The median survival of the single agent sunitinib cohort and the median survival of the untreated cohort are significantly different. However, the selleck bio median survival of the sunitinib plus rapamycin treated cohort is not significantly different than the median survival of the single agent rapamycin treated cohort. In summary, suni tinib as a single agent is effective at increasing survival, but not at reducing tumor growth, when compared to the untreated cohort. Single agent sunitinib is not as effective as rapamycin at decreasing tumor volume or increasing survival. Furthermore, adding sunitinib to rapamycin did not reduce disease severity when com pared to single agent rapamycin. Single agent bevacizumab improves survival and reduces Tsc2 tumor growth.

The day 30 average tumor volume for the bevacizumab cohort Inhibitors,Modulators,Libraries and the untreated cohort are significantly different. The average tumor volumes at day 65 Inhibitors,Modulators,Libraries for the bevacizumab plus rapamycin cohort and the rapamycin cohort are similar. The median survival of the single agent bevacizumab cohort and the median survival of the untreated cohort are significantly different. However, the median survival of the bevacizu mab plus rapamycin treated Inhibitors,Modulators,Libraries cohort is not sig nificantly different than the median survival of the single agent rapamycin treated cohort. The slightly lower median survival in the bevacizumab plus rapamycin combination group sug Inhibitors,Modulators,Libraries gests that adding bevacizumab to rapamycin may enhance tumor growth in some cases, although the mechanism is not known. In summary, bevacizumab as a single agent is effective at reducing tumor growth and increasing survival when compared to the untreated cohort.

Single agent bevacizumab is not as effective as rapamycin Inhibitors,Modulators,Libraries at decreasing tumor volume or increasing survival. Furthermore, adding bevacizumab to rapamycin did not reduce disease severity when compared to single agent rapamycin. Vincristine was not effective for the treatment of Tsc2 tumors. The day 23 average tumor volume for the vincristine cohort and the untreated cohort are not significantly different. The average tumor volumes at day 65 for the vincristine plus rapamycin cohort are similar. Survival data shows that the med ian survival of the single agent vincristine cohort does not differ significantly from the median sur vival of the untreated cohort.

The median sur vival of the vincristine plus rapamycin treated cohort is also not significantly different than the med ian survival of the single agent rapamycin treated cohort. In summary, vincristine as a single agent is not effective selleck at reducing tumor growth and increasing survival when compared to the untreated cohort or the single agent rapamycin cohort. Furthermore, adding vincristine to rapamycin did not reduce disease severity when compared to single agent rapamycin.