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BLM$_1$: A Boundless Large Model for Cross-Space, Cross-Task, and Cross-Embodiment Learning

arXiv:2510.24161v1 Announce Type: new Abstract: Multimodal large language models (MLLMs) have advanced vision-language reasoning and are increasingly deployed in embodied agents. However, significant limitations remain: MLLMs generalize poorly across digital-physical spaces and embodiments; vision-language-action models (VLAs) produce low-level actions yet lack robust high-level embodied reasoning; and most embodied large language models (ELLMs) are constrained to digital-space with poor generalization to the physical world. Thus, unified models that operate seamlessly across digital and physical spaces while generalizing across embodiments and tasks remain absent. We introduce the \textbf{Boundless Large Model (BLM$_1$)}, a multimodal spatial foundation model that preserves instruction following and reasoning, incorporates embodied knowledge, and supports robust cross-embodiment control. BLM$_1$ integrates three key capabilities -- \textit{cross-space transfer, cross-task learning, and cross-embodiment generalization} -- via a two-stage training paradigm. Stage I injects embodied knowledge into the MLLM through curated digital corpora while maintaining language competence. Stage II trains a policy module through an intent-bridging interface that extracts high-level semantics from the MLLM to guide control, without fine-tuning the MLLM backbone. This process is supported by a self-collected cross-embodiment demonstration suite spanning four robot embodiments and six progressively challenging tasks. Evaluations across digital and physical benchmarks show that a single BLM$_1$ instance outperforms four model families -- MLLMs, ELLMs, VLAs, and GMLMs -- achieving $\sim\!\textbf{6%}$ gains in digital tasks and $\sim\!\textbf{3%}$ in physical tasks.

Tumor microenvironment and drug resistance in lung adenocarcinoma: molecular mechanisms, prognostic implications, and therapeutic strategies

Discov Oncol. 2025 Feb 25;16(1):238. doi: 10.1007/s12672-025-01981-x.

ABSTRACT

The fight against lung adenocarcinoma (LUAD) is challenged by tumor microenvironment (TME)-mediated drug resistance, which limits effective treatment. This study examines the LUAD TME and identifies four distinct subtypes through multi-omics profiling: immune-rich, immune-exhausted, stromal-dominant, and TME-desert. Each subtype has unique molecular features, tumor diversity, and links to clinical outcomes. Immune-rich subtypes respond better to immune checkpoint inhibitors, while stromal-dominant and TME-desert subtypes show resistance to treatment and poor prognosis. Molecular analysis uncovers subtype-specific mutations, chromosomal instability, and altered signaling pathways, pointing to potential therapeutic targets. In silico drug screening identifies promising treatments for resistant subtypes. These findings, validated in independent cohorts, highlight the critical role of the TME in drug resistance and treatment response, providing insights for personalized treatment strategies in LUAD.

PMID:40000527 | PMC:PMC11861463 | DOI:10.1007/s12672-025-01981-x

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