STAT6 (Signal transducer and activator of transcription 6)

This study elucidates the mechanism through which IL-4/JAK2/STAT6-mediated M2 macrophages promote glycolysis in ESCC and demonstrates that ZGY disrupts this pathway by targeting JAK2 in macrophages. These findings provide a mechanistic foundation for developing ZGY as a promising tumor microenvironment-modifying therapy for ESCC.

Definitive diagnosis depends on histopathological and immunohistochemical confirmation. Complete surgical excision offers a favorable prognosis.

It also proposes future directions for translating bixin into a next-generation phytopharmaceutical through advanced formulation, mechanistic validation, and clinical evaluation. Collectively, the evidence positions bixin not merely as a natural colorant, but as a versatile bioactive molecule with significant promise in drug design, development, therapy, and delivery.

Collectively, the interference of DPPE-PEG with iNKT cells activation evidenced by reduced CD1d expression and IL-13 cytokine, with subsequently retarded activation of JAK1/STAT6 inflammatory signaling and preserved intestinal mucosa could, at least partly, contribute to impeding the progression of colitis. These findings reinforce our suggestion that DPPE-PEG could be an effective and promising candidate for retarding the advancement of ulcerative colitis.

The long disease-free interval raises the diagnostic dilemma of late recurrence versus a metachronous SFT, a distinction that remains challenging due to shared morphologic and molecular characteristics. This case underscores the limitations of metabolic imaging in indolent SFTs and highlights the importance of complete surgical resection and long-term, potentially lifelong, surveillance.

Diagnosis depends on histopathology and immunohistochemistry, particularly STAT6. Complete excision is usually curative, but long-term surveillance remains essential.

Consistently, ectopic expression of IL-4 receptor α in Mafb-deficient macrophages restored M2 phenotypes comparable to those of wild-type macrophages. These data highlight the critical cell-intrinsic role of MAFB in regulating M2-like TAMs and provide the first evidence that targeting MAFB enhances ICI efficacy in CRC by reprogramming TAMs toward an anti-tumorigenic M1-like phenotype.

Preclinical studies demonstrate CSF-1R inhibitors (e.g., pexidartinib) disrupt LSC-TAM crosstalk, while CAR-M therapy synergizes with phagocytosis-promoting agents. Despite challenges, macrophage-targeted therapies offer transformative potential by remodeling the TME, overcoming resistance, and augmenting immunotherapy. This review outlines mechanistic insights and translational strategies to harness macrophage plasticity for leukemia treatment.

Although the diagnosis was established based on morphology and immunoprofile, adverse histologic features, such as increased mitotic activity and high cellularity, suggest potential malignant behavior, warranting close clinical follow-up. This case underscores the importance of thorough histopathological and immunohistochemical evaluation in distinguishing SFT from other spindle cell lesions of the prostate, particularly given its extreme rarity and potential implications for patient management and follow-up.

This report highlights the challenges in diagnosing and treating oropharyngeal SFTs. It emphasizes the need for molecular confirmation and adds to the limited research on SFTs in rare head and neck locations.

This "pro-tumor vs. anti-tumor" duality underscores the pivotal yet paradoxical role of Type II immunity in tumor immunoregulation. Here, we systematically review the dual functions of Type II immune responses in tumor immunity and their translational potential for next-generation cancer immunotherapy.