Normal view
-
cs.AI, q-bio.NC updates on arXiv.org
-
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
-
cs.AI, q-bio.NC updates on arXiv.org
-
BacktestBench: Benchmarking Large Language Models for Automated Quantitative Strategy Backtesting
arXiv:2605.17937v2 Announce Type: replace-cross Abstract: Quantitative backtesting is essential for evaluating trading strategies but remains hampered by high technical barriers and limited scalability. While Large Language Models (LLMs) offer a transformative path to automate this complex, interdisciplinary workflow through advanced code generation, tool usage, and agentic planning, the practical realization is significantly challenged by the current lack of a large-scale benchmark dedicated t
BacktestBench: Benchmarking Large Language Models for Automated Quantitative Strategy Backtesting
-
Cell
-
Pan-neurodegeneration proteomics reveals disease subtypes and molecular signatures
A pan-neurodegeneration atlas built from multilayer, deep proteomics of 2,279 brain samples across 6 major diseases integrates whole proteome, detergent-insoluble proteome, and posttranslational modifications to enable intra- and inter-disease comparisons to reveal disease-specific subtypes and dysregulated pathways, while identifying shared changes such as GPNMB upregulation and NPTX2 downregulation.
Pan-neurodegeneration proteomics reveals disease subtypes and molecular signatures
-
(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
-
Characterization and regulatory mechanism evaluation of C8orf33 in hepatocellular carcinoma through multiomics profiling
Discov Oncol. 2026 Apr 11. doi: 10.1007/s12672-026-04951-z. Online ahead of print.ABSTRACTBACKGROUND: Hepatocellular carcinoma (HCC) is a major cause of cancer-related mortality. Chromosome 8 open reading frame 33 (C8orf33) has been noted as a potential oncogenic factor in several cancers, but its biological roles and regulatory mechanism in HCC microenvironment remain unknown.METHODS: We integrated bulk RNA sequencing, single-cell RNA sequencing (scRNA-seq), and spatial transcriptomics (ST) to
Characterization and regulatory mechanism evaluation of C8orf33 in hepatocellular carcinoma through multiomics profiling
Discov Oncol. 2026 Apr 11. doi: 10.1007/s12672-026-04951-z. Online ahead of print.
ABSTRACT
BACKGROUND: Hepatocellular carcinoma (HCC) is a major cause of cancer-related mortality. Chromosome 8 open reading frame 33 (C8orf33) has been noted as a potential oncogenic factor in several cancers, but its biological roles and regulatory mechanism in HCC microenvironment remain unknown.
METHODS: We integrated bulk RNA sequencing, single-cell RNA sequencing (scRNA-seq), and spatial transcriptomics (ST) to characterize the expression landscape of C8orf33. We then performed C8orf33 loss-of-function studies in HCC cell lines, including in vitro phenotypic assays and subcutaneous xenografts.
RESULTS: C8orf33 was broadly overexpressed and associated with unfavorable prognosis across multiple Cancers. In HCC, higher C8orf33 aligned with advanced stage and shorter overall survival. C8orf33 knockdown reduced proliferation and migration, impaired tumorigenic capacity, and increased apoptosis. ScRNA-seq analyses identified a malignant population of Epi3 with high C8orf33 expression. Cell-cell communication analysis suggested that C8orf33-high Epi3 state was associated with an enriched MIF-CD74/CXCR4/CD44 signaling program toward macrophage populations with M2-like features. ST analyses further confirmed the colocalization of C8orf33 with malignant features in tumor cores. In Huh7 cells, C8orf33 knockdown was accompanied by reduced mRNA and protein levels of MIF and its receptor components. Consistently, xenografts derived from C8orf33-silenced cells showed lower expression of these MIF-axis components and reduced infiltration of CD163 and CD206-positive macrophages.
CONCLUSION: These results support a tumor-promoting association of C8orf33 in HCC and suggest a potential link to macrophage-associated immunomodulatory features, nominating C8orf33 as a candidate biomarker and therapeutic target.
PMID:41965457 | DOI:10.1007/s12672-026-04951-z
-
Omics in Hepatocellular
-
Characterization and regulatory mechanism evaluation of C8orf33 in hepatocellular carcinoma through multiomics profiling
Discov Oncol. 2026 Apr 11. doi: 10.1007/s12672-026-04951-z. Online ahead of print.ABSTRACTBACKGROUND: Hepatocellular carcinoma (HCC) is a major cause of cancer-related mortality. Chromosome 8 open reading frame 33 (C8orf33) has been noted as a potential oncogenic factor in several cancers, but its biological roles and regulatory mechanism in HCC microenvironment remain unknown.METHODS: We integrated bulk RNA sequencing, single-cell RNA sequencing (scRNA-seq), and spatial transcriptomics (ST) to
Characterization and regulatory mechanism evaluation of C8orf33 in hepatocellular carcinoma through multiomics profiling
Discov Oncol. 2026 Apr 11. doi: 10.1007/s12672-026-04951-z. Online ahead of print.
