BACKGROUND
Behavioral and social science research (BSSR) is essential for understanding human behavior and informing interventions, policy, and health outcomes; however, such research faces persistent challenges related to fragmented knowledge, imprecise and inconsistent terminology, and limited interoperability across studies. Ontologies provide a promising solution by enabling standardized, machine-readable representations of concepts and relationships to support data integration, knowledge synthesis, and reproducibility.
RESULTS
We present an initial overview of the ACCELERATE-BASSO Research Network, an NIH-supported consortium established to advance BSSR through ontology-driven approaches. Specifically, we describe the role of the Dissemination and Coordination Center (DCC) and the Best Practices Working Group (BPWG) in supporting a network of projects focusing on accelerating BSSR through ontology development and use. Based on the consortium's early experiences, we summarize emerging ontology-driven practices, current interoperability efforts, and common methodological considerations identified across the participating projects. Rather than proposing a formal consensus framework, this work provides an initial consortium perspective on current ontology development activities and shared lessons learned. We also discuss the potential role of ontologies in supporting AI-related applications in BSSR.
CONCLUSIONS
This paper provides an initial consortium perspective on ontology-driven approaches for advancing BSSR. By synthesizing early experiences, emerging practices, and shared challenges across multiple projects, it offers insights to inform future ontology development, interoperability, and community consensus while laying the foundation for more systematic evaluation and broader adoption within the BSSR community.
Yue Yu, Lu Kang, Susan Michie et al.· Journal of Biomedical Semant...· 0 citations
Pancreatic ductal adenocarcinoma (PDAC) is the most lethal common cancer (5-year survival ∼13%), emerging through years-to-decades progression involving chronic fibro-inflammatory injury and precursor transformation processes including ADM and PanIN. KRAS-driven acinar-to-ductal metaplasia (ADM) is among the earliest experimentally tractable and potentially interceptable events; KRAS (mutated in >90% of PDAC) has remained difficult to therapeutically target, particularly for prevention; emerging KRAS inhibitors are developed for treatment of established malignancy rather than early interception. We aimed to prioritize KRAS-axis interception candidates via AI-guided network analysis of TCGA-PAAD restricted to a curated KRAS-driven ADM/PanIN-initiation mechanism module.
The 38-gene module (n=183 TCGA-PAAD samples; 37 genes available, PRSS2 absent) spans KRAS-MAPK, RTKs, TGF-β/SMAD, ECM, inflammation, transcription, tumor suppressors, and ductal/acinar genes from canonical pancreatic-cancer-progression biology, linking established-tumor transcriptomes to early-interception biology. A stability-selected Spearman-correlation network served as the network backbone (PCMCI+/NOTEARS extensions ongoing), paired with patient-level bootstrap filtering (B=200 resamples; ≥70% retention). A composite Interception Score I(v) = α·CB + β·Σ|w| + γ·U + δ·R integrating betweenness centrality, summed edge-weight influence, druggability (literature-curated drug-target prior), and bootstrap robustness ranked candidate interception nodes (unoptimized weights; tuning ongoing).
Spearman correlation yielded a 37-node, 248-edge network baseline; bootstrap resampling (B=200) evaluated 856 distinct candidate edges, of which 194 (22.7%) achieved ≥70% retention, defining the stable subgraph used for scoring. The Interception Score placed 7 KRAS-axis genes among the top-10 candidates: ERBB2 (0.953), KRAS (0.743), ERBB3 (0.742), MAPK1 (0.708), EGFR (0.675), MAP2K2 (0.605), and BRAF (0.589). Inflammation (IL6, 0.755), TGF-β/SMAD2 (0.726), and ECM/MMP2 (0.638) also ranked highly, recapitulating PDAC initiation mechanisms (stromal-epithelial crosstalk; inflammatory-fibrotic priming). ERBB2 (HER2), a clinically druggable RTK with approved inhibitors in other malignancies, emerged as the top-ranked candidate, supporting evaluation of HER2-axis signaling for interception in molecularly selected PDAC subsets. These findings align with canonical PDAC biology, supporting biological plausibility prior to formal weight optimization and external validation.
AI-guided network analysis of TCGA-PAAD prioritizes biologically coherent KRAS-axis and stromal-inflammatory candidates with clinically available HER2-, EGFR-, MEK-, BRAF-, and KRAS-pathway inhibitors, supporting hypothesis generation for future pancreatic cancer interception studies. Stage-resolved analysis, causal-inference extensions, and sex-/age-stratified validation are ongoing.
Jianfu Li, Yingyun Yang, Michael Wallace, Cui Tao, Yan Bi. AI-Driven Network-Based Discovery on TCGA-PAAD Identifies KRAS-Axis Drug-Repurposing Targets for Pancreatic Cancer Interception [abstract]. In: Proceedings of AACR Drug Discovery and Development (AACR D3) Conference; 2026 Jul 21-24; Boston, MA. Philadelphia (PA): AACR; Clin Cancer Res 2026;32(14_Suppl):Abstract nr A029.
Jianfu Li, Yingyun Yang, Michael B. Wallace et al.· Clinical Cancer Research· 0 citations
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