arXiv:2608. 05359v1 Announce Type: new Abstract: CASCADE is an agentic framework that predicts downstream transcriptional effects of gene perturbation from precomputed ARACNe regulatory networks, exposed via MCP.
arXiv:2607. 14097v1 Announce Type: new Abstract: We introduce RegNetAgents, an AI-oriented multi-agent framework for structured, query-driven regulatory candidate identification across heterogeneous gene regulatory networks.
arXiv:2606. 01042v1 Announce Type: cross Abstract: Perturbation experiments are central to understanding cellular mechanisms, but remain costly and sparse, motivating prediction of gene expression responses for unobserved conditions.
arXiv:2512. 22240v5 Announce Type: replace-cross Abstract: Machine learning models are primarily judged by predictive performance, especially in applied genomics, where explanations are read as biological findings.
Accurate prediction of patient-specific therapeutic response from pre-treatment transcriptomes is hindered by the scarcity of matched clinical response labels and post-treatment molecular profiles. Preclinical transfer-learning models can simulate drug-induced expression changes but are often hard to interpret and unstable, whereas knowledge-graph methods provide mechanistic context yet remain static and fail to capture drug-induced transcriptomic perturbation dynamics.
The paper introduces CELLAUDIT, a method for auditing whether inputs claimed to influence predictive models actually do so. By testing if an input can enter the computation, whether predictions depend on it, and if that dependence improves observed responses, the authors evaluate agent-generated predictors on a morphology‑transcriptomics benchmark (BBBC047). Their findings show that many models claim compound contributions that are not supported by the data, and that falsification‑guided revisions can recover genuine input effects while improving performance.
arXiv:2603. 02274v3 Announce Type: replace-cross Abstract: Precision oncology is currently limited by the small-N, large-P paradox, where high-dimensional genomic data is abundant but pharmacological response samples are sparse.
arXiv:2606. 09898v2 Announce Type: replace Abstract: Cancer treatment involves decisions across multiple clinical outcomes, yet pathway-informed deep learning models are typically evaluated in isolation, making their relative benefits unclear.
arXiv:2606. 30695v1 Announce Type: cross Abstract: Single-cell drug perturbation models should predict not only transcriptional response magnitude, but also whether a treatment alters the proliferative state of a cell.
arXiv:2607. 04557v1 Announce Type: cross Abstract: Accurate prediction of patient-specific therapeutic response from pre-treatment transcriptomes is hindered by the scarcity of matched clinical response labels and post-treatment molecular profiles.
arXiv:2608. 05982v1 Announce Type: new Abstract: Inadequate target--disease linkage accounts for 40--50\% of Phase~II efficacy failures, so anticipating which programmes will advance would let sponsors back the hypotheses most likely to reach patients.
The study evaluated nine transcriptomic models—five bulk RNA‑seq and four single‑cell RNA‑seq—designed to predict response to immune checkpoint inhibitors. Across independent datasets, bulk models performed near chance while single‑cell models offered only modest gains, and pathway analyses revealed inconsistent biomarker signals. The results highlight the limited cross‑cohort robustness and biological consistency of current transcriptomic ICI predictors.
arXiv:2606. 14823v1 Announce Type: cross Abstract: Genetic evidence is enriched among approved drug targets: in an observational analysis of 26,278 target-disease pairs from Open Targets and ChEMBL, targets with any genetic association had a 3.