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 | ++ | + | – | – | ± |