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Lock, J.

Publications and source records attributed to Lock, J..

3 recordsLinked to original sources

Uncertainty-Aware Deep Learning for Multi-Metric and Dose-Specific Prediction of Drug Synergy

Accurately predicting drug synergy is critical to accelerate the development of combination therapies for cancer and other complex diseases. Yet, the vast combinatorial drug and dose space poses a substantial challenge, even for modern deep learning approaches. Existing approaches often lack generalisability, collapse rich dose-response surfaces into single dose-averaged synergy scores, and fail to quantify predictive uncertainty. Here, we introduce AlgoraeOS, a biologically informed, attention-aware deep neural network designed to address these challenges. Trained on the largest harmonised dataset of experimentally tested drug combinations, AlgoraeOS simultaneously predicts multiple synergy metrics, while preserving their empirical correlations and accurately estimating both aleatoric and epistemic uncertainty. The model achieves state-of-the-art performance and strong out-of-distribution generalisability across diverse tissues and drug mechanisms, including rigorous zero- and few-shot evaluations. Notably, AlgoraeOS predicts the entire dose-response surface, providing dose-specific inhibition profiles with high precision and scalability to multi-million-point datasets. Prospective in vitro validation of dose-specific inhibition was performed using an anchor compound entirely absent from the training corpus, tested in combination with 24 mechanistically diverse partner drugs across three molecularly distinct cancer cell lines, yielding 2,592 dose-combination measurements. This evaluation demonstrated consistent rank-order fidelity (Spearmans {rho} = 0.51-0.59, p < 0.001) and strong directional agreement (Kendalls {tau} = 0.863), confirming reliable prediction under out-of-distribution conditions. Model-derived uncertainty estimates further stratified predictions by expected reliability, with lower-uncertainty predictions showing higher concordance with experimental outcomes. By integrating uncertainty-aware, multi-metric, and dose-resolved prediction into a single unified framework, AlgoraeOS offers a powerful solution for drug-combination discovery and establishes a new standard for model development and validation in the field.

bioinformatics↗

A selective inhibitor of oncogenic JNK signalling perturbs metastatic outgrowth of triple-negative breast cancer through metabolic blockade

Although c-Jun N-terminal Kinase (JNK) represents an attractive anti-cancer target, its pleiotropic functionality limits the use of direct JNK inhibitors. Here, we identify a distinct subcellular pattern of JNK activity as a therapeutic vulnerability in breast cancer, where cytoplasmic JNK activity predicts poor survival outcomes, is elevated in triple-negative breast cancers (TNBC) and is essential for metastatic outgrowth. Mechanistic analyses reveal cytoplasmic JNK acts through multiple mechanisms, with downstream targets involved in cellular metabolism and cytoskeletal regulation. On this basis, we leveraged actin-based phenotypic drug-screening and identified K12, an indirect but selective inhibitor of cytoplasmic JNK that blocks TNBC metastatic outgrowth in vivo. We reveal that K12 inhibits glutaminase-1 and the pyruvate dehydrogenase complex, and that this poly-pharmacology overcomes pyruvate anaplerosis, a known resistance mechanism of existing glutaminase inhibitors. These findings demonstrate the potential of selectively targeting the oncogenic function of JNK, offering new treatment options for early-stage metastatic TNBC.

cancer biology↗

Systematic perturbation screens decode regulators of inflammatory macrophage states and identify a role for TNF mRNA m6A modification

Macrophages adopt dynamic cell states with distinct effector functions to maintain tissue homeostasis and respond to environmental challenges. During chronic inflammation, macrophage polarization is subverted towards sustained inflammatory states which contribute to disease, but there is limited understanding of the regulatory mechanisms underlying these disease-associated states. Here, we describe a systematic functional genomics approach that combines genome-wide phenotypic screening in primary murine macrophages with transcriptional and cytokine profiling of genetic perturbations in primary human monocyte-derived macrophages (hMDMs) to uncover regulatory circuits of inflammatory macrophage states. This process identifies regulators of five distinct inflammatory states associated with key features of macrophage function. Among these, the mRNA m6A writer components emerge as novel inhibitors of a TNF-driven cell state associated with multiple inflammatory pathologies. Loss of m6A writer components in hMDMs enhances TNF transcript stability, thereby elevating macrophage TNF production. A PheWAS on SNPs predicted to impact m6A installation on TNF revealed an association with cystic kidney disease, implicating an m6A-mediated regulatory mechanism in human disease. Thus, systematic phenotypic characterization of primary human macrophages describes the regulatory circuits underlying distinct inflammatory states, revealing post-transcriptional control of TNF mRNA stability as an immunosuppressive mechanism in innate immunity.

immunology↗