Dr. Daniela Ungureanu is Associate Professor in Precision Oncology at the Disease Networks Research Unit, Faculty of Biochemistry and Molecular Medicine, University of Oulu, Finland. She leads an interdisciplinary research group at the interface of cancer biology, drug discovery, and single-cell genomics, with a focus on deciphering the molecular mechanisms that drive therapy resistance in solid tumours.
Dr. Ungureanu holds a 20-year track record in cancer cell signalling and drug discovery, having pioneered structural and functional characterization of cancer-related kinases and pseudokinases. Her research has since evolved to encompass tumour microenvironment biology, epigenetic regulation, and the development of high-throughput pharmacogenomic technologies. Her group’s flagship innovation — a 96-plex single-cell pharmacotranscriptomic platform — enables simultaneous profiling of transcriptional responses to pharmacological perturbations at single-cell resolution using primary tumor samples. This platform is now being applied to map context-dependent drug resistance mechanisms in cancers such as ovarian and prostate, with a particular emphasis on tumour-stroma crosstalk and epigenetic vulnerabilities.
A 96-Plex Pharmacotranscriptomic Platform to Decode Drug Resistance at Single Cell Level in Cancers
Understanding why tumours fail to respond to therapy remains one of the central challenges in oncology. Bulk transcriptomic and pharmacological approaches mask the cellular heterogeneity that underlies resistance, obscuring the contributions of distinct tumour cell populations and stromal compartments. To address this, we developed a 96-plex single-cell pharmacotranscriptomic platform that enables simultaneous profiling of up to 96 drug or perturbation conditions within a single experiment, resolving transcriptional responses at single-cell resolution with high throughput and reproducibility (Nature Chemical Biology, Dini et al., 2025).
In this talk, I will present the conceptual framework and technical implementation of the platform and illustrate its application through two cancer models. In high-grade serous ovarian carcinoma (HGSOC), a disease defined by frequent chemoresistance, we used the platform to dissect the mechanism of action of PI3K/AKT inhibitors, identifying a targetable vulnerability in CAV1-high tumors mediated by EGFR upregulation. In prostate cancer, single-cell drug profiling across tumour-stroma co-culture systems uncovered FAP signalling as a master regulator of cancer-associated fibroblast-mediated therapy resistance, demonstrating how the stromal compartment actively reprogrammed drug response at the transcriptional level.
Together, these findings illustrate the power of high-dimensional pharmacotranscriptomics to resolve the cellular and molecular heterogeneity of drug resistance, and to prioritize mechanistically grounded combination strategies for precision oncology.