Background: Colony-stimulating factor-1 (CSF-1) is a homodimeric glycoprotein. The main role of CSF-1 is as a hematopoietic growth factor that modulates proliferation, differentiation, and survival of macrophages. Moreover, CSF-1 has also been reported to be aberrantly expressed in several human cancers. However, the precise role of CSF-1 in upper tract urothelial carcinomas (UTUC) has not been studied. In this research, we examined the clinical significance of CSF-1 expression in UTUC.
Materials And Methods: One hundred twelve cancer tissue samples of UTUC from patients were included in this study, and the other cohort of 35 UTUC were paired cancer-adjacent normal samples. CSF-1 expression was evaluated by immunohistochemistry, and the association of CSF-1 expression with different clinicopathological variables was analyzed.
Results: CSF-1 expression was higher in UTUC than in the normal urothelium ( = 0.005). The CSF-1 expression was primarily localized in the nucleus and was significantly correlated with tumor size ( = 0.04) and patients who had a high stage ( < 0.001), distant metastasis ( = 0.006), recurrence ( = 0.003), and cancer death ( = 0.005). High CSF-1 expression was correlated with poor disease-free survival ( = 0.008) and cancer-specific survival ( = 0.001). Our results also used univariate and multivariable analyses, which found that high CSF-1 expression was an independent predictor of poor disease-free survival (hazard ratio = 2.56; = 0.007) and cancer-specific survival (hazard ratio = 5.14; = 0.022).
Conclusions: Our findings indicate that the expression of CSF-1 is a potential prognostic marker for predicting patient survival and recurrence in UTUC.
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http://dx.doi.org/10.1155/2019/2724948 | DOI Listing |
Scand J Immunol
January 2025
Department of Ophthalmology, Shanghai Jiangong Hospital, Shanghai, China.
Dry eye disease (DED) is an inflammatory disorder in which CD4 T cells play a significant role in its pathogenesis. A CD4 T cell subset termed granulocyte-macrophage colony-stimulating factor-producing T helper (ThGM) cells would contribute to DED pathogenesis. However, the mechanisms by which the activity of ThGM cells is modulated are not thoroughly understood.
View Article and Find Full Text PDFJ Interferon Cytokine Res
January 2025
The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia.
Suppressor of cytokine signaling (SOCS) 1 is a key negative regulator of interferon (IFN), interleukin (IL)12, and IL-2 family cytokine signaling through inhibition of the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway. To investigate the temporal induction of SOCS1 in response to cytokine in live cells and its selective regulation of signaling pathways, we generated a mouse expressing a Halo-tag-SOCS1 fusion protein (Halo-SOCS1) under control of the endogenous promoter. Homozygous Halo-SOCS1 mice () were viable with minor T cell abnormalities, most likely due to enhanced Halo-SOCS1 expression in thymocytes compared with the untagged protein.
View Article and Find Full Text PDFJCI Insight
January 2025
Department of Immunology and.
Tumor-associated macrophages (TAMs) are one of the key immunosuppressive components in the tumor microenvironment (TME) and contribute to tumor development, progression, and resistance to cancer immunotherapy. Several reagents targeting TAMs have been tested in preclinical and clinical studies, but they have had limited success. Here, we show that a unique reagent, FF-10101, exhibited a sustained inhibitory effect against colony-stimulating factor 1 receptor by forming a covalent bond and reduced immunosuppressive TAMs in the TME, which led to strong antitumor immunity.
View Article and Find Full Text PDFBackground: Microglial activation is one of the neuropathological hallmarks of Alzheimer's disease (AD). Evidence suggest that chronic activation of microglia cause neuroinflammation and neuronal injuries, contributing to cognitive impairment. Therefore, modulation of microglial pathway like CSF-1R represents an attractive therapeutic strategy.
View Article and Find Full Text PDFBiomark Res
January 2025
Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Background: Although immunotherapy has achieved great progress in advanced triple-negative breast cancer (TNBC), there are still numerous patients who do not benefit from immunotherapy. Therefore, identification of the key molecule that induces immune escape and clarification of its specific mechanism in TNBC are urgently needed.
Methods: In this research, single cell sequencing and bulk sequencing were conducted for biomarker screening.
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