Table 1 Advantages and limitations of preclinical HNSCC models
| Preclinical model | Major advantages | Limitations | Pathogenesis modelling | Low-throughput drug screening | High throughput drug screening | Precision oncologya | Immune-oncologyb |
|---|---|---|---|---|---|---|---|
| Immortalized cell lines |
- low expenses - ease of maintenance - amenable to genetic manipulation |
- chromosomal instability - low retention of genetic features | – | ++ | ++ | – | – |
| Primary 2D cultures |
- high take rate - moderate expenses - amenable to genetic manipulation | - no resemblance of tumor architecture and cellular microenvironment | – | ++ | + | ++ | – |
| Organoids |
- resemblance of tumor architecture - retention of genetic heterogeneity - reconstitution with stroma-immune components possible |
- time and cost consuming - poorly validated HNSCC model - unknown effects of mouse-derived ECM components on cell behavior | ++ | ++ | ± | ++ | ++ |
| Patient-derived xenografts |
- retention of histological and genetic features of original tumor - tumor- (mouse-) stroma interactions |
- time and cost consuming - reconstitution of immune system challenging | – | ++ | – | + | ± |
| Carcinogen induced mouse models |
- close resemblance of OC tumors - retention of genetic heterogeneity - immunocompetent model |
- extended time until development of carcinomas - not all HNSCC sites can be modelled | ++ | + | – | – | ± |
| Genetically engineered mouse models |
- recapitulation of tumor initiation and progression - modeling of complex processes, e.g. tumor angiogenesis - immunocompetent model |
- time and cost consuming - unpredictable frequency and latency of tumor formation - genetic alterations driving tumor formation rare in HNSCC | ++ | + | – | – | ± |