Table 1.
Induction of gliomas by RCAS vectors in tv-a transgenic mice
|
tv-a transgenes
|
Genes introduced with RCAS vectorsa
|
Genetic backgroundb
|
|||||
|---|---|---|---|---|---|---|---|
|
EGFR*
|
cdk4
|
bFGF
|
wild type
|
INK4a+/−
|
INK4a−/−
|
p53+/−
|
|
| Gtv-a | + | − | − | 0/21 | 1/17 | 2/6 | |
| Ntv-a | + | − | − | 0/24 | 13/25 | 8/19 | 0/16 |
| Ntv-a | + | + | − | 1/8 | 5/19 | 4/10 | 3/8 |
| Ntv-a | + | + | + | 3/29 | 4/7 | 6/16 | 17/39 |
Glioma formation, as measured by either histologic inspection of frozen brain sections or by clinical appearance of hydrocephalus, is tabulated for Gtv-a and Ntv-a transgenic mice from four different genetic backgrounds with respect to the tumor suppressors INK4a–ARF and p53, after infection of newborns with RCAS vectors carrying the indicated genes.
EGFR* (RCAS–EGFR*); cdk4 (RCAS–cdk4); bFGF (RCAS–bFGF). Tumors induced by infections with RCAS–EGFR* alone were scored at 8–10 weeks by histologic analysis of fixed frozen sections. Mice infected with combinations of RCAS–EGFR* and RCAS–cdk4 were scored for hydrocephalus between 3 and 8 weeks of age, after determining in >15 mice that early hydrocephalus is highly correlated with histologic features of gliomas.
INK4a+/− and INK4a−/− are heterozygous and homozygous for a targeted deletion of the INK4a–ARF tumor suppressor locus; and p53+/− is heterozygous for a targeted deletion of the p53 tumor suppressor gene.