CXCR1 (Chemokine (C-X-C motif) receptor 1)

This study reveals that CXCL8 drives OSCC metastasis via CXCR1/2-mediated JAK1/STAT3 activation leading to MMP1 transcriptional upregulation. Our findings establish CXCL8 as both a prognostic biomarker and a promising therapeutic target, and suggest that targeting this pathway offers significant therapeutic potential for preventing OSCC metastatic progression.

Low UFL1 expression synergized with anti-PD-1 therapy to prolong survival in orthotopic and spontaneous HCC models, whereas pharmacologic inhibition of CXCL8-CXCR1/2 signaling using SX-682 recapitulated these effects. Clinically, patients who responded to immunotherapy exhibited reduced UFL1, PRMT5 and CXCL8 expression; decreased neutrophil infiltration; elevated CD8+ T-cell activity; and lower serum CXCL8 levels. These findings reveal a UFL1-PRMT5-NF-κB p65-CXCL8 axis that governs neutrophil-driven immunosuppression and identify CXCL8 as both a predictive biomarker and therapeutic target to optimize immunotherapy in patients with HCC.

Comprehensive single-cell analysis identified selective chemokine recruitment signatures supporting γδ T-cell infiltration but revealed paradoxical corecruitment of immunosuppressive populations. Patient stratification through chemokine profiling, combined with γδ T-cell enrichment and targeted chemokine antagonism, represents a rational therapeutic strategy.

Pharmacological inhibition of the CXCR1/2 axis with reparixin effectively blocked OCM-mediated induction of both NFIX and FRY, suggesting that chemokine signaling initiates this pro-invasive loop. Collectively, these findings suggest that FRY is a macrophage-driven mediator of invasion and underscore its potential relevance in ovarian cancer.

Inhibition of SREBP2, pharmacological blockade of CXCL1, or perturbation of NETs markedly reduced PDAC growth in diabetic mouse models. Together, these multi-omics analyses and follow-up mechanistic studies constitute an integrated approach that elucidates a metabolic mechanism by which diabetes promotes PDAC development by remodeling the tumor immune microenvironment and highlights a potential therapeutic strategy for PDAC with DM.

This review establishes a unifying framework linking EBV-driven inflammation to neutrophil plasticity, NET biology, and NPC progression. Neutrophils are dynamic, targetable components with dual pro-tumor and anti-tumor roles. While neutrophil-related indices hold prognostic value, their clinical translation requires standardization and integration with other biomarkers. Targeting suppressive neutrophil programs and NETs offers promising strategies to improve therapeutic efficacy and overcome treatment resistance in NPC.

Finally, we outline actionable biomarkers, including transcriptomic signatures, plasma cytokine kinetics, myeloid/neutrophil metrics and spatial TME profiling, to stratify patients and guide dosing, sequencing and adaptive add-on strategies. Rational, biomarker-guided cytokine modulation offers a path to convert immune-excluded tumors into durable ICI responders.

The BsPNEC platform integrates tumor-targeted delivery, magnetic resonance imaging (MRI) contrast capabilities, and robust inhibition of tumor growth. Our findings present a synergistic immunotherapeutic strategy that simultaneously skews immunosuppressive TME and amplifies T cell immune response.

We outline current and emerging myeloid-reprogramming strategies-including PI3Kγ and CSF1-CSF1R targeting, TREM2 antagonism, COX-2-PGE2 blockade, and adenosine-axis inhibition-and their integration with PD-(L)1 therapy, alongside single-cell/spatial endpoints to quantify on-treatment remodeling. The purpose of this mini-review is to provide a mechanistic and technology-informed framework to reference rational trial design and clinical translation for overcoming checkpoint resistance in CRC.

Our findings highlight the versatility of FTPs in precise delivery of toxin payloads and provide a foundation for potential applications in antiviral and anticancer therapies targeting KSHV-associated diseases.

Our synthesis provides an appraisal of the evolving landscape of myeloid-informed precision immuno-oncology in HNSCC and outlines pragmatic standards and avenues for clinical translation. We hope these insights will assist researchers and clinicians as they endeavor to implement more effective, individualized regimens.