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Macrophage contribution to follicular lymphoma pathogenesis: CSF-1R as a novel prognostic factor and therapeutic target

ABSTRACT: Follicular lymphoma (FL) patient samples from lymph node biopsies were in co-culture or not with M2 macrophages (generated from healthy donors) for 48h We used microarrays to uncover the mechanisms underlying FL and macrophages crosstalk

ORGANISM(S): Homo sapiens

PROVIDER: GSE147211 | GEO | 2021/01/31

REPOSITORIES: GEO

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CSF-1R inhibition alters macrophage polarization and blocks gliomagenesis

Project description:Glioblastoma multiforme (GBM), the most common and aggressive primary brain tumor in adults, can be divided into several molecular subtypes including proneural GBM. Most clinical strategies aimed at directly targeting glioma cells in these tumors have failed. A promising alternative is to target stromal cells in the brain microenvironment, such as tumor-associated microglia and macrophages (TAMs). Macrophages are dependent upon colony stimulating factor (CSF)-1 for differentiation and survival; therefore, we used an inhibitor of its receptor, CSF-1R, to target macrophages in a mouse proneural GBM model. CSF-1R inhibition dramatically increased survival in mice and regressed established GBMs. Tumor cell apoptosis was significantly increased, and proliferation and tumor grade markedly decreased. Surprisingly, TAMs were not depleted in tumors treated with the CSF-1R inhibitor. Instead, analysis of gene expression in TAMs isolated from treated tumors revealed a decrease in alternatively activated/ M2 macrophage markers, consistent with impaired tumor-promoting functions. These gene signatures were also associated with better survival specifically in the proneural subtype of patient gliomas. Collectively, these results establish macrophages as valid therapeutic targets in proneural gliomas, and highlight the clinical potential for CSF-1R inhibitors in GBM. RNA was isolated from sorted tumor associated macrophages (TAMs) from murine gliomas following either 7 days of vehicle or BLZ945 treatment. Samples were collected from 16 total tumor burdened mice, with 8 replicates for each treatment group. BLZ945: a Colony-Stimulating Factor 1 Receptor (CSF-1R) inhibitor

2013-09-20 | E-GEOD-37475 | biostudies-arrayexpress

CSF-1R inhibition alters macrophage polarization and blocks gliomagenesis

2013-09-20 | GSE37475 | GEO

Gene expression profiling of Follicular Lymphoma (FL) cultured in the presence or absence of the Follicular Dendritic Cell (FDC) line HK

Project description:Cells from 2 FL patients and 1 FL cell line were cultured for up to 48h, with no stroma or on top of HK cells pre-establised layers. RNA from FL cells was isolated after 24 and 48h of culture The aim of this study was to uncover the molecular mechanisms underlying the FL-FDC crosstalk

2014-08-04 | GSE54158 | GEO

Macrophage contribution to follicular lymphoma pathogenesis: CSF-1R as a novel prognostic factor and therapeutic target

Project description:Macrophage contribution to follicular lymphoma pathogenesis: CSF-1R as a novel prognostic factor and therapeutic target

| PRJNA613435 | ENA

Effect of Idelalisib in follicular lymphoma monocultures and cocultured with follicular dendritic cells (FDC)

Project description:Follicular Lymphoma primary cells (FL) were treated with the PI3K delta inhibitor idelalisib (500nM, 48h) in the presence or absence of follicular dendritic cells We used microarrays to uncover the mechanisms underlying mechanism of resistance and sensitivity of FL to idelalisib

2020-09-15 | GSE130918 | GEO

Gene expression profiling of Follicular Lymphoma (FL) cultured in the presence or absence of the Follicular Dendritic Cell (FDC) line HK

2014-08-04 | E-GEOD-54158 | biostudies-arrayexpress

The receptor of the colony-stimulating factor-1 (CSF-1R) is a novel prognostic factor and therapeutic target in follicular lymphoma.

Project description: Not available

| S-EPMC8410584 | biostudies-literature

ASIC3-M-CSF-M2 macrophage-positive feedback loop modulates in skin fibrosis pathogenesis

Project description:Inflammation is one of the main pathological features leading to skin fibrosis and a key factor leading to the progression of skin fibrosis. Acidosis caused by a decrease in extracellular pH is a sign of the inflammatory process. Acid-sensing ion channels (ASICs) are ligand-gated ion channels on the cell membrane that sense the drop in extracellular pH. However, the molecular mechanisms by which skin fibroblasts are regulated by Acid-sensing ion channel 3(ASIC3) remain unknown. This study investigated whether ASIC3 is related to inflammation and skin fibrosis and explored the underlying mechanisms. We demonstrate that Macrophage colony-stimulating factor (M-CSF) is a direct target of ASIC3, and ASIC3 activation promotes M-CSF transcriptional regulation of macrophages for M2 polarization. The polarization of M2 macrophages transduced by the ASIC3-M-CSF signal promotes the differentiation of fibroblasts into myofibroblasts through transforming growth factor β1 (TGF-β1), thereby producing ASIC3-M-CSF-TGF-β1 positive feedback loop. Targeting ASIC3 may be a new treatment strategy for skin fibrosis.

2021-10-30 | GSE186739 | GEO

Prognostic Significance of CSF-1R Expression in Early Invasive Breast Cancer.

Project description: Not available

| S-EPMC8616299 | biostudies-literature

Human monocyte-derived macrophages polarized by GM-CSF or M-CSF

Project description:Identification of genes differentially expressed between human monocyte-macrophages generated in the presence of either GM-CSF (termed M1) or M-CSF (termed M2)

2012-04-13 | GSE27792 | GEO

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