Trellis tree-based analysis reveals stromal regulation of patient-derived organoid drug responses
Open accessAbstract
Patient-derived organoids (PDOs) can model personalized therapy responses; however, current screening technologies cannot reveal drug response mechanisms or how tumor microenvironment cells alter therapeutic performance. To address this, we developed a highly multiplexed mass cytometry platform to measure post-translational modification (PTM) signaling, DNA damage, cell-cycle activity, and apoptosis in >2,500 colorectal cancer (CRC) PDOs and cancer-associated fibroblasts (CAFs) in response to clinical therapies at single-cell resolution. To compare patient- and microenvironment-specific drug responses in thousands of single-cell datasets, we developed "Trellis"-a highly scalable, tree-based treatment effect analysis method. Trellis single-cell screening revealed that on-target cell-cycle blockage and DNA-damage drug effects are common, even in chemorefractory PDOs. However, drug-induced apoptosis is rarer, patient-specific, and aligns with cancer cell PTM signaling. We find that CAFs can regulate PDO plasticity-shifting proliferative colonic stem cells (proCSCs) to slow-cycling revival colonic stem cells (revCSCs) to protect cancer cells from chemotherapy.
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YAP inhibition reverses the revCSC phenotype and synergises with chemotherapy.
“Consequently, YAP inhibition reverses the revCSC phenotype and synergises with chemotherapy.148”
From Current and emerging concepts for systemic treatment of metastatic colorectal cancer (2025) · cites this paper as [148]
One common mechanism by which CAFs confer resistance to chemotherapy and other antimitotic drugs is the induction of a revival colonic stem cell (revCSC) phenotype in tumour cells.
“One common mechanism by which CAFs confer resistance to chemotherapy and other antimitotic drugs is the induction of a revival colonic stem cell (revCSC) phenotype in tumour cells.148”
From Current and emerging concepts for systemic treatment of metastatic colorectal cancer (2025) · cites this paper as [148]
RevCSCs are induced by stromal cues such as TGF-β in a YAP-dependent manner and are characterised by a slow-cycling, drug-persisting phenotype.
“RevCSCs are induced by stromal cues such as transforming growth factor beta (TGF-β) in a Yes-associated protein (YAP)-dependent manner and are characterised by a slow-cycling, drug persisting phenotype.148”
From Current and emerging concepts for systemic treatment of metastatic colorectal cancer (2025) · cites this paper as [148]
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- Authors
- Ramos Zapatero, M., Tong, A., Opzoomer, J. W., O’Sullivan, R., Cardoso Rodriguez, F., Sufi, J., Vlckova, P., Nattress, C., Qin, X., Claus, J., Hochhauser, D., Krishnaswamy, S., & Tape, C. J.
- Affiliations
- Yale University (US)
- University College London (GB)
- Corresponding author
- Krishnaswamy, Smita
- Tape, Christopher J.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2023-12
- Volume
- 186
- Issue
- 25
- Pages
- 5606-5619.e24
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W4389427718
- Cited by
- 72
- References
- 99
- Citations by year
- 2026: 19 · 2025: 26 · 2024: 24 · 2023: 3
- FWCI
- 8.73
- Type
- journal article
- Language
- en
- Update notices
- erratum (2024-12-12)
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cell (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion, cc-by)
- Funders
- Chan Zuckerberg Initiative (CZF2019-182702/CZF2019-002440, FG-2021-15883)
- National Institutes of Health (R01GM135929/R01GM130847)
- Cancer Research UK (C7893/A26233, C60693/A23783)
- Rosetrees Trust (M872/A2292)
- NIHR UCLH BRC (BRC422)
- National Science Foundation (2047856)
- UCLH Biomedical Research Centre
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Single-cell and spatial transcriptomics
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Keywords
- patient-derived organoids, colorectal cancer, cancer-associated fibroblasts, tumor microenvironment, drug response, mass cytometry, DNA damage, cell cycle, apoptosis, colonic stem cells, chemoresistance, single-cell screening, cancer stem cell plasticity
- MeSH terms
- Cancer-Associated Fibroblasts, Algorithms, Drug Evaluation, Preclinical, Humans, Organoids, Stem Cells, Signal Transduction, Apoptosis, Single-Cell Analysis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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