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Multi-Agent Agentic Graph Learning via Structural Signatures

10 September 2026 at 12:00
arXiv:2609.09565v1 Announce Type: new Abstract: Agentic graph learning (AGL) has recently achieved promising results on graph reasoning tasks, where an agent powered by a large language model (LLM) sequentially samples the graph as evidence to support its final prediction. Existing methods either employ a single agent or orchestrate multiple role-based agents to reason and learn over the entire graph, but both essentially rely on a shared reasoning policy across different graph regions, which can be suboptimal for graphs with heterogeneous structural and semantic patterns. Inspired by the progress of multi-agent collaboration on complex reasoning tasks, a natural remedy is to let multiple agents own different memory and collaborate; however, applying this paradigm to graphs directly faces two challenges. First, existing AGL methods typically verbalize graph structures into natural-language descriptions for LLM agents, making the reasoning process sensitive to the ordering of structural information and thereby breaking the permutation-invariant nature of graphs. Second, incorporating increasingly large sampled neighborhoods leads to rapidly growing contexts. To address these challenges, this paper introduces a multi-agent agentic graph learning (i.e., MAAGL) framework. MAAGL partitions the graph into communities and assigns an independent agent to each community for region-specific specialization. MAAGL represents structural and semantic evidence separately. Structural evidence is summarized by a dynamically updated structural signature that is permutation-invariant and fixed in size, while semantic evidence is filtered to the top-k nodes ranked by relevance. Based on historical trajectories with similar signatures, agents estimate their confidence and trigger debate-style collaboration when needed. Extensive experiments on four benchmark datasets show that MAAGL outperforms SOTA AGL methods.

Extracellular Vesicles in Osteosarcoma: Mechanisms, Diagnostics and Therapeutic Applications

20 March 2026 at 18:00

Drug Des Devel Ther. 2026 Jan 6;20:565059. doi: 10.2147/DDDT.S565059. eCollection 2026.

ABSTRACT

Osteosarcoma is a primary bone malignancy of adolescents and young adults with marked heterogeneity and a high metastatic propensity. Five-year survival exceeds 70% in localized disease but falls to about 20% with pulmonary metastasis or chemoresistance, and overall outcomes have plateaued for decades. Extracellular vesicles (EVs) have emerged as critical mediators of osteosarcoma progression and metastasis. EVs remodel the tumor microenvironment (TME) by promoting immune evasion, extracellular matrix reprogramming, and angiogenesis, while also facilitating invasion, epithelial-mesenchymal transition (EMT)-like plasticity, and formation of lung pre-metastatic niches through organotropic integrins and glycoproteins. Their cargo, including proteins, lipids, and nucleic acids, drives intercellular communication that sustains proliferation, migration, and therapy resistance under metabolic or hypoxic stress. Clinically, the stability of EVs in body fluids and their tumor-specific molecular signatures highlight their promise as liquid-biopsy biomarkers for early diagnosis, prognosis, and treatment monitoring. Therapeutically, EVs are being engineered as delivery vehicles for drugs or RNA therapeutics, and interventions targeting their biogenesis, cargo sorting, or uptake are under exploration. Future research should integrate single-EV multi-omics, longitudinal cohort validation, and causal perturbation models to delineate functional mechanisms. Rational strategies that modulate EV dynamics and incorporate standardized analytic pipelines may transform EVs into actionable biomarkers and therapeutic targets, offering new avenues to overcome resistance and improve clinical outcomes in osteosarcoma.

PMID:41858917 | PMC:PMC12998350 | DOI:10.2147/DDDT.S565059

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