CSF1R (Colony stimulating factor 1 receptor)

bMΦs emerge directly from axial vessels through an atypical endothelial-to-macrophage transition that is independent of Runx1 and Csf1r. Our findings reveal a previously unrecognized macrophage population dedicated to vascular immune surveillance, uncovering mechanisms that preserve blood and vessel integrity and offering potential therapeutic avenues for bloodborne and vascular diseases.

P2, N=222, Recruiting, National Cancer Institute (NCI) | Phase classification: P3 --> P2

CI has a manageable safety profile and leads to increased intratumoral cytotoxic effector T cells. https://clinicaltrials.gov/study/NCT03153410, identifier NCT03153410.

Proteomic profiling of these high-risk angiosarcomas within this cluster demonstrated upregulation of oxidative phosphorylation, angiogenesis, and neutrophil-associated pathways, alongside downregulation of extracellular matrix organization, indicating a metabolically distinct and immunologically myeloid-driven tumor state and immune phenotype. These findings identify CSF1R⁺ macrophage enrichment as a defining feature of high-risk angiosarcoma and suggest that improved biological understanding of the CSF1R axis may allow additional immunomodulatory therapeutic strategies in this rare and aggressive malignancy.

It also summarizes the design principles and adaptive strategies of biomimetic platforms and introduces an artificial intelligence (AI)-assisted closed-loop therapeutic framework encompassing identification, delivery, and feedback to support individualized and precise immunotherapy. Although the approach demonstrates strong potential for multidimensional integration, several challenges remain, including the standardization of spatial atlases, the stability of delivery systems, and cross-platform compatibility, all of which require further technological advancement.

P2, N=53, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jun 2026 --> Jan 2027

Overexpression of Mt1 restored metal ion homeostasis, normalized ROS production in microglia, and prevented the development of behavioral deficits, while Mt3 deletion had disease-enhancing effects. These findings demonstrate CSF-1R regulation of metal ion homeostasis via metallothioneins in the brain.

P2/3, N=87, Not yet recruiting, Universita Degli Studi Di Milano Bicocca

Furthermore, we examine emerging therapeutic strategies targeting glial-specific pathways, including NF-κB, JAK/STAT, CSF1R, and TREM2 signaling, as well as remyelinating agents and stem cell-based interventions. By integrating glial biology with therapeutic innovation, this review positions glial cells not as supporting actors but as central regulators and potential gatekeepers of dementia pathogenesis and treatment.

We also assess challenges in clinical translation, including tumor-type heterogeneity, insufficient biomarkers, and incomplete understanding of spatial immune architecture within bone lesions. Advancing myeloid-targeted interventions may enable more durable control of metastasis and improve outcomes for patients with skeletal involvement.

Also underscored are the existence of commercially available drugs and patented compounds, as well as translational candidates featuring the 2-aminobenzothiazole pharmacophore. The paper emphasises the dual mechanistic targetability of 2-aminobenzothiazole derivatives as valuable lead compounds targeting both kinases and other targets in an innovative manner aimed at future development of targeted anti-cancer therapies.

Our study demonstrates that the OPN/PI3K/AKT/CSF1-CSF1R axis plays a crucial role in CRC metastasis. Blocking the CSF1/CSF1R axis reduces M2-like TAMs infiltration and tumor metastasis, offering a promising strategy for metastatic CRC.