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Label-Guided Knowledge Distillation for 3D-CNNs in Action Recognition
Treatment with quercetin inhibits SARS-CoV-2 N protein-induced acute kidney injury by blocking Smad3-dependent G1 cell-cycle arrest
FoodMonitor: Benchmarking MLLMs for Explainable Compliance Analysis
Circulating Tumor Cells in Pancreatic Ductal Adenocarcinoma: The Systemic Execution Hub of Metastasis
Pharmacol Res. 2026 May 17:108253. doi: 10.1016/j.phrs.2026.108253. Online ahead of print.
ABSTRACT
Pancreatic ductal adenocarcinoma (PDAC) exemplifies early systemic dissemination, with circulating tumor cells (CTCs) at its core. We advance a unified conceptual framework that positions CTCs as the systemic execution hub of PDAC metastasis, dynamic entity that coordinates the metastatic cascade via four cardinal functions: Seeding, Adapting, Engineering, and Signaling. Integrating eco-evolutionary dynamics, this hub actively drives phenotypic selection, niche remodeling, and immune evasion, while providing real-time biologic intelligence through liquid biopsy. Robust clinical correlation has not yet translated into routine practice because of technical variability, biological complexity, and a lack of interventional evidence. We therefore propose an evidence-driven, phased roadmap: grounded in prospective clinical cohort data, progressing from immediate multi-center technical standardization and pragmatic trials, such as minimal residual disease (MRD)-triggered salvage therapy, to mid-term biomarker-driven adjuvant trials and long-term integration into multimodal liquid biopsy ecosystems, aimed at intercepting this execution hub. By reframing CTCs from correlative indicators to actionable therapeutic targets and dynamic sentinels, this framework charts a path toward transforming the management of this recalcitrant systemic disease.
PMID:42150733 | DOI:10.1016/j.phrs.2026.108253
Refined immune-based molecular subtypes of gastric cancer: Integrating mismatch repair status and tumor microenvironment for enhanced immunotherapy prediction
Chin J Cancer Res. 2026 Apr 30;38(2):234-251. doi: 10.21147/j.issn.1000-9604.2026.02.09.
ABSTRACT
OBJECTIVE: Gastric cancer (GC) is heterogeneous, and current mismatch repair (MMR)-based classifications incompletely predict response to immune checkpoint inhibitors (ICIs).
METHODS: RNA sequencing (RNA-seq) and immune infiltration profiles from 189 resected GC were used to derive four refined immune-MMR subtypes (R1-R4) by integrating MMR status, survival, and tumor microenvironment (TME) features. Multi-omics profiling and pathway analysis defined subtype biology. External transcriptomic cohorts and an ICI-treated cohort were classified with Nearest Template Prediction (NTP). Immune response-associated genes were identified from responder vs. non-responder comparisons within the ICI-sensitive subtype and validated by multiplex immunohistochemistry (mIHC).
RESULTS: R1 showed the best prognosis and highest immunotherapy response with objective response rate (ORR) 54.5%, while R4 had the worst prognosis. R2 represented an immune-unresponsive deficient mismatch repair (dMMR) subset, and R3 captured an immune-active proficient mismatch repair (pMMR) subgroup with moderate therapy sensitivity. Multi-omics integration revealed subtype-specific pathways (e.g., ECM remodeling in R1, metabolic reprogramming in R2). Reclassification of pMMR tumors based on transcriptional similarity to R1 identified a New R3 subset with enhanced immune features and higher ICI response. Eight immune response-associated genes (e.g., CXCL10, CXCL11, ELN, GAD1, IL32, MT1E, OR2I1P, SLC3A1) were identified and validated by mIHC for predictive relevance.
CONCLUSIONS: This immune-based molecular framework refines risk stratification beyond conventional MMR categories, identifies ICI-sensitive subsets among both dMMR and pMMR tumors, and proposes candidate biomarkers for patient selection.
PMID:42147371 | PMC:PMC13171420 | DOI:10.21147/j.issn.1000-9604.2026.02.09