Table 1.
An overview of common genetically engineered mouse models of pancreatic cancer and their key characteristics
| Genotype | Preneoplastic lesion | Cancer phenotype | Metastasis | Features | References |
|---|---|---|---|---|---|
| Pdx1; KRASG12D/+ | PanIN | PDAC | Yes | Long latency | 343 |
| Ptf1a+/Cre; KRASG12D/+ | PanIN | PDAC | Yes | Long latency | 343 |
| KRASG12D/+; Ela-TGFa | PanIN | IPMN | Yes (50%) | Moderate latency | 350 |
| Pdx1-Cre; LSL-KRASG12D/+; Ink4a/Arflox/lox | PanIN | PDAC | Yes (21%) | Short latency and high penetrance | 346 |
| Pdx1-Cre; LSL-KRASG12D/+; LSL-TP53R172H/+ | PanIN | PDAC | Yes (63%) | Accelerated development of metastatic PDAC | 345 |
| LSL-KRASG12D; TP53fl/fl (in situ electroporation of Cre recombinase and myrAkt2) | PanIN | PDAC | Yes (>60%) | High efficiency, short latency | 384 |
| Co-electroporation of SB13 transposase with a KRASG12V-expressing transposon, Cre recombinase and myrAkt2 in TP53fl/fl mice | PanIN | PDAC | Yes (>70%) | High efficiency, short latency | 384 |
| Pdx1-Cre; KRASG12D/+; Ink4a−/− TP53lox/lox | PanIN | PDAC | Yes (20%) | Short latency and high penetrance | 347 |
| Pdx1-Cre; KRASG12D/+; Smadlox/lox | IPMN | PDAC | Yes (38%) | Model of IPMN to PDAC progression | 351,352 |
| Ptf1a+/Cre; KRASG12D/+; Smadlox/lox | MCN | PDAC | Yes (18%) | MCNs resembling human disease | 385 |
| Ptf1a+/Cre; KRASG12D/+; ATMlox/lox | PanIN | PDAC | Yes (78%) | High metastasis tendency | 348 |
IPMN intraductal papillary mucinous neoplasm, MCN mucinous cystic neoplasm, PanIN pancreatic intraepithelial neoplasia, PDAC pancreatic ductal adenocarcinomas