Chemotherapy stimulates syndecan-1 shedding: a potentially negative effect of treatment that may promote tumor relapse - Wikidata - wikimedia - TriplyDB

Chemotherapy stimulates syndecan-1 shedding: a potentially negative effect of treatment that may promote tumor relapse

Chemotherapy stimulates syndecan-1 shedding: a potentially negative effect of treatment that may promote tumor relapse

http://www.wikidata.org/entity/Q42021140

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Proteoglycan form and function: A comprehensive nomenclature of proteoglycans Recent Insights into Cell Surface Heparan Sulphate Proteoglycans and Cancer Syndecan-1 in Cancer: Implications for Cell Signaling, Differentiation, and Prognostication Mechanisms of heparanase inhibitors in cancer therapy.Diagnostic and prognostic value of soluble syndecan-1 in pleural malignancies.Shed Syndecan-1 is involved in chemotherapy resistance via the EGFR pathway in colorectal cancer Shed syndecan-1 translocates to the nucleus of cells delivering growth factors and inhibiting histone acetylation: a novel mechanism of tumor-host cross-talk.Relationship between circulating syndecan-1 levels (CD138s) and serum free light chains in monoclonal gammopathies.Mitochondrial-Targeted Decyl-Triphenylphosphonium Enhances 2-Deoxy-D-Glucose Mediated Oxidative Stress and Clonogenic Killing of Multiple Myeloma Cells Soluble PD-L1: A biomarker to predict progression of autologous transplantation in patients with multiple myeloma.The role of syndecan-1 in cellular signaling and its effects on heparan sulfate biosynthesis in mesenchymal tumors Syndecans as modulators and potential pharmacological targets in cancer progression.What we mean when we talk about MRD in myeloma. A review of current methods. Part 1 of a two-part series.Chemotherapy induces expression and release of heparanase leading to changes associated with an aggressive tumor phenotype.Immunoglobulin Free Light Chains and GAGs Mediate Multiple Myeloma Extracellular Vesicles Uptake and Secondary NfκB Nuclear Translocation.A subset of high Gleason grade prostate carcinomas contain a large burden of prostate cancer syndecan-1 positive stromal cells.

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P2860

Chemotherapy stimulates syndecan-1 shedding: a potentially negative effect of treatment that may promote tumor relapse

http://www.wikidata.org/entity/Q42021140

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2013 nî lūn-bûn

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name

Chemotherapy stimulates syndec ...... that may promote tumor relapse

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Chemotherapy stimulates syndec ...... that may promote tumor relapse

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Chemotherapy stimulates syndec ...... that may promote tumor relapse

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Chemotherapy stimulates syndec ...... that may promote tumor relapse

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Chemotherapy stimulates syndec ...... that may promote tumor relapse

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Chemotherapy stimulates syndec ...... that may promote tumor relapse

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Chemotherapy stimulates syndec ...... that may promote tumor relapse

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Ralph D Sanderson

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Vishnu C Ramani

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P2860

Syndecans in tumor cell adhesion and signaling

Analyzing real-time PCR data by the comparative C(T) method

Biology of the syndecans: a family of transmembrane heparan sulfate proteoglycans

A disintegrin and metalloproteinase 17 (ADAM17) mediates inflammation-induced shedding of syndecan-1 and -4 by lung epithelial cells

Heparanase-enhanced shedding of syndecan-1 by myeloma cells promotes endothelial invasion and angiogenesis.

Transcriptional regulation of matrix metalloproteinase-1 and collagen 1A2 explains the anti-fibrotic effect exerted by proteasome inhibition in human dermal fibroblasts.

Chemotherapy-induced activation of ADAM-17: a novel mechanism of drug resistance in colorectal cancer.

Global gene expression profiling of multiple myeloma, monoclonal gammopathy of undetermined significance, and normal bone marrow plasma cells.

Heparanase plays a dual role in driving hepatocyte growth factor (HGF) signaling by enhancing HGF expression and activity

Heparanase-mediated loss of nuclear syndecan-1 enhances histone acetyltransferase (HAT) activity to promote expression of genes that drive an aggressive tumor phenotype

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215-222

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scholarly article

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10.1016/J.MATBIO.2013.10.005

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35

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2013-10-18T00:00:00Z

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