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Earth-Agent-Pro: Towards Real-World Full-Chain Earth Observation with Agents

arXiv:2609.12533v1 Announce Type: cross Abstract: Real-world Earth observation (EO) agents must translate high-level scientific questions into executable workflows to acquire observations, prepare data, perform domain computations, and derive conclusions from runtime evidence. Existing EO agents typically start from supplied observations, while benchmarks typically provide prepared inputs or candidate answers, leaving full-chain open-world EO execution largely untested. We present Earth-Agent-Pro, an execution-adaptive Plan-and-Execute framework using expert-authored skills to constrain planning and runtime tool use. Workflow-centered structured memory records planned steps, accepted evidence, and their dependencies, enabling repair of only the affected workflow suffix when runtime evidence invalidates a step. Separate large language model adapters use sequence-level supervised fine-tuning for planner workflow composition and node-level group relative policy optimization with locally verifiable rewards for executor tool-argument grounding. Earth-Bench-Pro instantiates 248 expert-curated task cores as 744 questions under three matched regimes. Its 248 Open-World Execution questions span RGB imagery, spectral observations, and remote sensing products, pairing high-level requests with runtime data requirements, executable trajectories, and open-ended answers grounded in execution evidence. With a shared GPT-5 backbone, Earth-Agent-Pro achieves 66.13% LLM-as-Judge accuracy, exceeding ReAct by 20.95 points in this metric and 24.44 points in Tools-In-Order. Joint adapter tuning raises Qwen3.5-9B LLM-as-Judge accuracy from 38.31% to 50.00%, an 11.69-point gain over the untuned configuration. Planning-only evaluation and execution with the reference workflow show that the adapters improve workflow composition and argument grounding, respectively. Code and datasets will be released soon.
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A Non-Canonical Role of SMAD4 in Regulating 3D Genome Architecture to Inhibit Lung Squamous Cell Carcinoma Development

Adv Sci (Weinh). 2026 May 26:e75839. doi: 10.1002/advs.75839. Online ahead of print.

ABSTRACT

Lung squamous cell carcinoma (LUSC) lacks clearly defined key drivers and effective targeted therapies, reflecting an incomplete understanding of its molecular pathogenesis. Here, we identify SMAD4 as a critical regulator of three-dimensional (3D) genome organization in LUSC and uncover a mechanistic link between tumor suppressor loss and oncogenic transcriptional activation. By integrating clinical datasets, genetically engineered mouse models, human and murine LUSC cell lines, and multi-omics analyses, we demonstrate that SMAD4 deficiency promotes LUSC progression by unleashing EP300-mediated enhancer-promoter looping at the SOX2 locus. Mechanistically, SMAD4 does not directly bind SOX2 regulatory elements but instead constrains chromatin looping by sequestering EP300 away from loop anchor regions. Loss of SMAD4 leads to enhanced H3K27ac deposition, aberrant SOX2 activation, and increased LUSC tumor cell proliferation. Together, these findings reveal a non-canonical role for a transcription factor (e.g., SMAD4) in regulating dysregulated 3D genome architecture to inhibit tumor development.

PMID:42189071 | DOI:10.1002/advs.75839

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A Non-Canonical Role of SMAD4 in Regulating 3D Genome Architecture to Inhibit Lung Squamous Cell Carcinoma Development

Adv Sci (Weinh). 2026 May 26:e75839. doi: 10.1002/advs.75839. Online ahead of print.

ABSTRACT

Lung squamous cell carcinoma (LUSC) lacks clearly defined key drivers and effective targeted therapies, reflecting an incomplete understanding of its molecular pathogenesis. Here, we identify SMAD4 as a critical regulator of three-dimensional (3D) genome organization in LUSC and uncover a mechanistic link between tumor suppressor loss and oncogenic transcriptional activation. By integrating clinical datasets, genetically engineered mouse models, human and murine LUSC cell lines, and multi-omics analyses, we demonstrate that SMAD4 deficiency promotes LUSC progression by unleashing EP300-mediated enhancer-promoter looping at the SOX2 locus. Mechanistically, SMAD4 does not directly bind SOX2 regulatory elements but instead constrains chromatin looping by sequestering EP300 away from loop anchor regions. Loss of SMAD4 leads to enhanced H3K27ac deposition, aberrant SOX2 activation, and increased LUSC tumor cell proliferation. Together, these findings reveal a non-canonical role for a transcription factor (e.g., SMAD4) in regulating dysregulated 3D genome architecture to inhibit tumor development.

PMID:42189071 | DOI:10.1002/advs.75839

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