Figure 1

Exogenous expression of p190B increases tumor multiplicity. (a) Kaplan-Meier tumor-free survival curve of rtTA/Neu, tetO/Neu, and p190B transgenic mice reveals that p190B does not affect MMTV-Neu tumor latency. The median time to tumor onset was approximately 275 days for each of the three groups. Log-rank test analysis showed no significant differences between the groups (P > 0.05). (b) P190B transgenic mice developed an average of two tumors whereas control mice developed an average of one tumor per mouse indicating that exogenous p190B expression increases tumor multiplicity. A Mann-Whitney test revealed statistically significant differences in tumor multiplicity between the groups. (c) Tumor location by gland is graphed demonstrating statistically significant increased tumor formation in mammary gland pairs 1, 4, and 2/3 in the p190B transgenic mice as compared to rtTA/Neu control mice (P < 0.05) and in mammary gland pairs one and four compared to tetO/Neu control mice (P < 0.05). (d) Western blotting to detect expression of ErbB2/Neu, p190B, and ErbB3 in rtTA/Neu and p190B transgenic tumors. Equal amounts of protein were pooled from 11 mice per genotype. Similar levels of ErbB2 and p190B were detected in the two groups. Arrow indicates a lower molecular weight form of ErbB3 that was detected concomitant with a decrease in total protein in p190B transgenic tumor lysates. β-actin is shown as a loading control. (e) Luciferase activity is graphed indicating that the tetO-p190B-IRES-luciferase transgene is expressed in the majority of p190B tumors. Luciferase activity is never detected in control tumors. (f) RT-PCR on cDNA prepared from exogenous p190B expressing and rtTA/Neu control tumors shows mRNA expression of the human p190B transgene in p190B transgenic, but not rtTA/Neu control tumors. RT-PCR for GAPDH is shown as a positive control and samples prepared without RT were negative (data not shown).