CSF1 expression

Furthermore, α5-nAChR expression was strongly linked to pSTAT3, SOX2 and M2 macrophage marker CD206 expression and negatively correlated with M1 macrophage marker CD86 expression in vivo. It is indicated that M2 macrophages are mediated by the new α5-nAChR /SOX2/CSF-1 axis in nicotine-related LUAD, which is a potential therapeutic strategy for cancer.

MIP-1α expression was significantly correlated with average CXCR4 CAML expression (P = 0.003). We discovered larger CAML size was associated with SAT-dominant obesity with increased macrophage-related and proinflammatory markers in obese than in nonobese breast cancer patients.

The patient was treated with pegylated interferon and imatinib, which resulted in stable disease after three months...Analysis of ligand-receptor interactions showed significant communication between neoplastic cells and macrophages mediated by CSF1 and CSF1R. Our findings emphasize the importance of comprehensive molecular analysis in diagnosing and treating rare malignancies like TGCT.

POLA2 induced macrophage infiltration in the tumor microenvironment by upregulating the expression CSF1 and VEGFA expression. POLA2 is a novel diagnostic and prognostic biomarker of HCC with potential clinical value.

We observed in vitro that the activation of lymphocytes mediated by pembrolizumab was hindered by the treatment of PBMC with recombinant CSF-1, suggesting that CSF-1 creates a systemic immunosuppressive state that interferes with ICI treatment. In conclusion, baseline CSF-1 levels represent a potential predictive marker to ICI treatment in NSCLC.

Our findings provide additional evidence that the CSF1/CSF1R pathway is involved in the pathogenesis of XGET/KPGCT. These findings suggest a possible role for CSF1R inhibition in the treatment of unresectable or metastatic XGET/KPGCT.

Single-cell analysis of human lung cancers revealed a significant reduction in the immunosuppressive TAMs in former smokers compared with individuals who had never smoked. These findings demonstrate that carcinogen exposure impairs the development of an immunosuppressive TME and indicate a novel link between carcinogens and cancer immunogenicity.

This phenomenon extended to human lung cancers, as evidenced by TAM reprogramming in smokers versus nonsmokers. This study substantially advances our understanding of carcinogen-mediated effects on cancer immunogenicity, potentially redirecting approaches to cancer immunotherapy.

Inhibition of Brd4 not only reduces tumor invasion and lung metastasis, but also reduces circulating Csf-1 levels. Overall, our results establish a novel p53-R172H-dependent Brd4-Csf-1 axis that promotes ESCC lung metastasis, and suggest avenues for therapeutic strategies for this difficult-to-treat disease.

Pts with TGCT not amenable to surgery who received prior anti-CSF1/CSF1R therapy (including pexidartinib, cabiralizumab, or vimseltinib) were enrolled and treated with vimseltinib 30 mg twice weekly (recommended phase 2 dose). Longer follow-up demonstrated that vimseltinib continued to be well tolerated with a manageable safety profile in pts with TGCT not amenable to surgery who received prior anti-CSF1/CSF1R therapy. Antitumor activity continued to improve in this pretreated population, with an increased ORR. At week 25, all responders experienced ≥30% reductions in worst and average pain.

Pts with TGCT not amenable to surgery and no prior anti-CSF1/CSF1R therapy (previous treatment with imatinib or nilotinib was allowed) were enrolled and treated with vimseltinib 30 mg twice weekly (recommended phase 2 dose). Longer follow-up demonstrated that vimseltinib continued to be well tolerated with a manageable safety profile in pts with TGCT not amenable to surgery with no prior anti-CSF1/CSF1R therapy. Antitumor activity continued to improve with a promising overall ORR. At week 25, the majority of responders experienced ≥30% reductions in worst and average pain.

To assess the mechanism of CSF-1-mediated suppression of immunotherapy, Isolated PBMC, activated with phytohemagglutinin (PHA) with or without pembrolizumab (20 nM), were cultured alone, or in the presence of macrophages or on an established NSCLC monolayer...The use of Pexidartinib (PLX-3397), a CSF-1R inhibitor, reversed the effects of CSF-1 by restoring lymphocyte activation. However, these effects were dependent on the presence of monocytes/macrophages, suggesting that the immune suppression mediated by CSF-1 was an indirect effect resulting from the stimulation of monocytes that promote their differentiation into macrophages. Conclusions Our study suggests that plasma levels of CSF-1 could serve as a useful predictive biomarker for resistance to ICIs, while targeting the CSF-1/CSF-1R signaling pathway could potentially overcome resistance to ICIs in patients with NSCLC.