Fig. 3.

Rapamycin treatments of MPR mice at the onset of tumor delayed growth of pancreatic neuroendocrine tumors (PanNETs) and pituitary neuroendocrine tumors (PitNETs). a Western blot analysis of Menin, Pten, phospho-AKT (p-Akt), total Akt, phospho-Rps6 (p-Rps6), total Rps6, and Gapdh proteins from 5 PanNETs and 5 PitNETs of MPR mice shown in Lanes 1–5. Lane S is the spleen from one of the five MPR mice. The molecular weight markers (in kD) were labeled on the left side of the blots. b–d Rapamycin treatment of MPR mice at the onset of tumor delayed growth of PitNETs and death but did not inhibit PitNET development and death in MPR mice. b Rapamycin-treated mice (n = 14) showed longer life span than vehicle-treated MPR mice (n = 10) (p < 0.003) in the first trial. c Size of PitNETs of vehicle-treated mice (n = 10) was significantly larger than rapamycin-treated mice (n = 7) of the same age (p < 0.001); size of PitNETs of rapamycin-treated mice (n = 7) at death/end of treatment was similar to that of vehicle-treated mice at death (p = 0.5). d Gross pathology of pituitary in vehicle-treated or rapamycin-treated MPR mice in the first trial. e Rapamycin treatments delayed the growth of PanNET in MPR mice—H & E of pancreas in vehicle-treated or rapamycin-treated MPR mice in the first trial. f Rapamycin was not toxic to mice. Weekly body weight change of rapamycin- and vehicle-treated mice was shown