5q31.1 are associated with systemic lupus erythematosus susceptibility and subphenotypes in the Han Chinese population.FTY720 induces apoptosis in B16F10-NEX2 murine melanoma cells, limits metastatic development in vivo, and modulates the immune system.FTY720 induces apoptosis of chronic myelogenous leukemia cells via dual activation of BIM and BID and overcomes various types of resistance to tyrosine kinase inhibitors.
P2860
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P2860
Essential requirement for PP2A inhibition by the oncogenic receptor c-KIT suggests PP2A reactivation as a strategy to treat c-KIT+ cancers
description
2010 nî lūn-bûn
@nan
2010 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
Essential requirement for PP2A ...... rategy to treat c-KIT+ cancers
@ast
Essential requirement for PP2A ...... rategy to treat c-KIT+ cancers
@en
Essential requirement for PP2A ...... rategy to treat c-KIT+ cancers
@nl
type
label
Essential requirement for PP2A ...... rategy to treat c-KIT+ cancers
@ast
Essential requirement for PP2A ...... rategy to treat c-KIT+ cancers
@en
Essential requirement for PP2A ...... rategy to treat c-KIT+ cancers
@nl
prefLabel
Essential requirement for PP2A ...... rategy to treat c-KIT+ cancers
@ast
Essential requirement for PP2A ...... rategy to treat c-KIT+ cancers
@en
Essential requirement for PP2A ...... rategy to treat c-KIT+ cancers
@nl
P2093
P2860
P1433
P1476
Essential requirement for PP2A ...... rategy to treat c-KIT+ cancers
@en
P2093
Alistair T R Sim
Amanda M Smith
Daniel Thomas
Danilo Perrotti
Fiona McDougall
Helen Carpenter
Jason A Powell
Kathryn G Roberts
Leonie K Ashman
Mark A Guthridge
P2860
P304
P356
10.1158/0008-5472.CAN-09-2544
P407
P577
2010-06-15T00:00:00Z