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The Menu Is an Execution Prior: State-Path Tool Menus for Online Agents

arXiv:2609.09395v1 Announce Type: new Abstract: Language models act through tools, yet practical agents face libraries containing thousands of interfaces. We introduce the tool menu as the short, ordered subset of available tools shown to an agent before execution. The agent can call only tools in this menu. Multi-step tasks require the final action and the prerequisite tools that create its inputs in a usable order. Current constructors rank tools by request relevance, which can surface the final action while omitting or delaying less obvious producers. We introduce the state path, a pre-execution route from the observable request state to the desired outcome, and propose State-Path Tool Menu to learn it. Our framework treats the menu as an execution prior over these routes. Its encoder represents which tools can run from the current state, how their outputs satisfy later inputs, and which orders recur in training paths. A retriever covers an executable entry, the missing-input producers, and the final action. A reranker then places producers before consumers. On ToolBench, our menu raises online success from 0.737 to 0.898 and outperforms retrieval, reranking, generation, and routing baselines without changing the agent. The State-Path menu also covers more complete chains with 32 tools than the official list covers with 128, and its success gain persists across executor families with different model capacities. Our code is at https://github.com/Met2348/State-Path.
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Integrative Pan-Cancer Characterization of lncRNA UPK1A-AS1 and Its Role in Hypoxia-Associated Sorafenib Resistance in Hepatocellular Carcinoma

Anal Cell Pathol (Amst). 2026;2026(1):e1554526. doi: 10.1155/ancp/1554526.

ABSTRACT

Long noncoding RNAs (lncRNAs) are emerging as critical regulators of tumor initiation and progression through transcriptional and posttranscriptional mechanisms. UPK1A antisense RNA 1 (UPK1A-AS1), a cancer-associated lncRNA, has been reported to participate in oncogenic processes; however, its overall landscape across human malignancies and its biological role in therapy resistance remain poorly understood. Given the increasing importance of identifying functional lncRNAs with prognostic and therapeutic potential, this study presents a comprehensive multiomics characterization of UPK1A-AS1 and its experimental validation in hepatocellular carcinoma (HCC). We integrated datasets from The Cancer Genome Atlas (TCGA), the Genotype-Tissue Expression Project (GTEx), the cancer immunology data engine (CIDE), and the cBioPortal for cancer genomics (cBioPortal) to systematically assess its expression pattern, genomic alterations, clinical significance, and immunological associations. Our analyses revealed that UPK1A-AS1 is significantly upregulated in multiple tumor types, with copy-number amplification as the predominant genomic alteration driving its overexpression. Elevated UPK1A-AS1 expression was correlated with advanced disease stage, poor differentiation, immune exclusion, and unfavorable prognosis, supporting its potential as a cancer type-dependent biomarker. In parallel, functional studies demonstrated that hypoxia transcriptionally induces UPK1A-AS1 in HCC, where it promotes sorafenib resistance by suppressing apoptosis. Silencing UPK1A-AS1 restored apoptotic and enhanced sorafenib efficacy both in vitro and in vivo. Collectively, our findings suggest that UPK1A-AS1 is a hypoxia-inducible oncogenic lncRNA that plays dual roles in cancer, with cancer type-dependent associations with progression and immune modulation across malignancies and mechanistically mediating hypoxia-associated drug resistance in HCC.

PMID:42678131 | PMC:PMC13532061 | DOI:10.1155/ancp/1554526

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