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--- annexin_a1 [2025/07/06 17:19] – administrador
+++ annexin_a1 [2025/07/06 17:28] (current) – administrador
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   * Promotes immune evasion and tumor progression
-((Discov Oncol. 2025 Jul;16(1):1269. doi:10.1007/s12672-025-03112-y))
+In a [[Translational research]] with bulk [[RNA sequencing analysis]], scRNA-seq, and [[in vitro]] [[validation]]
+Hong Hu *et al.*
+from the Harbin Medical University
+published in the **Journal:** [[Discover Oncology]]
+to elucidate how [[methionine]] metabolism contributes to the immunosuppressive [[tumor microenvironment]] in [[glioma]]s, with a focus on [[macrophage]] polarization mediated by [[ANXA1]].
+Elevated methionine metabolism in [[glioma cell]]s correlates with higher [[WHO]] [[tumor]] [[grade]] and an immunosuppressive microenvironment. High [[methionine]] metabolic activity fosters M2 macrophage polarization via ANXA1, which is downregulated upon methionine deprivation
+((Hu H, Huang Y, Li J, Liu R, Li H, Cai M, Chen H, Wang N, Yang S, Wang K, Teng L, Liu H. [[Glioma]] promotes [[macrophage immunosuppressive phenotype]] through [[ANXA1]] in a [[methionine metabolism]]-dependent manner. Discov Oncol. 2025 Jul 6;16(1):1269. doi: 10.1007/s12672-025-03112-y. PMID: 40618309.)).
+==== Critical Review ====
+This study leverages [[multi-omics]] datasets, particularly MMA-scoring and scRNA-seq, to draw a novel link between methionine metabolism and the immune suppressive phenotype in gliomas, focusing on macrophage polarization. The authors make a credible case for metabolic reprogramming as a driver of glioma malignancy. However, there are caveats:
+- **Strengths:** The integration of bulk and single-cell RNA-seq enhances resolution, and the use of in vitro validation lends support to mechanistic claims. The correlation between MMA-scores and glioma grade is statistically compelling.
+- **Limitations:** Despite the innovative premise, the study relies heavily on correlative data. Functional validation, particularly in vivo or using clinical samples, is lacking. The assertion that ANXA1-mediated macrophage polarization is solely Met-dependent needs further biochemical interrogation. Furthermore, patient sample heterogeneity and potential confounders are not adequately addressed.
+- **Mechanistic Gap:** While ANXA1 expression is shown to respond to Met availability, its downstream effects on macrophage behavior are inferred rather than mechanistically dissected.
+- **Clinical Implications:** The study's translational relevance is speculative. No clinical outcome data (e.g., survival stratified by MMA-score) are presented, and therapeutic exploitation remains conceptual.
+**Final Verdict:** Ambitious and methodologically diverse, but insufficiently validated for [[clinical translation]].
+**Takeaway for the Practicing Neurosurgeon:** While methionine metabolism may signal tumor aggressiveness and immune evasion, it is not yet a practical biomarker or therapeutic target without deeper functional validation.
+**Bottom Line:** Promising hypothesis linking [[glioma metabolism]] to immune suppression via [[ANXA1]]; more robust causal evidence is needed before clinical application.
+**Rating:** 6.5/10
+**Title:** Glioma promotes macrophage immunosuppressive phenotype through ANXA1 in a methionine metabolism-dependent manner
+**Citation:** Hu H *et al.* Discover Oncology. 2025 Jul 6;16(1):1269. doi:10.1007/s12672-025-03112-y
+**Publication Date:** July 6, 2025
+**Corresponding Author Email:** liuhuaileinsdm@hrbmu.edu.cn
 === Summary ===