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Kretzschmar, K.

Publications and source records attributed to Kretzschmar, K..

4 recordsLinked to original sources

NELLY enables patient-centric drug prioritization through interpretable drug-conditioned gene weighting

Precision oncology seeks to match each tumor with the most effective anti-cancer therapy. Advances in pharmacogenomics and machine learning enabled drug response prediction models with strong performance in cancer cell lines. Nonetheless, patient-centric evaluation of drug prioritization and systematic assessment of model generalization in patient-derived systems across cancer types remain largely absent. Here we introduce a translational framework combining patient-centric benchmarking with a pan-cancer pharmacogenomic atlas of patient-derived organoids, together with NELLY, a deep learning model integrating transcriptomic and chemical information to predict drug response and prioritize therapies. NELLY outperformed existing methods for patient-specific drug prioritization across cancer cell lines and patient-derived organoids, including under out-of-distribution evaluation. Its dynamic weighting mechanism provided patient-specific gene attributions, offering a route to connect predicted drug response to molecular programs associated with drug resistance. Our results support NELLY as a promising framework for translationally relevant and interpretable drug response prediction in precision oncology.

cancer biology↗

Chromatin Remodeling in Patient-Derived Colorectal Cancer Models

Patient-Derived Organoids (PDO) and Xenografts (PDX) are the current gold standards for patient derived models of cancer (PDMC). Nevertheless, how patient tumor cells evolve in these models and the impact on drug response remains unclear. Herein, we compared the transcriptomic and chromatin accessibility landscapes of six matched sets of colorectal cancer (CRC) PDO, PDX, PDO-derived PDX (PDOX), and original patient tumors (PT) and discovered two major remodeling axes. The first axis delineates PDX and PDO from PT, and the second axis distinguishes PDX and PDO. PDOX were more similar to PDX than they were to PDO, indicating that the growth environment is a driving force for chromatin adaptation. Using bivariate genomic footprinting analysis, we identified transcription factors (TF) that differentially bind to open chromatins between matched PDO and PDOX. Among them, KLF14 and EGR2 footprints were enriched in all six PDOX relative to matched PDO, and silencing of KLF14 or EGR2 promoted tumor growth. Furthermore, EPHA4, a shared downstream target gene of KLF14 and EGR2, altered tumor sensitivity to MEK inhibitor treatment. Altogether, patient-derived CRC cells undergo both common and distinct chromatin remodeling in PDO and PDX/PDOX, driven largely by their respective microenvironments, which results in differences in growth and drug sensitivity and needs to be taken into consideration when interpreting their ability to predict clinical outcome.

cancer biology↗

Behavioral-transcriptomic landscape of engineered T cells targeting human cancer organoids

Cellular immunotherapies are rapidly gaining clinical importance, yet predictive platforms for modeling their mode of action are lacking. Here, we developed a dynamic immuno-organoid 3D imaging-transcriptomics platform; BEHAV3D, to unravel the behavioral and underlying molecular mechanisms of solid tumor targeting. Applied to an emerging cancer metabolome-sensing immunotherapy: TEGs, we first demonstrate targeting of multiple breast cancer subtypes. Live-tracking of over 120,000 TEGs revealed a diverse behavioral landscape and identified a super engager cluster with serial killing capability. Inference of single-cell behavior with transcriptomics identified the gene signature of super engager killer TEGs, which contained 27 genes with no previously described T cell function. Furthermore, guided by a dynamic type 1 interferon (IFN-I) signaling module induced by high TEG-sensitive organoids, we show that IFN-I can prime resistant organoids for TEG-mediated killing. Thus, BEHAV3D characterizes behavioral-phenotypic heterogeneity of cellular immunotherapies and holds promise for improving solid tumor-targeting in a patient-specific manner.

cancer biology↗

Modelling cancer immunomodulation using epithelial organoid cultures

Here we utilize organoid technology to study immune-cancer interactions and assess immunomodulation by colorectal cancer (CRC). Transcriptional profiling and flow cytometry revealed that organoids maintain differential expression of immunomodulatory molecules present in primary tumours. Finally, we established a method to model antigen-specific epithelial cell killing and cancer immunomodulation in vitro using CRC organoids co-cultured with cytotoxic T cells (CTLs).

cancer biology↗