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AutoResearchClaw: Self-Reinforcing Autonomous Research with Human-AI Collaboration

arXiv:2605.20025v2 Announce Type: replace Abstract: Automating scientific discovery requires more than generating papers from ideas. Real research is iterative: hypotheses are challenged from multiple perspectives, experiments fail and inform the next attempt, and lessons accumulate across cycles. Existing autonomous research systems often model this process as a linear pipeline: they rely on single-agent reasoning, stop when execution fails, and do not carry experience across runs. We present AutoResearchClaw, a multi-agent autonomous research pipeline built on five mechanisms: structured multi-agent debate for hypothesis generation and result analysis, a self-healing executor with a \textsc{Pivot}/\textsc{Refine} decision loop that transforms failures into information, verifiable result reporting that prevents fabricated numbers and hallucinated citations, human-in-the-loop collaboration with seven intervention modes spanning full autonomy to step-by-step oversight, and cross-run evolution that converts past mistakes into future safeguards. On ARC-Bench, a 25-topic experiment-stage benchmark, AutoResearchClaw outperforms AI Scientist v2 by 54.7%. A human-in-the-loop ablation across seven intervention modes reveals that precise, targeted collaboration at high-leverage decision points consistently outperforms both full autonomy and exhaustive step-by-step oversight. We position AutoResearchClaw as a research amplifier that augments rather than replaces human scientific judgment. Code is available at https://github.com/aiming-lab/AutoResearchClaw.

M$^\star$: Every Task Deserves Its Own Memory Harness

arXiv:2604.11811v2 Announce Type: replace-cross Abstract: Large language model agents rely on specialized memory systems to accumulate and reuse knowledge during extended interactions. Recent architectures typically adopt a fixed memory design tailored to specific domains, such as semantic retrieval for conversations or skills reused for coding. However, a memory system optimized for one purpose frequently fails to transfer to others. To address this limitation, we introduce M$^\star$, a method that automatically discovers task-optimized memory harnesses through executable program evolution. Specifically, M$^\star$ models an agent memory system as a memory program written in Python. This program encapsulates the data Schema, the storage Logic, and the agent workflow Instructions. We optimize these components jointly using a reflective code evolution method; this approach employs a population-based search strategy and analyzes evaluation failures to iteratively refine the candidate programs. We evaluate M$^\star$ on four distinct benchmarks spanning conversation, embodied planning, and expert reasoning. Our results demonstrate that M$^\star$ improves performance over existing fixed-memory baselines robustly across all evaluated tasks. Furthermore, the evolved memory programs exhibit structurally distinct processing mechanisms for each domain. This finding indicates that specializing the memory mechanism for a given task explores a broad design space and provides a superior solution compared to general-purpose memory paradigms.

GPX8<sup>+</sup> cancer-associated fibroblast-derived lactate contributes to lenvatinib resistance by facilitating BRPF1 expression through histone H3 lysine 18 lactylation in hepatocellular carcinoma

Oncogene, Published online: 22 May 2026; doi:10.1038/s41388-026-03711-1

GPX8+ cancer-associated fibroblast-derived lactate contributes to lenvatinib resistance by facilitating BRPF1 expression through histone H3 lysine 18 lactylation in hepatocellular carcinoma

Exploring the prognostic role of senescence-related genes in gastric cancer through multi-omics integration and machine learning

Hum Genomics. 2026 May 9. doi: 10.1186/s40246-026-00979-y. Online ahead of print.

ABSTRACT

Cellular senescence plays a context-dependent role in gastric cancer (GC), functioning both through tumor-suppressive arrest and the tumor-promoting senescence-associated secretory phenotype. However, its systematic integration into prognostic models remains limited. Here, we develop a novel interpretable framework to identify and validate a robust senescence-related gene signature for GC prognosis. We first introduce a dual-model interpretable feature selection strategy that integrates a biologically informed Kolmogorov-Arnold Network with a tabular foundation model to identify cancer-associated senescence genes. From the initial candidates, an ensemble of ten machine learning algorithms distills a core 4-gene signature to construct a Senescence Risk Score (SRS). The SRS proves to be a powerful and independent prognostic indicator, effectively stratifies patients into high- and low-risk groups with distinct overall survival across multiple cohorts. High-risk patients exhibit an "immune-hot" but potentially dysfunctional tumor microenvironment, characterized by enriched immune cell infiltration, elevated checkpoint expression, and distinct metabolic reprogramming favoring pathways such as angiogenesis and epithelial-mesenchymal transition (EMT). Furthermore, the SRS correlates with differential somatic mutation profiles and suggests potential sensitivity to specific chemotherapeutic agents. In vitro functional assays confirmed the oncogenic role of SERPINE1, a top-ranked core gene, in promoting GC cell proliferation. Regulatory network analysis revealed potential upstream transcription factors and miRNAs governing the signature. Collectively, we present a validated senescence-related prognostic signature that enables effective risk stratification of patients with gastric cancer.

PMID:42106891 | DOI:10.1186/s40246-026-00979-y

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