Table 1.
Site-specific brain metastasis produced by B16-BL6 and K-1735 C4 melanoma cells in syngeneic and B6C3F1 cross mice
| C57BL/6
 | 
B6C3F1 | 
|||
|---|---|---|---|---|
| Cell line | Leptomeninges, ventricles | Parenchyma | Leptomeninges, ventricles | Parenchyma | 
| B16-BL6 | 14/14 | 0/14 | 4/4 | 0/4 | 
| B16-BL6/vector control | 15/15 | 0/15 | 5/5 | 0/5 | 
| B16-BL6/TGF-β2 OE | 19/19 | 5/19* | 5/5 | 1/5* | 
| C3H/HeN
 | 
B6C3F1
 | 
|||
| Cell line | Leptomeninges, ventricles | Parenchyma† | Leptomeninges, ventricles | Parenchyma | 
| 
 | ||||
| K-1735 C4 | 0/20 | 20/20 | 0/5 | 5/5 | 
| K-1735 C4/shRNA control | 0/19 | 19/19 | 0/5 | 5/5 | 
| K-1735 C4/TGF-β2 shRNA | 0/20 | 17/20‡ | 0/4 | 4/4 | 
B16-BL6 cells overexpressing the TGF-β2 cytokine produced microscopic tumor lesions in the brain parenchyma.
K-1735 C4 cells and derivative cells produced grossly visible tumors in the brain parenchyma. The production of parenchymal lesions was significantly delayed in mice injected with K-1735 C4/TGF-β2 shRNA cells.
Three mice killed 24 d after tumor injection had no visible brain parenchymal lesions.