Tasquinimod Is an Allosteric Modulator of HDAC4 survival signaling within the compromised cancer microenvironment - Test2 - elhamkhani - TriplyDB

Tasquinimod Is an Allosteric Modulator of HDAC4 survival signaling within the compromised cancer microenvironment

Tasquinimod Is an Allosteric Modulator of HDAC4 survival signaling within the compromised cancer microenvironment

http://www.wikidata.org/entity/Q24618224

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Quantitative profiling of chromatome dynamics reveals a novel role for HP1BP3 in hypoxia-induced oncogenesis Chemical genetics approaches for selective intervention in epigenetics A Perspective of Immunotherapy for Prostate Cancer Tasquinimod in the treatment of castrate-resistant prostate cancer - current status and future prospects Evolving landscape and novel treatments in metastatic castrate-resistant prostate cancer Novel non-AR therapeutic targets in castrate resistant prostate cancer Bone-targeting agents in prostate cancer.HDAC4: mechanism of regulation and biological functions Long-term survival and biomarker correlates of tasquinimod efficacy in a multicenter randomized study of men with minimally symptomatic metastatic castration-resistant prostate cancer Restoration of impaired endothelial myocyte enhancer factor 2 function rescues pulmonary arterial hypertension.Tasquinimod modulates suppressive myeloid cells and enhances cancer immunotherapies in murine models HDAC4, a prognostic and chromosomal instability marker, refines the predictive value of MGMT promoter methylation.The anti-tumor effect of the quinoline-3-carboxamide tasquinimod: blockade of recruitment of CD11b(+) Ly6C(hi) cells to tumor tissue reduces tumor growth Tasquinimod triggers an early change in the polarization of tumor associated macrophages in the tumor microenvironment.Assessing angiogenic responses induced by primary human prostate stromal cells in a three-dimensional fibrin matrix assay.Methylseleninic acid elevates REDD1 and inhibits prostate cancer cell growth despite AKT activation and mTOR dysregulation in hypoxia.A review of tasquinimod in the treatment of advanced prostate cancer.Mechanisms of action of tasquinimod on the tumour microenvironment.Castration-resistant prostate cancer: latest evidence and therapeutic implications.Selective class IIa HDAC inhibitors: myth or reality.Prostate Cancer Immunotherapy with Sipuleucel-T: Current Standards and Future Directions.Clinical development of immunotherapy for prostate cancer.Tasquinimod inhibits prostate cancer growth in bone through alterations in the bone microenvironment.Progress in the mechanism and drug development of castration-resistant prostate cancer.Anti-cancer potency of tasquinimod is enhanced via albumin-binding facilitating increased uptake in the tumor microenvironment.Tasquinimod: a novel drug in advanced prostate cancer.Phase Ib Trial of Cabazitaxel and Tasquinimod in Men With Heavily Pretreated Metastatic Castration Resistant Prostate Cancer (mCRPC): The CATCH Trial.Beyond the Immune Suppression: The Immunotherapy in Prostate Cancer.Epigenetic regulation of interleukin-8 expression by class I HDAC and CBP in ovarian cancer cells.DNA vaccines for prostate cancer.

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Tasquinimod Is an Allosteric Modulator of HDAC4 survival signaling within the compromised cancer microenvironment

http://www.wikidata.org/entity/Q24618224

description

2013 nî lūn-bûn

@nan

2013 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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2013 թվականի փետրվարին հրատարակված գիտական հոդված

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

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name

Tasquinimod Is an Allosteric M ...... omised cancer microenvironment

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Tasquinimod Is an Allosteric M ...... omised cancer microenvironment

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Tasquinimod Is an Allosteric M ...... omised cancer microenvironment

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Cancer Research

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Tasquinimod Is an Allosteric M ...... omised cancer microenvironment

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Anders Björk

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Anders Olsson

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Hans Hammers

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John T Isaacs

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Jun Luo

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Li Xing

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Lizamma Antony

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Michel Wissing

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Per Björk

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Stephanie Gerber

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P2860

S100A9 interaction with TLR4 promotes tumor growth

Identification of human S100A9 as a novel target for treatment of autoimmune disease via binding to quinoline-3-carboxamides

Tasquinimod (ABR-215050), a quinoline-3-carboxamide anti-angiogenic agent, modulates the expression of thrombospondin-1 in human prostate tumors

Enzymatic activity associated with class II HDACs is dependent on a multiprotein complex containing HDAC3 and SMRT/N-CoR

Structural and functional analysis of the human HDAC4 catalytic domain reveals a regulatory structural zinc-binding domain

HDAC5 is a repressor of angiogenesis and determines the angiogenic gene expression pattern of endothelial cells

FOXP3 up-regulates p21 expression by site-specific inhibition of histone deacetylase 2/histone deacetylase 4 association to the locus

HDAC4 represses p21(WAF1/Cip1) expression in human cancer cells through a Sp1-dependent, p53-independent mechanism

Transcriptional activation of hypoxia-inducible factor-1alpha by HDAC4 and HDAC5 involves differential recruitment of p300 and FIH-1

Sirtuin 1 modulates cellular responses to hypoxia by deacetylating hypoxia-inducible factor 1alpha

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