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70 results for “CSF1R”
Involvement of the optic nerve in mutated CSF1R-induced hereditary diffuse leukoencephalopathy with axonal spheroids
<p><strong>Figure 1:</strong> Family pedigree. The arrow indicates the proband (present patient). Her mother developed a motor disorder at 40 years of age and died at 60 years of age. Her grandparents, father, brothers, sisters, and daughters were not affected.</p> <p><strong>Figure 2: Brain MRI, DWI, DTI, and MRS images. T2/Flair showed multifocal periventricular white matter lesions (A, B, and C), without enhancement (D). DWI shows high-signal intensities in periventricular white matters and corpus callosum (E, F). DTI shows decreased numbers of corpus callosum fibers, while subcortical arcuate fibers are spared (G). MRS shows increased Cho levels, while NAA levels are decreased in the white matter lesions (H, I).</strong></p> <p><strong>Figure 3: </strong>Optic nerves on MRI, showing that bilateral optic nerves are injured (red arrows). </p> <p><strong>Figure 4: </strong>OCT shows that the right peripapillary retinal nerve fiber layer (pRNFL) is atrophic in the temporal quadrant, and the left pRNFL is thinning in the temporal superior quadrants. Green represents pRNFL thickness, which is within normal limits; yellow represents pRNFL thickness, which is below borderline; red represents pRNFL thickness, which is below normal limits.</p> <p><strong>Figure 5:</strong> VEP shows reduced bilateral P100 amplitudes, although P100 latencies are normal in both eyes.</p> <p><strong>Figure 6:</strong> Visual fields in the right eye are partially missing in the upper right, lower right, and lower left quadrants, especially in the lower right quadrant. Visual fields in the left eye are partially missing in the four quadrants, especially in the upper left and lower right quadrants.</p> <p><strong>Figure 7:</strong> Gene analysis of <em>CSF1R</em>. The sequencing result from exon 18 of <em>CSF1R</em> (NM_005211.3) indicates a heterozygous c.2345 G>A (p.782Arg>His) substitution in the patient.</p>
Supplemental information for: Inhibition of CSF1R and KIT with pexidartinib reduces inflammatory signaling and cell viability in endometriosis
<p>Endometriosis is a common and debilitating disease, affecting ~170 million women worldwide. Affected patients have limited therapeutic options such as hormonal suppression or surgical excision of the lesions, though therapies are often not completely curative. Targeting receptor tyrosine-kinases (RTKs) could provide a nonhormonal treatment option for endometriosis. We determined that two RTKs, Macrophage colony stimulating factor receptor (CSF1R) and Mast/stem cell growth factor receptor KIT (KIT), are overexpressed in endometriotic lesions and could be novel nonhormonal therapeutic targets for endometriosis. The kinase activity of CSF1R and KIT is suppressed by pexidartinib, a small molecule inhibitor that was recently approved by the US Food and Drug Administration (FDA). Using immunohistochemistry, we detected CSF1R and KIT in endometriotic tissues obtained from peritoneal lesions, colorectal lesions, and endometriomas. Specifically, we show that KIT is localized to the epithelium of the lesions, while CSF1R is expressed in the stroma and macrophages of the endometriotic lesions. Given the high epithelial expression of CSF1R and KIT, 12Z endometriotic epithelial cells were used to evaluate the efficacy of dual CSF1R and KIT inhibition with pexidartinib. We found that pexidartinib suppressed activation in 12Z cells of JNK, STAT3 and AKT signaling pathways, which control key pro-inflammatory and survival networks within the cell. Using quantitative real time PCR, we determined that pexidartinib suppressed interleukin 8 (<em>IL8) </em>and cyclin D1 (<em>CCND1) </em>expression<em>.</em> Lastly, we demonstrated that pexidartinib decreased cell growth and viability.<em> </em>Overall, these results indicate that pexidartinib-mediated CSF1R and KIT inhibition reduces pro-inflammatory signaling and cell viability in endometriosis.</p>
Supplemental information for: Inhibition of CSF1R and KIT with pexidartinib reduces inflammatory signaling and cell viability in endometriosis
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Involvement of the optic nerve in mutated CSF1R-induced hereditary diffuse leukoencephalopathy with axonal spheroids
