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$M^3-Verse$: A "Spot the Difference" Challenge for Large Multimodal Models
Bottom-Up Synthesis of Molecular Nanodiamond from Nanographene
Nature, Published online: 26 May 2026; doi:10.1038/s41586-026-10669-3
Bottom-Up Synthesis of Molecular Nanodiamond from NanographeneFDX1 as a predictive biomarker and therapeutic target for lymph node metastasis in gastric cancer
Clin Exp Med. 2026 May 10. doi: 10.1007/s10238-026-02160-0. Online ahead of print.
ABSTRACT
The prognostic values of cuproptosis-related genes (CRGs) in gastric cancer with lymph node metastasis (GCLM), especially in the tumor immune microenvironment (TIME), remain unclear. We analyzed the expression, mutation, immunity, drug sensitivity, and prognostic value of CRGs in GCLM using TCGA and GEO cohorts. Consensus clustering was performed to identify CRG subtypes, with differences characterized by multi-omics analysis. A CRG-based prognostic risk score and immune score were constructed for individualized assessment, and the role of CRGs was validated through in vitro and in vivo experiments. Consensus clustering revealed that CRGs were significantly enriched in biological processes related to mitosis and energy metabolism, as well as in immune-related and cancer-associated pathways. Four distinct CRG subtypes were identified, showing marked differences in expression profiles, prognosis, genetic alterations, TIME, and chemotherapeutic drug sensitivity. We developed an exploratory CRG-based prognostic risk score for preliminary individualized assessment, and the functional relevance of CRGs in GCLM was further validated through in vitro experiments. Among these, FDX1, LIAS, DLAT, MTF1, and GLS were identified as key determinants of overall survival in patients with GCLM, with FDX1 emerging as a potential independent prognostic factor. Notably, upregulation of FDX1 significantly suppressed lymph node metastasis of gastric cancer cells in a mouse popliteal lymph node metastasis model. Our data uncovers FDX1 might be a potential favorable prognostic factors in GCLM patients. These findings may improve our understanding of CRGs in GCLM and provide new in-sights for assessing prognosis and developing more effective treatment strategies.
PMID:42107026 | DOI:10.1007/s10238-026-02160-0
CoMaTrack: Competitive Multi-Agent Game-Theoretic Tracking with Vision-Language-Action Models
InCoder-32B: Code Foundation Model for Industrial Scenarios
Targeting sialic acid metabolism: a therapeutic strategy against gastric cancer driven by WZ35
Cell Oncol (Dordr). 2026 Mar 23;49(2):60. doi: 10.1007/s13402-026-01194-6.
ABSTRACT
Glycolytic reprogramming is closely associated with the occurrence and progression of gastric cancer. Specifically, the energy derived from glucose metabolism and the cellular proteins by its intermediate products influence gastric cancer development. However, as an important branch of glucose metabolism, sialic acid metabolism and its mediated sialylation modifications remain insufficiently studied in gastric cancer, and their specific relationship with malignant tumor progression requires further exploration. This study employed a multi‑omics approach, integrating metabolomics, single‑cell RNA sequencing, and bulk RNA sequencing analyses, to investigate the metabolic landscape of gastric cancer and its associated alterations. The results indicated that sialic acid is a characteristic metabolite in malignant gastric cancer tissues. It modulates biological functions such as immune response, proliferative activity, and metabolic remodeling within gastric cancer tissues by influencing sialylation modifications. Furthermore, we identified the drug WZ35, which can inhibit the malignant proliferation of gastric cancer by targeting both sialic acid metabolism and sialylated protein modifications. We put forward a conjecture that the metabolism and modification of sialic acid promote the malignant development of gastric cancer, and we discovered that the drug WZ35 has an inhibitory effect on the sialic acid metabolism of gastric cancer.
GRAPHICAL ABSTRACT:
PMID:41870836 | PMC:PMC13009457 | DOI:10.1007/s13402-026-01194-6
CoMaTrack: Competitive Multi-Agent Game-Theoretic Tracking with Vision-Language-Action Models
Targeting sialic acid metabolism: a therapeutic strategy against gastric cancer driven by WZ35
Cell Oncol (Dordr). 2026 Mar 23;49(2):60. doi: 10.1007/s13402-026-01194-6.
NO ABSTRACT
PMID:41870836 | DOI:10.1007/s13402-026-01194-6
MovieTeller: Tool-augmented Movie Synopsis with ID Consistent Progressive Abstraction
Narrative Weaver: Towards Controllable Long-Range Visual Consistency with Multi-Modal Conditioning
Unraveling the Link Between Azathioprine and Acute Pancreatitis: Integrating Network Toxicology, Machine Learning, and Mendelian Randomization
CPT Pharmacometrics Syst Pharmacol. 2026 Mar;15(3):e70178. doi: 10.1002/psp4.70178.
ABSTRACT
Azathioprine (AZA), a widely used immunosuppressant, can induce acute pancreatitis (AP), yet the underlying molecular mechanisms remain unclear. This study employed an integrative multiomics strategy-combining network toxicology, machine learning, Mendelian randomization (MR), and molecular docking-to elucidate the biological basis of AZA-induced AP. AZA-associated genes were first identified through bioinformatics databases and analyzed using protein-protein interaction networks and GO/KEGG functional enrichment. Least absolute shrinkage and selection operator (LASSO) regression and support vector machine recursive feature elimination (SVM-RFE) were applied to prioritize key differentially expressed genes for diagnostic modeling. MR was then used to examine potential causal links between gene expression and AP risk, followed by molecular docking to assess AZA-protein interactions. Sixty-eight candidate genes related to AZA-induced AP were identified. Enrichment analyses indicated involvement in lipid metabolic regulation, inflammatory pathways, and energy homeostasis. Machine learning highlighted seven key genes-CES1, CTSK, JAK1, NR3C2, PLIN5, WEE1, and RORA-as central to AP development. MR analysis further demonstrated that decreased expression of CES1 and CTSK may mediate AZA-related AP susceptibility. Docking simulations revealed strong, specific binding between AZA and both CES1 and CTSK. Overall, this study identifies CES1 and CTSK as genetically protective factors and mechanistic mediators in AZA-triggered AP. These findings offer new molecular insights into the genomic and biochemical pathways underlying this adverse drug reaction.
PMID:41832938 | DOI:10.1002/psp4.70178
Risk-adaptive therapy guided by dynamic ctDNA in nasopharyngeal carcinoma
Nature, Published online: 11 March 2026; doi:10.1038/s41586-026-10244-w
A clinical trial testing whether monitoring ctDNA clearance during treatment for nasopharyngeal cancer could be used to inform decisions about an individual’s subsequent therapeutic programme shows promising results.