SLC40A1 (Solute Carrier Family 40 Member 1)

These findings suggest that dysregulated gene expression may contribute to the activation of stromal cells and macrophages within the spleen, facilitating malignant transformation. Overall, these findings deliver novel transcriptomic insights into canine splenic tumorigenesis that may improve diagnostic precision, inform prognostic assessment, and support the development of targeted therapeutic strategies in veterinary oncology.

These findings identify SLC40A1 as a key regulator of the antitumor immune response in EOC. High SLC40A1 expression is associated with enhanced macrophage-mediated tumor suppression and improved response to immunotherapy, highlighting its potential as both a prognostic biomarker and a therapeutic target.

METTL14 knockdown remits HG-induced HK-2 cell apoptosis, inflammation, and ferroptosis via promoting SLC40A1. In addition, E2F4 enhances SLC40A1 transcription. This research provides new potential targets and insights for the treatment of DN.

Therapeutically, administration of an AGR2-targeting peptide synergizes with ferroptosis inducers, significantly enhancing cell death in PDAC models. Our findings not only elucidate a novel AGR2/p53/FPN1 regulatory axis in ferroptosis control but also propose innovative combination strategies for pancreatic cancer treatment.

Our findings reveal that high expression of LGALS9 suppresses T cell function, fosters a strongly immunosuppressive tumor microenvironment, and is associated with chemotherapy resistance, ineffective immunotherapy, and poor prognosis. LGALS9 may serve as a biomarker for predicting immunotherapy response. This knowledge has the potential to facilitate early diagnosis, precise molecular typing, accurate prognosis evaluation, and the development of personalized treatment strategies that can overcome tumor drug resistance and improve patient outcomes.

SLC40A1 upregulation enhanced the inhibitory effect of APS on immune escape in CC. APS inhibits immune escape of CC by targeting NR3C2 and activating SLC40A1.

Thus, this study highlights potential avenues for NHL therapy tailored by EBV status and provides a unique resource to examine tumor-TME interactions in the HIV-immunocompromised context. Spatial transcriptomic landscapes resolve cell-of-origin- and EBV-associated HIV-NHL heterogeneity including immunosuppressive myeloid responses to EBV+ tumorsSpatial gradients including CXCL12 and CXCL13 indicate that tumor-stromal interactions mimic lymphoid tissue organization and depend on B cell development stageDevelopment of a direction-agnostic method to calculate spatial expression gradients relative to annotated tissue and cell types of interest Predicted pharmacologic vulnerabilities in clinical samples are replicated in vitro and confirmed by small molecule screening.

Although preclinical studies suggest that iron metabolism and inflammatory signalling form an interconnected axis closely linked to CRC, translating this pathway into reliable clinical biomarkers and effective therapeutic strategies remains a significant challenge. Future biomarker-guided clinical trials are essential to determine the clinical relevance and to establish precision medicine strategies targeting the iron-inflammation crosstalk in CRC.

Our findings establish a PDO-T cell platform for precision immunotherapy screening and identify JIB04 as a promising epigenetic agent that induces ferroptosis and sensitizes PDAC to immune checkpoint blockade. This ferroptosis-based reprogramming provides a potential strategy to overcome resistance and improve clinical outcomes in PDAC.

ID is closely associated with aggressive tumor biology, suboptimal response to neoadjuvant therapy, and impaired postoperative recovery. Dysregulation of iron homeostasis and ferroptosis pathways in ID patients may contribute to CRC progression. These findings highlight ID as a potential biomarker for risk stratification and suggest that targeting iron metabolism could improve therapeutic outcomes in CRC management.

This study identifies key α-HB-related targets and biomarkers for sepsis, offering new insights into its pathophysiology. The findings highlight the potential of α-HB in modulating immune responses and suggest that α-HB-related targets could serve as promising therapeutic targets for sepsis management.

CRC with enriched CCL20+ and APOE+ TAMs were characterized by high prevalence of deficient-mismatch repair (27.9%) and might achieve more benefit from immunotherapy. This single-cell study established an accurate classification system of CRC TAMs, unveiling their diverse roles in modulating tumor biology and assisting in treatment options of CRC patients.