期刊
DISEASE MODELS & MECHANISMS
卷 11, 期 11, 页码 -出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/dmm.037366
关键词
Cancer; Cell line; Tissue culture; Tumor cell line; Genetic heterogeneity
资金
- Wellcome Trust [WT209199/Z/17/Z, WT107963/Z/15/Z]
- Cancer Research UK (CRUK) Lung Cancer Centre of Excellence
- Roy Castle Lung Cancer Foundation
- CRUK Lung Cancer Centre of Excellence
- Biotechnology and Biological Sciences Research Council
- Rosetrees Trust
- UCL Hospitals Charitable Foundation
- UCLH Biomedical Research Centre
- MRC [G108/596] Funding Source: UKRI
The extent of genetic and epigenetic diversity between and within patient tumors is being mapped in ever more detail. It is clear that cancer is an evolutionary process in which tumor cell intrinsic and extrinsic forces shape clonal selection. The pre-clinical oncology pipeline uses model systems of human cancer - including mouse models, cell lines, patient-derived organoids and patient-derived xenografts - to study tumor biology and assess the efficacy of putative therapeutic agents. Model systems cannot completely replicate the environment of human tumors and, even within the same cancermodel, data are often irreproducible between laboratories. One hypothesis is that ongoing evolutionary processes remain relevant in laboratorymodels, leading to divergence over time. In a recent edition of Nature, Ben-David and colleagues showed that different stocks of widely used cancer cell lines - a staple of cancer research over many decades - are highly heterogeneous in terms of their genetics, transcriptomics and responses to therapies. The authors find compelling evidence of positive selection based on ongoing mutational processes and chromosomal instability. Thus, the origin, culture conditions and cumulative number of population doublings of cell lines likely influence experimental outcomes. Here, we summarize the key findings of this important study and discuss the practical implications of thiswork for researchers using cell lines in the laboratory.
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