PP2A-activating drugs selectively eradicate TKI-resistant chronic myeloid leukemic stem cells. - Wikidata - wikimedia - TriplyDB

PP2A-activating drugs selectively eradicate TKI-resistant chronic myeloid leukemic stem cells.

PP2A-activating drugs selectively eradicate TKI-resistant chronic myeloid leukemic stem cells.

http://www.wikidata.org/entity/Q37200863

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The broken "Off" switch in cancer signaling: PP2A as a regulator of tumorigenesis, drug resistance, and immune surveillance Chronic myeloid leukemia: reminiscences and dreams The emerging role of FTY720 (Fingolimod) in cancer treatment The non-genomic loss of function of tumor suppressors: an essential role in the pathogenesis of chronic myeloid leukemia chronic phase Protein Phosphatase 2A as a Therapeutic Target in Acute Myeloid Leukemia Kinase-independent mechanisms of resistance of leukemia stem cells to tyrosine kinase inhibitors Inhibition of STAT5: a therapeutic option in BCR-ABL1-driven leukemia EMT, CTCs and CSCs in tumor relapse and drug-resistance Dual targeting of p53 and c-MYC selectively eliminates leukaemic stem cells FTY720 inhibits mesothelioma growth in vitro and in a syngeneic mouse model The role of SET/I2PP2A in canine mammary tumors.From the Biology of PP2A to the PADs for Therapy of Hematologic Malignancies JAK2/STAT5 inhibition by nilotinib with ruxolitinib contributes to the elimination of CML CD34+ cells in vitro and in vivo.Therapeutic Re-Activation of Protein Phosphatase 2A in Acute Myeloid Leukemia BCR-ABL1-associated reduction of beta catenin antagonist Chibby1 in chronic myeloid leukemia Combined STAT3 and BCR-ABL1 inhibition induces synthetic lethality in therapy-resistant chronic myeloid leukemia Leukemia stem cells: the root of chronic myeloid leukemia Discovery of a small molecule targeting SET-PP2A interaction to overcome BCR-ABLT315I mutation of chronic myeloid leukemia.A novel mouse model identifies cooperating mutations and therapeutic targets critical for chronic myeloid leukemia progression.Targeting leukemia stem cells in vivo with antagomiR-126 nanoparticles in acute myeloid leukemia β-Catenin is required for intrinsic but not extrinsic BCR-ABL1 kinase-independent resistance to tyrosine kinase inhibitors in chronic myeloid leukemia.PPARγ ligands increase antileukemic activity of second- and third-generation tyrosine kinase inhibitors in chronic myeloid leukemia cells Imatinib and Nilotinib increase glioblastoma cell invasion via Abl-independent stimulation of p130Cas and FAK signalling.PLA2G16 promotes osteosarcoma metastasis and drug resistance via the MAPK pathway.Antagonistic activities of the immunomodulator and PP2A-activating drug FTY720 (Fingolimod, Gilenya) in Jak2-driven hematologic malignancies Targeting methyltransferase PRMT5 eliminates leukemia stem cells in chronic myelogenous leukemia.Cooperation of imipramine blue and tyrosine kinase blockade demonstrates activity against chronic myeloid leukemia.Stable SET knockdown in head and neck squamous cell carcinoma promotes cell invasion and the mesenchymal-like phenotype in vitro, as well as necrosis, cisplatin sensitivity and lymph node metastasis in xenograft tumor models.CML cells actively evade host immune surveillance through cytokine-mediated downregulation of MHC-II expression.Novel B55α-PP2A mutations in AML promote AKT T308 phosphorylation and sensitivity to AKT inhibitor-induced growth arrest.Phosphorylation of a constrained azacyclic FTY720 analog enhances anti-leukemic activity without inducing S1P receptor activation.Preclinical approaches in chronic myeloid leukemia: from cells to systems Sex chromosome loss and the pseudoautosomal region genes in hematological malignancies.The novel anticancer agent JNJ-26854165 is active in chronic myeloid leukemic cells with unmutated BCR/ABL and T315I mutant BCR/ABL through promoting proteosomal degradation of BCR/ABL proteins.Antagonism of SET using OP449 enhances the efficacy of tyrosine kinase inhibitors and overcomes drug resistance in myeloid leukemia.Different BCR/Abl protein suppression patterns as a converging trait of chronic myeloid leukemia cell adaptation to energy restriction.Kinase-inhibitor-insensitive cancer stem cells in chronic myeloid leukemia.Genetic events other than BCR-ABL1.Maintaining low BCR-ABL signaling output to restrict CML progression and enable persistence Concise review: cancer cells escape from oncogene addiction: understanding the mechanisms behind treatment failure for more effective targeting.

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PP2A-activating drugs selectively eradicate TKI-resistant chronic myeloid leukemic stem cells.

http://www.wikidata.org/entity/Q37200863

description

article científic

@ca

article scientifique

@fr

articolo scientifico

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artigo científico

@pt

bilimsel makale

@tr

scientific article published on 03 September 2013

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

PP2A-activating drugs selectiv ...... c myeloid leukemic stem cells.

@en

PP2A-activating drugs selectiv ...... c myeloid leukemic stem cells.

@nl

type

label

PP2A-activating drugs selectiv ...... c myeloid leukemic stem cells.

@en

PP2A-activating drugs selectiv ...... c myeloid leukemic stem cells.

@nl

prefLabel

PP2A-activating drugs selectiv ...... c myeloid leukemic stem cells.

@en

PP2A-activating drugs selectiv ...... c myeloid leukemic stem cells.

@nl

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Journal of Clinical Investigation

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PP2A-activating drugs selectiv ...... c myeloid leukemic stem cells.

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Adrienne M Dorrance

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Alistair Reid

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Besim Ogretmen

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Bin Zhang

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Carolyn A Paisie

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Chaode Sun

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Ching-Shih Chen

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Christopher J Walker

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Claudia S Huettner

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Danilo Perrotti

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P2860

Bcr-Abl stabilizes beta-catenin in chronic myeloid leukemia through its tyrosine phosphorylation

Protein phosphatase 2A and rapamycin regulate the nuclear localization and activity of the transcription factor GLI3

Wilms tumor suppressor WTX negatively regulates WNT/beta-catenin signaling

Involvement of protein phosphatase 2A in the interleukin-3-stimulated Jak2-Stat5 signaling pathway

A role for Wnt signalling in self-renewal of haematopoietic stem cells

Regulation of beta-catenin signaling by the B56 subunit of protein phosphatase 2A

Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CML

The Rac GTPase effector p21-activated kinase is essential for hematopoietic stem/progenitor cell migration and engraftment.

Isolation of a highly quiescent subpopulation of primitive leukemic cells in chronic myeloid leukemia.

AML xenograft efficiency is significantly improved in NOD/SCID-IL2RG mice constitutively expressing human SCF, GM-CSF and IL-3.

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4144-4157

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scholarly article

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10.1172/JCI68951

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10

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123

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Stefano Volinia

Steffen Koschmieder

Tessa L Holyoake

Jorge Eduardo Cortes

Carlo Maria Croce

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2013-09-03T00:00:00Z

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23999433

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3784537

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