ABSTRACT
BACKGROUND: Hepatocellular carcinoma (HCC) is a major cause of cancer-related mortality. Chromosome 8 open reading frame 33 (C8orf33) has been noted as a potential oncogenic factor in several cancers, but its biological roles and regulatory mechanism in HCC microenvironment remain unknown.
METHODS: We integrated bulk RNA sequencing, single-cell RNA sequencing (scRNA-seq), and spatial transcriptomics (ST) to characterize the expression landscape of C8orf33. We then performed C8orf33 loss-of-function studies in HCC cell lines, including in vitro phenotypic assays and subcutaneous xenografts.
RESULTS: C8orf33 was broadly overexpressed and associated with unfavorable prognosis across multiple Cancers. In HCC, higher C8orf33 aligned with advanced stage and shorter overall survival. C8orf33 knockdown reduced proliferation and migration, impaired tumorigenic capacity, and increased apoptosis. ScRNA-seq analyses identified a malignant population of Epi3 with high C8orf33 expression. Cell-cell communication analysis suggested that C8orf33-high Epi3 state was associated with an enriched MIF-CD74/CXCR4/CD44 signaling program toward macrophage populations with M2-like features. ST analyses further confirmed the colocalization of C8orf33 with malignant features in tumor cores. In Huh7 cells, C8orf33 knockdown was accompanied by reduced mRNA and protein levels of MIF and its receptor components. Consistently, xenografts derived from C8orf33-silenced cells showed lower expression of these MIF-axis components and reduced infiltration of CD163 and CD206-positive macrophages.
CONCLUSION: These results support a tumor-promoting association of C8orf33 in HCC and suggest a potential link to macrophage-associated immunomodulatory features, nominating C8orf33 as a candidate biomarker and therapeutic target.
PMID:41965457 | DOI:10.1007/s12672-026-04951-z
-
Nature Cancer
-
Harnessing foundation models for digital pathology without re-training
Nature Cancer, Published online: 03 April 2026; doi:10.1038/s43018-025-01108-9Applications of digital pathology in clinical oncology have largely depended on the requirement for labeled data and model re-training. A study now presents PRET, a training-free framework with robust performance for pan-cancer diagnosis that adapts pathology foundation models to diverse tasks at inference stage, from screening and subtyping tasks to segmentation and metastasis detection tasks.
Harnessing foundation models for digital pathology without re-training
Nature Cancer, Published online: 03 April 2026; doi:10.1038/s43018-025-01108-9
Applications of digital pathology in clinical oncology have largely depended on the requirement for labeled data and model re-training. A study now presents PRET, a training-free framework with robust performance for pan-cancer diagnosis that adapts pathology foundation models to diverse tasks at inference stage, from screening and subtyping tasks to segmentation and metastasis detection tasks.-
cs.AI, q-bio.NC updates on arXiv.org
-
Adaptation of Agentic AI: A Survey of Post-Training, Memory, and Skills
arXiv:2512.16301v3 Announce Type: replace Abstract: Large language model (LLM) agents are moving beyond prompting alone. ChatGPT marked the rise of general-purpose LLM assistants, DeepSeek showed that on-policy reinforcement learning with verifiable rewards can improve reasoning and tool use, and OpenClaw highlights a newer direction in which agents accumulate persistent memory and reusable skills. Yet the research landscape remains fragmented across post-training, retrieval, memory, and skill
Adaptation of Agentic AI: A Survey of Post-Training, Memory, and Skills
-
cs.AI, q-bio.NC updates on arXiv.org
-
ConEQsA: Concurrent and Asynchronous Embodied Questions Scheduling and Answering
arXiv:2509.11663v2 Announce Type: replace-cross Abstract: This paper formulates the Embodied Questions Answering (EQsA) problem, introduces a corresponding benchmark, and proposes an agentic system to tackle the problem. Classical Embodied Question Answering (EQA) is typically formulated as answering one single question by actively exploring a 3D environment. Real deployments, however, often demand handling multiple questions that may arrive asynchronously and carry different urgencies. We form
ConEQsA: Concurrent and Asynchronous Embodied Questions Scheduling and Answering
-
cs.AI, q-bio.NC updates on arXiv.org
-
ToolSelf: Unifying Task Execution and Self-Reconfiguration via Tool-Driven Intrinsic Adaptation
arXiv:2602.07883v2 Announce Type: replace Abstract: Agentic systems powered by Large Language Models (LLMs) have demonstrated remarkable potential in tackling complex, long-horizon tasks. However, their efficacy is fundamentally constrained by static configurations governing agent behaviors, which are fixed prior to execution and fail to adapt to evolving task dynamics. Existing approaches, relying on manual orchestration or heuristic-based patches, often struggle with poor generalization and f