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Advancing Graph Few-Shot Learning via In-Context Learning

arXiv:2605.24410v1 Announce Type: new Abstract: Graph few-shot learning, which aims to classify nodes from novel classes with only a few labeled examples, is a widely studied problem in graph learning. However, existing methods often face two key limitations. First, the predominant graph few-shot learning paradigm relies on supervised tasks, failing to leverage the vast number of unlabeled nodes in the graph. Second, many approaches require complex task adaptation or fine-tuning during inference, limiting their efficiency and applicability. Inspired by the powerful in-context learning capabilities of large language models, we propose a novel model named VISION for adVancIng graph few-Shot learning via In-cOntext LearNing to address these challenges. Our model reframes graph few-shot learning as a fine-tuning-free sequence reasoning problem. At its core is a context-aware network that initializes nodes with role embeddings and employs a dual-context fusion module to synergistically integrate local topological structures and global task-level dependencies. This allows our model to dynamically generate class-aware representations for the query set conditioned on the support set context in a single forward pass. To effectively train our model, we introduce an unsupervised task generator that creates structure-adaptive features and constructs diverse pseudo-tasks from abundant unlabeled data. Our method unifies unsupervised meta-learning with graph in-context learning, achieving efficient inference. Extensive experiments on multiple benchmark datasets demonstrate the superiority of our model. Our public code can be found

Multi-omics integration identifies ribosome biogenesis-active macrophage subpopulation and its key gene GNL2 in driving liver hepatocellular carcinoma progression and mechanisms

14 May 2026 at 18:00

Cancer Cell Int. 2026 May 14. doi: 10.1186/s12935-026-04330-2. Online ahead of print.

ABSTRACT

BACKGROUND: Liver hepatocellular carcinoma (LIHC) is a common malignancy, yet the core genes driving its progression and potential therapeutic targets remain insufficiently explored. Ribosome biogenesis (RB) is a critical biological process linked to various cancers; however, its systematic role in LIHC remains unclear.

METHODS: This study integrated LIHC single-cell RNA-Seq, bulk RNA-Seq, and spatial transcriptomic data with ribosome biogenesis-related gene sets to construct a single-cell atlas of LIHC. Weighted Gene Co-expression Network Analysis (WGCNA) was employed to characterize myeloid cell subsets. Furthermore, an LIHC prognostic risk model based on RB-related genes was developed using 117 machine-learning algorithm combinations. Key findings were subsequently corroborated through experimental validation and clinical sample analysis.

RESULTS: We identified a distinct macrophage subpopulation with high ribosome biogenesis activity, termed ribosome biogenesis-active macrophages (RAMs). These cells exhibited strong communication with inflammatory macrophages, potentially mediated by MIF-related receptor-ligand interactions. We further constructed an 8-gene prognostic model (PA2G4, GNL2, PWP1, DDX49, NOC4L, GDI2, CST7, and RCL1), which showed good predictive performance. Drug sensitivity analysis suggested that the high-risk group may be more responsive to several agents, including docetaxel. Among these genes, GNL2 was selected for further investigation. Elevated GNL2 expression was associated with increased stemness features in myeloid cells. Molecular docking analysis identified several candidate compounds with potential binding affinity to GNL2. Functionally, GNL2 knockdown in macrophages reduced TGF-Ξ² and TNF-Ξ± expression and was associated with decreased proliferation, migration, and invasion of LIHC cells.

CONCLUSION: We identified a highly active ribosome biogenesis-macrophage subpopulation (RAM), and constructed a robust risk model to aid in the diagnosis, prognosis, and treatment of LIHC. GNL2 is associated with increased expression of TGF-Ξ² and TNF-Ξ± and may contribute to LIHC progression.

PMID:42135716 | DOI:10.1186/s12935-026-04330-2

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