<p>Figure legends</p> <p>Figure 1: Family pedigree. The arrow indicates the proband (present patient). Her mother developed a motor disorder at 40 years of age and died at 60 years of age. Her grandparents, father, brothers, sisters, and daughters were not affected.</p> <p> </p> <p>Figure 2: Brain MRI, DWI, DTI, and MRS images. T2/Flair showed multifocal periventricular white matter lesions (A, B, and C), without enhancement (D). DWI shows high-signal intensities in periventricular white matters and corpus callosum (E, F). DTI shows decreased numbers of corpus callosum fibers, while subcortical arcuate fibers are spared (G). MRS shows increased Cho levels, while NAA levels are decreased in the white matter lesions (H, I).</p> <p> </p> <p>Figure 3: Optic nerves on MRI, showing that bilateral optic nerves are injured (red arrows).</p> <p> </p> <p>Figure 4: OCT shows that the right peripapillary retinal nerve fiber layer (pRNFL) is atrophic in the temporal quadrant, and the left pRNFL is thinning in the temporal superior quadrants. Green represents pRNFL thickness, which is within normal limits; yellow represents pRNFL thickness, which is below borderline; red represents pRNFL thickness, which is below normal limits.</p> <p> </p> <p>Figure 5: VEP shows reduced bilateral P100 amplitudes, although P100 latencies are normal in both eyes.</p> <p> </p> <p>Figure 6: Visual fields in the right eye are partially missing in the upper right, lower right, and lower left quadrants, especially in the lower right quadrant. Visual fields in the left eye are partially missing in the four quadrants, especially in the upper left and lower right quadrants.</p> <p> </p> <p>Figure 7: Gene analysis of CSF1R. The sequencing result from exon 18 of CSF1R (NM_005211.3) indicates a heterozygous c.2345 G>A (p.782Arg>His) substitution in the patient.</p>
CSF1R scRNAseq Data
<p>CSF1R Data for mutant and controls</p>
Pacritinib, a Kinase Inhibitor of CSF1R, IRAK1, JAK2, and FLT3, in Adults and Pediatric Participants 12 Years of Age or Older With Myelodysplastic Syndromes or Myelodysplastic/Myeloproliferative Neopl
ClinicalTrials.gov study NCT06303193. IPD Sharing: YES. Countries: 1. Publications: 1.
Effect of the CSF1R inhibitor AZD7507 on a relapse mouse model of high-grade serous ovarian cancer
GEO Series GSE158812. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
single-cell RNA-seq profile of microglia under acute Csf1r inhibition and early repopulation in adult brain
GEO Series GSE150169. Mus musculus. 9 samples. Type: Expression profiling by high throughput sequencing.
G3BP1::CSF1R: a new and actionable gene fusion in acute megakaryoblastic leukemia
GEO Series GSE279844. Homo sapiens. 12 samples. Type: Expression profiling by high throughput sequencing.
Glioblastoma Genetic Drivers Dictate the Function of Tumor-Associated Macrophages/Microglia and Responses to CSF1R Inhibition
GEO Series GSE185420. Mus musculus. 18 samples. Type: Expression profiling by high throughput sequencing.
The CSF1R-Microglia Axis Has Protective Host-Specific Roles During Neurotropic Picornavirus Infection
GEO Series GSE160660. Mus musculus. 13 samples. Type: Expression profiling by high throughput sequencing.
An EGR1-dependent cascade modulates genome architecture at the CSF1R locus [RNA-Seq]
GEO Series GSE283663. Homo sapiens. 10 samples. Type: Expression profiling by high throughput sequencing.
CSF1R inhibition by PLX5622 affects multiple immune cell compartments with tissue-specific metabolic effects
GEO Series GSE189434. Mus musculus. 13 samples. Type: Expression profiling by high throughput sequencing.
Molecular consequences of Csf1R (M-CSF receptor) inhibition by PLX3397 in the pilocarpine-induced chronic epileptic mouse hippocampus
GEO Series GSE77578. Mus musculus. 56 samples. Type: Expression profiling by array.
Global N6-methyladenosine RNA profiling reveals CSF1R as a target of METTL14 in non-small cell lung cancer [meRIP-seq]
GEO Series GSE179657. Homo sapiens. 16 samples. Type: Methylation profiling by high throughput sequencing.
scRNA-seq data of CSF1R WT/WT, naïve CSF1R WT/I792T and Mr BMT-treated CSF1R WT/I792T (deficient gene replaced by normal gene) mice brain cells.
GEO Series GSE270262. Mus musculus. 3 samples. Type: Expression profiling by high throughput sequencing.
CSF1R inhibition rescues tau pathology and neurodegeneration in an A/T/N model with combined AD pathologies, while preserving plaque associated microglia
GEO Series GSE176032. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
Transcriptome analysis using RNA sequencing of the perilesional cortex in traumatic brain injury mice treated with CSF1R inhibitor or vehicle
GEO Series GSE196121. Mus musculus. 20 samples. Type: Expression profiling by high throughput sequencing.
Metabolic reprogramming of skeletal muscle by resident macrophages points to CSF1R inhibitors as muscular dystrophy therapeutics (scRNA-Seq).
GEO Series GSE198055. Mus musculus. 10 samples. Type: Expression profiling by high throughput sequencing.
Sustained inhibition of CSF1R signaling augments antitumor immunity through inhibiting tumor-associated macrophages
GEO Series GSE242937. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
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International Brain Laboratory public data
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OpenNeuro
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