Background: The composition of the gut microbiota is associated with the response to immunotherapy for different cancers. However, the majority of previous studies have focused on a single cancer and a single immune checkpoint inhibitor. Here, we investigated the relationship between the gut microbiota and the clinical response to anti-programmed cell death protein 1 (PD-1) immunotherapy in patients with advanced cancers. Method: In this comprehensive study, 16S rRNA sequencing was performed on the gut microbiota of pre-immunotherapy and post-immunotherapy, of 72 advanced cancer patients in China. Results: At the phylum level, Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria were the main components of the microbiota in the 72 advanced cancer patients. At the genus level, Bacteroides and Prevotella were the dominant microbiota among these 72 patients. The PD_whole_tree, Chao1, Observed_species and Shannon indices of R.0 and R.T were higher than those of NR.0 and NR.T. The results of LEfSe showed that Archaea, Lentisphaerae, Victivallaceae, Victivallales, Lentisphaeria, Methanobacteriaceae, Methanobacteria, Euryarchaeota, Methanobrevibacter, and Methanobacteriales were significantly enriched in the response group before immunotherapy (R.0), and the Clostridiaceae was significantly enriched in the non-response group before immunotherapy (NR.0) (p < 0.05). Lachnospiraceae and Thermus were significantly enriched in the response group after immunotherapy (R.T), and Leuconostoc was significantly enriched in R.0 (p < 0.05). ROC analysis showed that the microbiota of R.T (AUC = 0.70) had obvious diagnostic value in differentiating Chinese cancer patients based on their response to immunotherapy. Conclusions: We demonstrated that the gut microbiota was associated with the clinical response to anti-PD-1 immunotherapy in cancer patients. Taxonomic signatures enriched in responders were effective biomarkers to predict the clinical response. Our findings provide a new strategy to improve the efficiency of responses to immunotherapy among cancer patients.

This study aimed to investigate the prognostic value of volumetric parameters on 18F- fluoro-2-deoxy-D-glucose (18F-FDG) positron emission tomography/computed tomography (PET/CT) in gastric-cancer patients, according to the expression status of c-MET (MET proto-oncogene, receptor tyrosine kinase), which was previously unclear. The study included 61 patients with advanced gastric cancer. Data on the baseline 18F-FDG PET/CT, clinical-pathological information, progression-free survival (PFS), and overall survival (OS) were collected. The maximum standardized uptake value (SUVmax), peak SUV (SUVpeak), metabolic tumor volume (MTV), and total lesion glycolysis (TLG) of gastric tumors in situ were measured on PET/CT. The expression status of c-MET was recorded based on immunohistochemical staining. Associations between the parameters on PET/CT and patients’ survival outcomes were analyzed in relation to expression status of c-MET. Patients with positive c-MET expression had significantly shorter PFS (11.5 vs. 17.6 months, P = 0.039) and OS (17.0 vs. 24.3 months, P = 0.043), and had gastric tumors with a larger MTV (70.8 ± 53.11 vs. 41.1 ± 52.32, P = 0.034) and TLG (428.39 ± 442.95 vs. 205.7 ± 354.40, P = 0.039), compared with those with negative c-MET expression. However, SUVmax (9.6 ± 7.40 vs. 8.0 ± 4.91, P = 0.335) and SUVpeak (7.7 ± 5.99 vs. 6.62 ± 4.08, P = 0.438) were similar between these two patient groups. In patients with c-MET-positive tumors, MTV and TLG were independent factors in predicting patient OS after correction by distant metastasis (hazards ratio = 1.014 and 1.002, respectively; P = 0.024 and 0.027, respectively), while these associations were not significant in patients with c-MET-negative tumors. Patients with c-MET-positive gastric cancer had higher MTV and TLG values compared to those with c-MET-negative gastric cancer. In patients with c-MET-positive gastric cancer, volumetric parameters on 18F-FDG PET/CT have prognostic value for patient overall survival.

Introduction: To compare the prognosis of adjuvant SOX (S-1 and oxaliplatin) vs XELOX (capecitabine and oxaliplatin) chemotherapy in Chinese patients with gastric cancer (GC) after D2 gastrectomy. Methods: This was a real-world study of patients with GC (stages II–III) who underwent D2 gastrectomy and received adjuvant SOX or XELOX between 01/2010 and 06/2017 in Zhongshan Hospital affiliated to Fudan University. The patients were matched by propensity score matching. The primary and secondary endpoints were disease-free survival (DFS) and overall survival (OS), respectively. Adverse events (AEs) were compared. Results: A total of 552 patients were included. The median follow-up time was 24.9 months. There were no differences in DFS (median, 44.4 vs 41.2 months; HR=1.17, 95% CI: 0.92– 1.48) and OS (median, 61.5 vs 65.3 months; HR=1.01, 95% CI: 0.73– 1.39) between the XELOX and SOX groups. Both DFS and OS had no significant differences between SOX and XELOX for all subgroups based on sex (P=0.949, P=0.990), age (P=0.303, P=0.392), Lauren type (P=0.362, P=0.573), type of gastrectomy (P=0.607 P=0.989), and pathological TNM stage (P=0.899, P=0.888). A total of 86 patients in the SOX subgroup (34.2%) experienced AEs, similar to the rate found in the XELOX subgroup (104 patients or 41.4%; P=0.098). Discussion: The results suggested that adjuvant SOX chemotherapy has similar survival benefits compared to XELOX chemotherapy in Chinese patients with pathological stage II or III GC after D2 gastrectomy.

Metal ions are key regulators of the neuro–immune–tumor axis. Recent studies provide concrete evidence that neuronal Ca ²⁺ pulses drive tumor–neuron integration and shape immune signaling. Synaptic Zn ²⁺ and ZIP transporters modulate synaptic transmission and tumor growth. Tumor iron accumulation fuels proliferation while creating a clear ferroptosis vulnerability. Copper promotes angiogenesis, lysyl oxidase (LOX)‐mediated extracellular matrix (ECM) remodeling and metastasis, and implicates cuproptosis as a therapeutic target. Mn potentiates cyclic GMP‐AMP synthase (cGAS)–STING signaling and serves as both an immune adjuvant and manganese‐enhanced magnetic resonance imaging (MEMRI) contrast. Besides, Mg and K ⁺ regulate kinase/T‐cell receptor (TCR) function and tumor–neuron excitability, respectively. Despite these advances, major gaps persist, notably limited spatial and temporal mapping of labile metal pools, a paucity of cell‐type‐specific causal perturbations, and underdeveloped tumor‐targeted metal‐modulating therapies with proven safety. We therefore propose a focused research agenda: integrate spatial metallomics with single‐cell multiomics, deploy metal‐sensitive longitudinal imaging, apply conditional genetic and chemogenetic perturbations and organotypic models to dissect neuro–immune cross‐talk, and implement preclinical pipelines emphasizing tumor‐selective delivery and comprehensive safety testing.