PO.BCS01.03 · 生物信息与计算

PTMax:一个整合文献挖掘与多组学、用于癌症中磷酸化功能解读的AI赋能平台

PTMax: An AI-enabled platform integrating literature mining and multi-omics for functional interpretation of phosphorylation in cancer

海报缩略图:PTMax:一个整合文献挖掘与多组学、用于癌症中磷酸化功能解读的AI赋能平台
编号 2703 展板 28 时间 4/20 02:00–05:00 区域 Section 1 主讲 Yanling Sun, BS;PhD
分会场 Application of Bioinformatics to Cancer Biology 3
查看 PDF 下载 PDF 🔒 查看 / 下载完整 PDF 需登录并开通下载套餐 · 查看套餐 / 开通 AACR 官方页面

作者与单位 Authors & Affiliations

Yanling Sun, Sara S. Savage, John M. Elizarraras, Eric Jaehnig, Bing Zhang

Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, TX

摘要 Abstract

中文摘要
磷酸化是蛋白功能和致癌信号传导的核心调控因子,而质谱技术的进步现已能够对癌症相关磷酸化位点进行无偏的、蛋白质组范围的鉴定。然而,大多数位点的功能相关性仍不甚了解,且分散于文献之中。为弥补这一空白,我们开发了PTMax,一个AI赋能的资源,整合全面的文献挖掘与系统性的多组学数据,以推进癌症中磷酸化的功能解读。为标准化已发表研究中报道的磷酸化位点信息,我们改进了文献挖掘流程,以高效地从全文文章和通路图中提取位点级证据及相关功能信息。从这些来源汇总的证据被用于生成功能摘要,并通过自动化和人工质量评估进行评价。PTMax还纳入了数十个基于质谱的磷酸化蛋白质组学数据集以及来自CPTAC癌症队列的多组学数据,包括RNA、蛋白、磷酸化位点丰度和表型关联。对于每个磷酸化位点,我们计算了两个证据评分,分别量化文献衍生的信息丰富度和数据驱动的支持度。我们还构建了特征集,按癌症标志、共同提及的基因或疾病以及通路图关联对磷酸化位点进行分组,并生成了共调控磷酸化网络,以促进通路和网络层面的解读。PTMax目前包含超过40,000个文献衍生的磷酸化位点,提取自逾500,000个句子和1,400张通路图,涵盖了PhosphoSitePlus中约70%经低通量验证的位点和约80%经调控注释的位点。值得注意的是,超过30,000个位点缺乏先前的调控证据,凸显了AI驱动的文献挖掘的价值。与多组学资源的整合新增了约200,000个独特磷酸化位点,包括65,000个具有定量关联的位点和26,000个与癌症表型相关联的位点。PTMax界面使用户能够查询单个基因或磷酸化位点,并检索全面、富含背景的信息以及友好易用的可视化内容。此外,基于通路和网络的分析模块有助于将磷酸化位点列表转化为功能和信号传导层面的见解。总之,PTMax将文献和图谱挖掘与大规模实验数据集相统一,提供了一个全面、多维度的资源,推进癌症中磷酸化的功能研究。
查看英文原文 English abstract
Phosphorylation is a central regulator of protein function and oncogenic signaling, and advances in mass spectrometry now enable unbiased, proteome-wide identification of cancer-associated phosphosites. However, the functional relevance of most sites remains poorly understood and scattered across the literature.To address this gap, we developed PTMax, an AI-enabled resource that integrates comprehensive literature mining with systematic multi-omics data to advance functional interpretation of phosphorylation in cancer.To standardize phosphosite information reported across published studies, we enhanced our literature-mining pipeline to efficiently extract site-level evidence and associated functional information from full-text articles and pathway figures. Evidence aggregated from these sources was used to generate functional summaries, which were evaluated through both automated and manual quality assessments. PTMax additionally incorporates dozens of mass spectrometry-based phosphoproteomics datasets and multi-omics data from CPTAC cancer cohorts, including RNA, protein, phosphosite abundance, and phenotype associations. For each phosphosite, we computed two evidence scores that quantify literature-derived information richness and data-driven support, respectively. We also constructed signature sets that group phosphosites by cancer hallmarks, co-mentioned genes or diseases, and pathway figure associations, and generated a co-regulated phosphorylation network to facilitate pathway- and network-level interpretation.PTMax currently contains more than 40,000 literature-derived phosphosites extracted from over 500,000 sentences and 1,400 pathway figures, capturing ~70% of low-throughput-validated and ~80% of regulatory-annotated phosphosites in PhosphoSitePlus. Notably, over 30,000 sites lack prior regulatory evidence, underscoring the value of AI-driven literature mining. Integration with multi-omics resources adds ~200,000 unique phosphosites, including 65,000 sites with quantitative associations and 26,000 linked to cancer phenotypes. The PTMax interface enables users to query individual genes or phosphosites and retrieve comprehensive, context-rich information together with user-friendly visualizations. In addition, pathway and network-based analysis modules help translate phosphosite lists into functional and signaling insights. In summary, PTMax unifies literature and figure mining with large-scale experimental datasets to deliver a comprehensive, multi-dimensional resource that advances the functional study of phosphorylation in cancer.
利益披露 Disclosure
Y. Sun, None.. S. S. Savage, None.. J. M. Elizarraras, None.. E. Jaehnig, None.. B. Zhang, None.

← 返回 AACR 2026 检索