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cs.AI, q-bio.NC updates on arXiv.org
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Modality-Decoupled Federated Learning for Privacy-Preserving Embodied Intelligence in 6G
arXiv:2609.09591v1 Announce Type: cross Abstract: Sixth-generation (6G) wireless networks are expected to provide a key infrastructure for large-scale embodied intelligence, where heterogeneous robots collaborate through low-latency connectivity, edge intelligence, and distributed sensing. Vision-language-action (VLA) models offer a foundation by integrating visual perception, language understanding, and action generation into a unified closed-loop policy. However, training and adapting VLA mod
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(Multiomics OR Omics) AND (Pancreatic)
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CAFs shape the immunosuppressive microenvironment of pancreatic cancer through the Lin28b-STING Axis
Nat Commun. 2026 Aug 7;17(1):9491. doi: 10.1038/s41467-026-76495-3.ABSTRACTCancer-associated fibroblasts comprise diverse functionally distinct cellular subsets, with certain subpopulations exerting pivotal influence in shaping the pancreatic cancer immune microenvironment. Here we show that Lin28b+ cancer-associated fibroblasts contribute to establishing an immunologically cold tumor microenvironment in pancreatic ductal adenocarcinoma. Mechanistically, Lin28b directly binds to STING mRNA and p
CAFs shape the immunosuppressive microenvironment of pancreatic cancer through the Lin28b-STING Axis
Nat Commun. 2026 Aug 7;17(1):9491. doi: 10.1038/s41467-026-76495-3.
ABSTRACT
Cancer-associated fibroblasts comprise diverse functionally distinct cellular subsets, with certain subpopulations exerting pivotal influence in shaping the pancreatic cancer immune microenvironment. Here we show that Lin28b+ cancer-associated fibroblasts contribute to establishing an immunologically cold tumor microenvironment in pancreatic ductal adenocarcinoma. Mechanistically, Lin28b directly binds to STING mRNA and promotes its degradation, thereby suppressing STING expression and downstream type I interferon signaling. Loss of Lin28b in cancer-associated fibroblasts activates the cGAS-STING-interferon signaling cascade, enhancing dendritic cell antigen presentation and CD8+ T cell cytotoxic function. Importantly, genetic inhibition of Lin28b in cancer-associated fibroblasts enhances sensitivity to anti-PD-L1 immune checkpoint blockade therapy. These findings reveal that targeting the Lin28b-STING axis represents a promising therapeutic strategy for overcoming the intrinsic resistance of pancreatic ductal adenocarcinoma to immunotherapy.
PMID:42693143 | PMC:PMC13542369 | DOI:10.1038/s41467-026-76495-3