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Key Lipid Reprogramming Revealed in Gastric Signet Ring Cell Carcinoma by Spatial Mass Spectrometry Metabolomics

J Am Soc Mass Spectrom. 2025 Aug 6;36(8):1598-1608. doi: 10.1021/jasms.4c00505. Epub 2025 Jul 2.

ABSTRACT

Gastric signet ring cell carcinoma (GSRC) is an aggressive subtype of gastric cancer (GC) with a poor prognosis. The lack of a systematic molecular and metabolic heterogeneity overview has led to slow progress in clinical practice. This study used mass spectrometry imaging (MSI) to investigate the metabolic landscape of GSRC in GC tissue with various differentiation grades. Our comprehensive spatial profiling of metabolites and lipids unveiled distinct metabolic signatures across different tissue subregions. A substantial number of lipidomic biomarkers associated with GSRC were identified, including phosphatidylethanolamine N-methyl (PE-NMe), phosphatidylethanolamine (PE), sphingomyelin (SM), diacylglycerol (DG), phosphatidic acid (PA), and phosphatidylcholine (PC), which may provide insights into its pathogenesis and potential therapeutic targets. Furthermore, multi-omics network analysis revealed intricate metabolic pathways involved in GSRC progression. Our findings highlight the importance of understanding the metabolic heterogeneity of GSRC and pave the way for future studies exploring its clinical implications and therapeutic strategies.

PMID:40600435 | DOI:10.1021/jasms.4c00505

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Rescuing dendritic cell interstitial motility sustains antitumour immunity

Nature, Published online: 25 June 2025; doi:10.1038/s41586-025-09202-9

Disruption of dendritic cell (DC) interstitial motility in the tumour microenvironment promotes immune evasion, and enhancement of DC interstitial motility offers a route for DC-centric immunotherapy.
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Multi-omics models for predicting prognosis in non-small cell lung cancer patients following chemotherapy and radiotherapy: A multi-center study

Radiother Oncol. 2025 Jan 10;204:110715. doi: 10.1016/j.radonc.2025.110715. Online ahead of print.

ABSTRACT

BACKGROUND AND PURPOSE: Quantifying tumor heterogeneity from various dimensions is crucial for precise treatment. This study aimed to develop and validate multi-omics models based on the computed tomography images, pathological images, dose and clinical information to predict treatment response and overall survival of non-small cell lung cancer (NSCLC) patients undergoing chemotherapy and radiotherapy.

MATERIALS AND METHODS: This retrospective study included 220 NSCLC patients from three centers. Following feature extraction and selection, single-omics and multi-omics models were built for treatment response and overall survival prediction. The performance of treatment response models was evaluated using the area under the curve (AUC) and box plots. For overall survival analysis, the model's evaluation included AUC, concordance index (C-index), Kaplan-Meier curves, and calibration curves. Shapley values were used to assess the contribution of different features to multi-omics models.

RESULTS: Multi-omics models consistently exhibited superior discriminative ability compared to single-omics models in predicting both treatment response and overall survival. For treatment response, the three all-modality models achieved AUC values of 0.87, 0.91, and 0.82 in the external validation set, respectively. In overall survival analysis, the three all-modality models demonstrated AUC values and C-index of 0.73/0.72, 0.80/0.77, 0.79/0.78 in the external validation set, respectively.

CONCLUSION: Multi-omics prediction models demonstrated superior predictive ability with robustness and interpretability. By predicting treatment response and overall survival in NSCLC patients, these models have the potential to assist clinician optimizing treatment plans, supporting individualized treatment strategies, improving the tumor control probability and prolonging the patients' survival.

PMID:39800269 | DOI:10.1016/j.radonc.2025.110715

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ZNF655 accelerates progression of pancreatic cancer by promoting the binding of E2F1 and CDK1

Oncogenesis, Published online: 04 August 2022; doi:10.1038/s41389-022-00418-2

ZNF655 accelerates progression of pancreatic cancer by promoting the binding of E2F1 and CDK1
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