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Early quantification of systemic inflammatory (INF) and cardiovascular disease (CVD) proteins predicts long-term treatment response to Tofacitinib and Etanercept (INF data set)

ABSTRACT: Proteomic profiles of 92 inflammatory proteins were measured in the blood of psoriasis patients both before and after treatment with tofacitanib or etanercept. These proteomic profiles were used to develop statistical classifiers for predicting PASI75 responses to tofacitinib and etancercept

ORGANISM(S): Homo sapiens

PROVIDER: GSE136434 | GEO | 2019/11/22

REPOSITORIES: GEO

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Early quantification of systemic inflammatory (INF) and cardiovascular disease (CVD) proteins predicts long-term treatment response to Tofacitinib and Etanercept (CVD data set)

Project description:Proteomic profiles of 91 cardiovascular disease proteins were measured in the blood of psoriasis patients both before and after treatment with tofacitanib or etanercept. These proteomic profiles were used to develop statistical classifiers for predicting PASI75 responses to tofacitinib and etancercept

2019-11-22 | GSE136431 | GEO

Early quantification of systemic inflammatory (INF) and cardiovascular disease (CVD) proteins predicts long-term treatment response to Tofacitinib and Etanercept

Project description:Early quantification of systemic inflammatory (INF) and cardiovascular disease (CVD) proteins predicts long-term treatment response to Tofacitinib and Etanercept

| PRJNA562531 | ENA

Early quantification of systemic inflammatory (INF) and cardiovascular disease (CVD) proteins predicts long-term treatment response to Tofacitinib and Etanercept (CVD data set)

Project description:Early quantification of systemic inflammatory (INF) and cardiovascular disease (CVD) proteins predicts long-term treatment response to Tofacitinib and Etanercept (CVD data set)

| PRJNA562533 | ENA

Early quantification of systemic inflammatory (INF) and cardiovascular disease (CVD) proteins predicts long-term treatment response to Tofacitinib and Etanercept (INF data set)

| PRJNA562534 | ENA

Early quantification of systemic inflammatory (INF) and cardiovascular disease (CVD) proteins predicts long-term treatment response to Tofacitinib and Etanercept

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-11-22 | GSE136435 | GEO

Cellular and Molecular Changes in Psoriasis Lesions Induced by Ustekinumab: Distinct Differences in Responders vs. Non-Responders

Project description:A gene expression profiling sub-study was conducted in which skin biopsy samples (n=192) were collected for RNA extraction and hybridization to microarrays from patients with moderate-to-severe psoriasis who participated in ACCEPT, an IRB-approved Phase 3, multicenter, randomized trial. This analysis identified gene expressions significantly modulated in psoriasis lesions (LS) following ustekinumab or etanercept treatment at week 12 compared to baseline. Molecular expression of mRNA was found to be different in ustekinumab PASI75 responders vs. nonresponders. Differential modulation of selected mRNAs was also observed between ustekinumab and etanercept PASI75 responders.

2019-02-01 | GSE106992 | GEO

MoDCs grown with/without Etanercept TNF inhibitor

Project description:The process for making monocyte derived DCs (moDCs) has been previously described (46). All analysis was performed on “day 5” immature DCs. Etanercept 10mg/mL was added to experimental wells on days 0, 2, and 4. We chose this concentration of etanercept as it approximates the plasma concentration of drug when given 50mg BIW. Keywords: Inhibition assay

2007-10-06 | GSE9239 | GEO

Effect of Etanercept on Active Pulmonary Tuberculosis in Rabbits

Project description:Treatment of chronic inflammatory diseases with tumor necrosis factor alpha antagonists has been associated with increased risk of tuberculosis (TB). We examined the usefulness of the rabbit model of active pulmonary TB for studying the impact of the human immune modulatory reagent etanercept on the host immune response. Control of Mycobacterium tuberculosis (Mtb) infection, disease pathology and the global transcriptional response in Mtb-infected lungs of rabbits were studied. Etanercept treatment exacerbated disease pathology and reduced bacillary control in the lungs, compared to infected untreated animals. The microarray experiments involves comparison of changes in gene expression between Mtb-HN878 infected and Etanercept treated and untreated rabbit lungs at 4 and 8 weeks post-treatment, starting at 4 weeks post-infection.

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Early tissue responses to etanercept in psoriasis lesions

Project description:Anti-TNF-alpha therapy has made a significant impact on the treatment of psoriasis. Despite being designed to neutralize TNF-alpha activity, the mechanism of action of these agents in the resolution of psoriasis remains unclear. The aim of this study was to better understand the mechanism of action of etanercept by examining very early changes in the lesional skin of psoriasis patients. 20 chronic plaque psoriasis patients were enrolled and received 50mg etanercept twice weekly. Skin biopsies were obtained before treatment and on days 1, 3, 7 and 14 post-treatment. Skin mRNA expression was analysed by microarray.

2014-06-07 | GSE47751 | GEO

Repurposing tofacitinib as an anti-myeloma therapeutic to reverse growth-promoting effects of the bone marrow microenvironment

Project description:The myeloma bone marrow microenvironment drives proliferation of malignant plasma cells and promotes resistance to therapy. Interleukin-6 (IL-6) and downstream JAK/STAT signaling are thought to be central components of these microenvironment-induced phenotypes. In a prior drug repurposing screen, we identified tofacitinib, a pan-JAK inhibitor FDA-approved for rheumatoid arthritis, as an agent that may reverse the tumor-stimulating effects of bone marrow mesenchymal stromal cells.Here, we validated both in vitro, in stromal-responsive human myeloma cell lines, and in vivo, in orthotopic disseminated murine xenograft models of myeloma, that tofacitinib showed both single-agent and combination therapeutic efficacy in myeloma models. Surprisingly, we found that ruxolitinib, an FDA-approved agent targeting JAK1 and JAK2, did not lead to the same anti-myeloma effects. Combination with a novel irreversible JAK3-selective inhibitor also did not rescue ruxolitinib effects. RNA-seq and unbiased phosphoproteomics revealed that marrow stromal cells drive a JAK/STAT-mediated proliferative program in myeloma plasma cells, and tofacitinib reversed the large majority of these pro-growth signals. Taken together, our results suggest that tofacitinib specifically reverses the growth-promoting effects of the tumor microenvironment through blocking an IL-6-mediated signaling axis. As tofacitinib is already FDA-approved, these results can be rapidly translated into potential clinical benefits for myeloma patients.

2018-10-24 | PXD006581 | Pride

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