Patient-derived xenografts undergo mouse-specific tumor evolution
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Abstract
Patient-derived xenografts (PDXs) have become a prominent cancer model system, as they are presumed to faithfully represent the genomic features of primary tumors. Here we monitored the dynamics of copy number alterations (CNAs) in 1,110 PDX samples across 24 cancer types. We observed rapid accumulation of CNAs during PDX passaging, often due to selection of preexisting minor clones. CNA acquisition in PDXs was correlated with the tissue-specific levels of aneuploidy and genetic heterogeneity observed in primary tumors. However, the particular CNAs acquired during PDX passaging differed from those acquired during tumor evolution in patients. Several CNAs recurrently observed in primary tumors gradually disappeared in PDXs, indicating that events undergoing positive selection in humans can become dispensable during propagation in mice. Notably, the genomic stability of PDXs was associated with their response to chemotherapy and targeted drugs. These findings have major implications for PDX-based modeling of human cancer.
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Long-term passage of PDXs in mice can alter tumour behaviour, but strategic use of low-passage lines curbs this mouse-specific drift and remains useful for osteosarcoma biology, precision medicine, and preclinical testing.
“Although prolonged passage in mice can alter the behaviour of tumours maintained as PDXs 227 , strategic use of low-passage PDX lines limits this mouse-specific evolution and is a useful tool in the study of osteosarcoma biology 228 , precision medicine approaches and preclinical validation of therapeutic candidates.”
From Osteosarcoma (2022) · cites this paper as [227]
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- Authors
- Ben-David, U., Ha, G., Tseng, Y.-Y., Greenwald, N. F., Oh, C., Shih, J., McFarland, J. M., Wong, B., Boehm, J. S., Beroukhim, R., & Golub, T. R.
- Affiliations
- Broad Institute (US)
- Corresponding author
- Beroukhim, Rameen
- Golub, Todd R
- ORCID
- Venue
- Nature Genetics
- Published
- 2017-10-09
- Volume
- 49
- Issue
- 11
- Pages
- 1567-1575
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC5659952
- OpenAlex
- W2737053924
- Cited by
- 716
- References
- 72
- Citations by year
- 2026: 40 · 2025: 63 · 2024: 67 · 2023: 74 · 2022: 83 · 2021: 106 · 2020: 103 · 2019: 83 · 2018: 90 · 2017: 6 · 2014: 1
- FWCI
- 25.85
- Type
- journal article
- Language
- en
- Open access
- green
- doi.org
- Locations
- Nature Genetics (publishedVersion)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- National Cancer Institute (R01CA188228)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomic variations and chromosomal abnormalities
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- patient-derived xenografts, copy number alterations, tumor evolution, aneuploidy, genetic heterogeneity, clonal selection, genome stability, chemotherapy response, targeted therapy response, tumor models
- MeSH terms
- Aneuploidy, Animals, Antineoplastic Agents, Clone Cells, Disease Models, Animal, DNA, Neoplasm, Humans, Neoplasms, Selection, Genetic, Species Specificity, Tumor Cells, Cultured, Mice, DNA Copy Number Variations, Clonal Evolution, Heterografts
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