❌

Normal view

Tongyi DeepResearch Technical Report

arXiv:2510.24701v1 Announce Type: cross Abstract: We present Tongyi DeepResearch, an agentic large language model, which is specifically designed for long-horizon, deep information-seeking research tasks. To incentivize autonomous deep research agency, Tongyi DeepResearch is developed through an end-to-end training framework that combines agentic mid-training and agentic post-training, enabling scalable reasoning and information seeking across complex tasks. We design a highly scalable data synthesis pipeline that is fully automatic, without relying on costly human annotation, and empowers all training stages. By constructing customized environments for each stage, our system enables stable and consistent interactions throughout. Tongyi DeepResearch, featuring 30.5 billion total parameters, with only 3.3 billion activated per token, achieves state-of-the-art performance across a range of agentic deep research benchmarks, including Humanity's Last Exam, BrowseComp, BrowseComp-ZH, WebWalkerQA, xbench-DeepSearch, FRAMES and xbench-DeepSearch-2510. We open-source the model, framework, and complete solutions to empower the community.

Fatty acid-binding proteins in cancers

Int J Surg. 2025 Jul 15. doi: 10.1097/JS9.0000000000003049. Online ahead of print.

ABSTRACT

Fatty acid-binding proteins (FABPs) are intracellular lipid chaperones with molecular weights of approximately 14-15 kDa. By binding and transporting fatty acids and lipid-related molecules, FABPs precisely regulate metabolic pathways, signal transduction, and gene expression, playing a central role in cancer initiation and progression. The 11 identified subtypes (FABP1-FABP12; FABP11 is identical to FABP3) exhibit tissue-specific expression and influence tumor progression through metabolic reprogramming, immune microenvironment modulation, and therapy resistance. Metabolically, FABPs enhance fatty acid uptake, β-oxidation, and synthesis, meeting the high proliferative demands of tumors. In immune regulation, FABP4+ macrophages secrete IL-6 to suppress T cell activity, while FABP6 downregulates MHC-I molecule expression to reduce CD8+ T cell infiltration, fostering an immunosuppressive microenvironment. Regarding therapy resistance, FABP4 enhances mitochondrial β-oxidation to reduce apoptosis in ovarian cancer, and FABP5 promotes chemoresistance in HCC via the HIF-1α pathway. Functional heterogeneity exists among subtypes: FABP7 drives glioblastoma stem cell migration via RXRα signaling, while FABP5 exhibits context-dependent roles, promoting HCC progression but suppressing colorectal cancer (CRC) through mTOR-mediated autophagy. Clinically, FABPs serve as diagnostic biomarkers and therapeutic targets. However, challenges such as insufficient target specificity, cross-cancer heterogeneity, and normal tissue toxicity remain. Future studies should integrate multi-omics and single-cell technologies to elucidate cell-specific mechanisms and develop precise combination therapies for clinical translation.

PMID:40717587 | DOI:10.1097/JS9.0000000000003049

❌