Table 2.
Genetically engineered mouse models of esophageal cancer.
| GEMM | GENES ALTERED | PHENOTYPE | REFERENCES |
|---|---|---|---|
| ED-L2/Cyclin D1 | Cyclin D1 overexpression | – Mild dysplasia by 8–10 months of age – Severe dysplasia by 15–16 months of age |
48 |
| ED-L2/Cyclin D1; p53−/− | Cyclin D1 overexpression and p53 deficiency | – Severe dysplasia by 5–6 months of age – Morbidity beyond 5 months for ED-L2/Cyclin D1; p53−/− mice – ESCC by 12 months of age in ED-L2/Cyclin D1; p53+/− mice – 25% of ED-L2/Cyclin D1; p53+/− mice develop lymph-node metastases |
69 |
| ED-L2/Cre; Klf4L/L | Klf4 conditional knockout | – Dysplasia by 6 months of age | 49 |
| ED-L2/Klf4 | Klf4 overexpression | – Chronic inflammation and dysplasia at 6 months of age – ESCC by 20–24 months of age |
7 |
| ED-L2/Cre; p120L/L | p120-catenin conditional knockout | – Dysplasia at 4–6 months of age – Invasive ESCC at 9–12 months of age |
6 |
| K5/Sox2 | Sox2 overexpression | – SCC nodules in the forestomach within 13 weeks of age | 76 |
| ED-L2/IL-1β | IL-1β overexpression | – Moderate inflammation by 6 months of age – Severe columnar metaplasia by 12–15 months of age – Severe dysplasia and/or dysplasia by 20–22 months of age |
85 |
| p63−/− | p63 global knockout | – Presence of metaplasia resembling BE in E18 embryos – p63 null mice do not survive into adulthood |
88 |