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CXCL8/CXCR2 signaling is Enriched in Fibrotic Myeloproliferative Neoplasms and is Vulnerable to Therapeutic Inhibition

ABSTRACT: CXCL8/CXCR2 signaling is Enriched in Fibrotic Myeloproliferative Neoplasms and is Vulnerable to Therapeutic Inhibition

PROVIDER: PRJNA785451 | ENA |

REPOSITORIES: ENA

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CXCL8/CXCR2 signaling is Enriched in Fibrotic Myeloproliferative Neoplasms and is Vulnerable to Therapeutic Inhibition [RNA-Seq]

Project description:Pro-inflammatory signaling is a hallmark feature of human cancer, including in myeloproliferative neoplasms (MPNs), most notably myelofibrosis (MF). Dysregulated inflammatory signaling contributes to fibrotic progression in MF; however, the individual cytokine mediators elicited by malignant MPN cells to promote collagen-producing fibrosis and disease evolution remain yet to be fully elucidated. Previously we identified a critical role for combined constitutive JAK/STAT and aberrant NF-kB pro-inflammatory signaling in myelofibrosis development. Using single-cell transcriptional and cytokine-secretion studies of primary MF patient cells and two separate murine models of myelofibrosis, we extend this previous work and delineate the role of CXCL8/CXCR2 signaling in MF pathogenesis and bone marrow fibrosis progression. MF patient hematopoietic stem/progenitor cells are enriched in a CXCL8/CXCR2 gene signature and display dose-dependent proliferation and fitness in response to exogenous CXCL8 ligand in vitro. Genetic deletion of Cxcr2 in the hMPLW515L adoptive transfer model abrogates fibrosis and extends overall survival, and pharmacologic inhibition of the CXCR1/2 pathway improves hematologic parameters, attenuates bone marrow fibrosis, and synergizes with JAK inhibitor therapy. Our mechanistic insights provide a rationale for therapeutic targeting of the CXCL8/CXCR2 pathway in MF patients at risk for continued fibrotic progression.

2023-05-12 | GSE189979 | GEO

CXCL8/CXCR2 signaling is Enriched in Fibrotic Myeloproliferative Neoplasms and is Vulnerable to Therapeutic Inhibition [ATAC-Seq]

2023-05-12 | GSE189978 | GEO

CXCL8/CXCR2 signaling is Enriched in Fibrotic Myeloproliferative Neoplasms and is Vulnerable to Therapeutic Inhibition [ATAC-Seq]

Project description:CXCL8/CXCR2 signaling is Enriched in Fibrotic Myeloproliferative Neoplasms and is Vulnerable to Therapeutic Inhibition [ATAC-Seq]

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CXCL8/CXCR2 signaling is Enriched in Fibrotic Myeloproliferative Neoplasms and is Vulnerable to Therapeutic Inhibition [RNA-Seq]

Project description:CXCL8/CXCR2 signaling is Enriched in Fibrotic Myeloproliferative Neoplasms and is Vulnerable to Therapeutic Inhibition [RNA-Seq]

| PRJNA785456 | ENA

Myelodysplastic/myeloproliferative neoplasms

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Project description:Cardiovascular events are the leading cause of death in patients with JAK2V617F myeloproliferative neoplasms. Their mechanisms are poorly understood. To investigate the role of microvesicles in these events, we performed a proteomic analysis of microvesicles derived from red blood cells from mice with a myeloproliferative neoplasms (Jak2V617F Flex/WT ;VE-cadherin-Cre) vs. littermate controls.

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CXCL8/CXCR2 signaling is Enriched in Fibrotic Myeloproliferative Neoplasms and is Vulnerable to Therapeutic Inhibition

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

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Project description:Targeting the CALR Interactome in Myeloproliferative Neoplasms