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What Are We Actually Decoding? Source Attribution for Non-Invasive Brain-to-Language Retrieval
Rethinking Federated Unlearning via the Lens of Memorization
HoloFair: Unified T2I Fairness Evaluation and Fair-GRPO Debiasing
Selective Test-Time Compute Scaling for Click-Through Rate Prediction via Uncertainty-Triggered Feature Path Exploration
Test-Time Self-Adaptive Conditioning for Stable Audio-Driven Talking-Head Generation
IPR-1: Interactive Physical Reasoner
All Leaks Count, Some Count More: Interpretable Temporal Contamination Detection and Mitigation in LLM Backtesting
AutoResearchClaw: Self-Reinforcing Autonomous Research with Human-AI Collaboration
Advancing solar and wind penetration in China through energy complementarity
Nature, Published online: 20 May 2026; doi:10.1038/s41586-026-10570-z
Using high-resolution satellite imagery combined with a deep-learning-based framework to build a national energy inventory enables a data-driven assessment of solar–wind complementarity strategies to reduce power variability and enhance renewable energy penetration across China.EBV strain interacts with host HLA to drive nasopharyngeal carcinoma risk
Nature, Published online: 15 April 2026; doi:10.1038/s41586-026-10416-8
A genome-to-genome association study identifies host and viral risk factors that interact to drive nasopharyngeal carcinoma endemicity in southern China.GPNMB Drives Brain Metastasis by Sculpting a Pathological Endothelial-Immune Interactome
Cancer Discov. 2026 Apr 15. doi: 10.1158/2159-8290.CD-25-1663. Online ahead of print.
ABSTRACT
Brain metastases (BM) remain a devastating disease with dismal prognosis. How circulating tumor cells (CTCs) penetrate the blood brain barrier (BBB) and reprogram the brain microenvironment remain unclear. Using spatially resolved multi-omic profiling of CTCs and brain metastases, integrated with experimental and clinical analyses, we identified Glycoprotein Non-Metastatic Melanoma Protein B (GPNMB) as a CTC-secreted driver of vascular disruption and brain colonization. CBX3 upregulation induced GPNMB expression, which bound endothelial EGFR, triggering CBL-mediated ubiquitination and degradation. Attenuated EGFR signaling suppressed FTO and disrupted endothelial junctions via YTHDF2-dependent TJP1 m6A methylation. Remarkably, GPNMB-induced BBB remodeling promoted immune infiltration via CXCL12-CXCR4 axis, and induced time course-dependent T cell exhaustion within the brain microenvironment. Clinically, elevated CBX3⁺GPNMB⁺ CTCs and plasma CXCL12 were significantly associated with BM progression in lung cancer and melanoma. Therapeutically, dual blockade of GPNMB and PD1 enhanced anti-BM efficacy in mice, unveiling GPNMB as a promising target for precision immunotherapy.
PMID:41973996 | DOI:10.1158/2159-8290.CD-25-1663