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Biology subjects

Kivioja, J.

Publications and source records attributed to Kivioja, J..

2 recordsLinked to original sources

Domain-adversarial learning predicts clinically actionable drug combination synergy in leukemia patients using bulk transcriptomics data

Deep learning has gained popularity in drug combination synergy prediction; however, DL models require large training datasets from cell line pharmacogenomic screens that poorly capture the heterogeneity in transcriptomic features and phenotypic responses seen in patients. To that end, we developed a domain-adversarial neural network (DANN) for personalized drug synergy prediction that accounts for systematic differences between cell line and patient domains. In applications to AML and CLL patient samples, we demonstrate how DANN boosts prediction accuracy under realistic data constraints. The model predictions demonstrated elevated synergy among clinically used combinations, such as venetoclax-based regimens, supporting its ability to identify both pharmaceutically and clinically meaningful combinations. DANN estimates prediction uncertainty and prioritizes high-confidence combination predictions to aid clinical translation. Together, DANN provides a systematic approach to improving accuracy and reliability in cross-domain drug synergy prediction, advancing the development of methods that are aligned with the translational requirements of precision hematology.

cancer biology↗

Inferring tumor-specific cancer dependencies through integrating ex-vivo drug response assays and drug-protein profiling

The development of cancer therapies may be improved by the discovery of tumor-specific molecular dependencies. The requisite tools include genetic and chemical perturbations, each with its strengths and limitations. Drug perturbations can be readily applied to primary cancer samples at a large scale, but mechanistic understanding of hits and further pharmaceutical development is often complicated by the fact that a small compound has a range of affinities to multiple proteins. To computationally infer the molecular dependencies of individual cancers from their ex-vivo drug sensitivity profiles, we developed a mathematical model that deconvolutes these data using measurements of protein-drug affinity profiles. Our method, DepInfeR, correctly identified known dependencies, including EGFR dependence in Her2+ breast cancer cell line, FLT3 dependence in AML tumors with FLT3-ITD mutations and the differential dependencies on the B-cell receptor pathway in two major subtypes of chronic lymphocytic leukemia (CLL). Furthermore, our method uncovered new subgroup-specific dependencies, including a previously unreported dependence of high-risk CLL on Checkpoint kinase 1 (CHEK1). The method also produced a more accurate map of the molecular dependencies in a heterogeneous set of 117 CLL samples. The ability to deconvolute polypharmacological phenotypes into underlying causal molecular dependencies should increase the utility of high-throughput drug response assays for functional precision oncology.

bioinformatics↗