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CODESKILL: Learning Self-Evolving Skills for Coding Agents

arXiv:2605.25430v1 Announce Type: new Abstract: Coding agents produce rich trajectories while solving software-engineering tasks. To enable agent self-evolution, these trajectories can be distilled into reusable procedural skills that compactly encode experience to guide future behavior. However, existing skill construction and maintenance methods often rely on fixed prompts and heuristic update rules, leaving it unclear how knowledge should be selected, abstracted, and maintained to best serve downstream agents. We propose CODESKILL, an LLM-based framework that reformulates skill extraction and skill-bank maintenance as a learnable management policy. CODESKILL extracts multi-granularity procedural skills from coding-agent trajectories, evolves skills with new experience, and maintains a compact skill bank for future task solving. We train CODESKILL with reinforcement learning, using a hybrid reward that combines dense rubric-based skill-quality feedback with sparse verifiable execution feedback from the frozen downstream agent. Experiments on EnvBench, SWE-Bench Verified, and Terminal-Bench 2 show that CODESKILL improves average pass rate by 9.69 over the no-skill baseline and by 4.01 over the strongest prompt-based or memory baseline, while maintaining the skill bank at a stable size during iterative construction.

Weakly Supervised Camouflaged Object Detection Based on the SAM Model and Mask Guidance

arXiv:2605.25385v1 Announce Type: cross Abstract: Camouflaged object detection (COD) from a single image is a challenging task due to the high similarity between objects and their surroundings. Existing fully supervised methods require labor-intensive pixel-level annotations, making weakly supervised methods a viable compromise that balances accuracy and annotation efficiency. However, weakly supervised methods often experience performance degradation due to the use of coarse annotations. In this paper, we introduce a new weakly supervised approach for camouflaged object detection to overcome these limitations. Specifically, we propose a novel network, MGNet, which tackles edge ambiguity and missed detections by utilizing initial masks generated by our custom-designed Cascaded Mask Decoder (CMD) to guide the segmentation process and enhance edge predictions. We introduce a Context Enhancement Module(CEM) to reduce the missing detection, and a Mask-guided Feature Aggregation Module (MFAM) for effective feature aggregation. For the weak supervision challenge, we propose BoxSAM, which leverages the Segment Anything Model (SAM) with bounding-box prompts to generate pseudo-labels. By employing a redundant processing strategy, high quality pixel-level pseudo-labels are provided for training MGNet. Extensive experiments demonstrate that our method delivers competitive performance against current state-of-the-art methods.

ANP32E drives lung adenocarcinoma progression via GSK3beta-mediated glycolytic reprogramming

14 April 2026 at 18:00

Cell Death Dis. 2026 Apr 14. doi: 10.1038/s41419-026-08712-2. Online ahead of print.

ABSTRACT

Lung adenocarcinoma (LUAD), a leading cause of cancer mortality, involves incompletely understood epigenetic-metabolic crosstalk. We identified ANP32E as a key regulator through multi-omics (TCGA, scRNA-seq) and clinical analyses, finding its overexpression correlates with poor prognosis. Functionally, ANP32E knockdown suppressed proliferation, migration, and glycolysis in LUAD cells (A549/H1975) and attenuated xenograft growth, while overexpression promoted tumorigenesis. Mechanistically, ANP32E transcriptionally upregulates histone demethylase KDM3B, reducing repressive H3K9me2 marks at the EGFR promoter to enhance EGFR transcription. This activates PI3K/AKT signaling, inducing inhibitory GSK3Ξ² phosphorylation. Combined with ANP32E-mediated GSK3Ξ² suppression, this dual inactivation liberates oncogenic glycolysis. Crucially, KDM3B silencing or EGFR inhibition (Cetuximab) abrogated ANP32E-driven phenotypes. High-throughput screening identified Penta-O-galloyl-Ξ²-D-glucose (PGG) as an ANP32E-targeting compound, with molecular dynamics confirming binding. PGG dose-dependently inhibited the ANP32E/KDM3B/EGFR axis in vitro and suppressed tumor growth in vivo. Thus, ANP32E drives LUAD progression via KDM3B/EGFR-mediated GSK3Ξ² inactivation, representing a prognostic biomarker and therapeutic target validated by PGG.

PMID:41980942 | DOI:10.1038/s41419-026-08712-2

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