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Evaluation of tofacitinib in cutaneous sarcoidosis [Olink Explore 1536]

ABSTRACT: Sarcoidosis is a multisystem inflammatory disease and no molecularly targeted therapies exist. Here we evaluate the efficacy of tofacitinib (a JAK1/3 inhibitor) in an open-label trial of 10 patients with sarcoidosis and correlate clinical improvement with molecular parameters in blood and skin.

ORGANISM(S): Homo sapiens

PROVIDER: GSE169148 | GEO | 2022/03/30

REPOSITORIES: GEO

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Evaluation of tofacitinib in cutaneous sarcoidosis [scRNA-seq]

Project description:Sarcoidosis is a multisystem inflammatory disease and no molecularly targeted therapies exist. Here we evaluate the efficacy of tofacitinib (a JAK1/3 inhibitor) in an open-label trial of 10 patients with sarcoidosis and correlate clinical improvement with molecular parameters in blood and skin.

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Evaluation of tofacitinib in cutaneous sarcoidosis

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

2022-03-30 | GSE169149 | GEO

Molecular profiling and gene expression analysis in cutaneous sarcoidosis (CS)

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Molecular profiling and gene expression analysis in cutaneous sarcoidosis (CS)

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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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