Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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DRIVE: Modeling Skills at the Reasoning and Interaction Levels for Web Agents under Continual Learning
arXiv:2605.23939v1 Announce Type: new Abstract: Web agents require both high-level reasoning (for task decomposition) and low-level interactions (for page elements manipulation) to conduct different tasks. However, these knowledge types differ fundamentally: reasoning knowledge (e.g., booking a flight requires first searching for routes) is abstract and transferable across websites, while interaction knowledge (e.g., clicking the Search button at a specific coordinate on Site A) depends heavily
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cs.AI, q-bio.NC updates on arXiv.org
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CoSPlay: Cooperative Self-Play at Test-Time with Self-Generated Code and Unit Test
arXiv:2605.23491v2 Announce Type: replace-cross Abstract: Recently, Reinforcement Learning with Verifiable Rewards (RLVR) and Test-Time Scaling (TTS) have advanced LLM code generation through executable verification. Yet Ground-Truth Unit Tests (GT UTs) remain a bottleneck: SOTA RLVR methods require them for costly training, while existing TTS methods lose competitiveness without them. This motivates GT-free TTS, where existing methods directly use self-generated UTs to refine and select code c
CoSPlay: Cooperative Self-Play at Test-Time with Self-Generated Code and Unit Test
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Omics in Hepatocellular
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PRXL2B facilitates the progression of hepatocellular carcinoma and the therapeutic efficacy of oncolytic adenovirus H101 through the PI3K/AKT/PD-L1 axis
Biosci Trends. 2026 May 21. doi: 10.5582/bst.2026.01000. Online ahead of print.ABSTRACTOncolytic adenovirus H101 has shown antitumor activity in hepatocellular carcinoma (HCC), but the molecular determinants of treatment response remain unclear. In this study, a Hepa1-6 subcutaneous tumor model was established in C57BL/6 mice and treated with intratumoral H101, followed by integrated transcriptomic and proteomic analyses to identify candidate genes associated with H101 response. PRXL2B was selec
PRXL2B facilitates the progression of hepatocellular carcinoma and the therapeutic efficacy of oncolytic adenovirus H101 through the PI3K/AKT/PD-L1 axis
Biosci Trends. 2026 May 21. doi: 10.5582/bst.2026.01000. Online ahead of print.
ABSTRACT
Oncolytic adenovirus H101 has shown antitumor activity in hepatocellular carcinoma (HCC), but the molecular determinants of treatment response remain unclear. In this study, a Hepa1-6 subcutaneous tumor model was established in C57BL/6 mice and treated with intratumoral H101, followed by integrated transcriptomic and proteomic analyses to identify candidate genes associated with H101 response. PRXL2B was selected for further investigation using public multi-omics datasets, tissue microarray-based immunohistochemistry, in vitro functional assays, mechanistic analyses, and in vivo validation experiments. Integrated multi-omics analyses identified PRXL2B as a candidate gene downregulated after H101 treatment. Public datasets and tissue-based validation further showed that PRXL2B was upregulated in HCC tissues. In MHCC97H and HCCLM3 cells, PRXL2B knockdown inhibited proliferation, migration, and invasion, promoted apoptosis and cell-cycle arrest, and enhanced the antitumor effect of H101. Mechanistically, PRXL2B silencing reduced AKT phosphorylation and PD-L1 expression. In vivo, PRXL2B knockdown suppressed tumor growth, and the combination of PRXL2B knockdown and H101 produced the strongest antitumor effect. These findings indicate that PRXL2B promotes malignant phenotypes in HCC and may modulate H101 efficacy through the PI3K/AKT/PD-L1 axis. Targeting PRXL2B may therefore represent a potential strategy to enhance the therapeutic efficacy of oncolytic virus therapy in HCC.
PMID:42161529 | DOI:10.5582/bst.2026.01000