Our study reveals a previously unrecognized CaMK2A-ZDHHC3-GPX4 signaling axis that couples ferroptosis resistance to immunosuppressive TAM polarization. Targeting GPX4 or disrupting exosomal CaMK2A signaling may reprogram the TME and potentiate immune checkpoint therapy in GC.

Notably, combining Cu-R837@CM with PD-L1 blockade achieved complete tumor regression and significantly prolonged survival. Collectively, Cu-R837@CM offers a clinically translatable nanoadjuvant paradigm that integrates cuproptosis-driven cGAS-STING activation with TLR7 co-stimulation for hepatocellular carcinoma immunotherapy.

After which, the patient received two cycles of immunotherapy with durvalumab, and received continued administration with anlotinib; follow-up evaluation revealed a partial response. At present, the patient remains alive with no evidence of disease progression, achieving a progression-free survival of >42 months. The present case report highlights the potential of immunotherapy combined with anti-angiogenic targeted therapy in treating PD-L1-positive mediastinal SC, despite the life-threatening adverse reactions, offering a viable treatment option for similar clinical cases.

Tumor cell-intrinsic regulators govern ferroptosis sensitivity and, in turn, can influence the success of immune-mediated tumor control. Here, we discuss the growing understanding of regulation of ferroptosis and examine the complex interplay between tumor cell-intrinsic ferroptosis pathways and the host immune response, with an emphasis on how ferroptosis might be leveraged to potentiate immunotherapy efficacy.

Our multimodal analyses highlight key differences between irAEs and CIDs, indicating that irAEs constitute a distinct inflammatory ecosystem that differentiates them from CIDs. Our study provides insights into potential biomarkers and therapeutic targets for improved irAE management.

This study established an interpretable ERlncRNA-based prognostic framework for melanoma and highlighted the biological and clinical relevance of ER stress-related lncRNAs. These findings provide insights into tumor heterogeneity, immune-related characteristics, and potential therapeutic stratification in melanoma, and suggest that selected ERlncRNAs may contribute to melanoma progression partly through modulation of ER stress-associated apoptotic signaling.

Functional assays showed that high HMGA1 expression conferred sensitivity to metabolic inhibitors but resistance to proteasome inhibitors, while HMGA1 knockout suppressed tumor growth and enhanced anti-PD-1 efficacy. By integrating bulk modeling with spatial validation, this study establishes a GC-mitophagy-based classification and highlights HMGA1 as a promising biomarker for prognostic stratification and personalized immunotherapy in LUAD.

In an in vivo experiment, dBsAb demonstrated a 68% reduction in tumor growth, with increased macrophage infiltration, M1 polarization, and elevated antigen presentation without observable systemic toxicity. This chemical assembly approach offers a practical alternative to recombinant methods for constructing bispecific antibodies and may facilitate the development of macrophage-directed immunotherapies.

BC remains the most frequently diagnosed malignancy among women worldwide and a major cause of cancer-related death. We systematically mapped the knowledge structure and development trends of CAR-T research in BC, identifying major research contributors and emerging research hotspots, which may provide valuable insights for future basic research and clinical exploration in this field.

In LONESTAR, serial SCENT-inferred PD-L1 status showed a borderline association with 3-month progression without paired post-treatment tissue confirmation. SCENT is a generalizable CT-based virtual biopsy for baseline PD-L1 prediction and complementary tissue IHC stratification, with longitudinal use requiring prospective validation.

As a result, this nano-pyroptosis inducer overcomes resistance to anti-PD-1 therapy, triggering potent systemic anti-tumor immunity and significantly inhibiting tumor growth. Overall, our findings establish a novel therapeutic paradigm for reversing ICB resistance via orchestrated pyroptosis amplification.

Our study uncovers how cancer cell plasticity shapes spatially organized tumor-immune ecosystems that critically modulate adjuvant ICI efficacy in melanoma. These findings highlight melanoma cell plasticity as a key driver of immune evasion via macrophages reprogramming, through targetable interactions that may represent novel therapeutic avenues to enhance ICI efficacy.