Recruited Cells Can Become Transformed and Overtake PDGF-Induced Murine Gliomas In Vivo during Tumor Progression
Figure 2
Homozygous tumor suppressor loss at glioma initiation enhances tumor formation and expands the recruited glioma cell fraction.
(a) Kaplan-Meyer analysis for symptomatic gliomas in various Ntv-a mouse strains listed above the graph, injected with RCAS-PSG and RCAS-Cre, if applicable. Each curve represents survival analysis for n≥30 animals. (b,c) Quantification of percentages of progeny cells in Ntv-a gliomas, which are wild-type, deleted for Ink4a/Arf, or for Ink4a/Arf and Pten, as measured by FACS. Tumor suppressor loss expands the recruited component in mouse gliomas. (d–f) DAPI-stained images of frozen sections of murine gliomas, showing virally encoded eGFP in RCAS-PSG-induced Ntv-a GBMs deleted for Ink4a/Arf (d,e) or Ink4a/Arf and Pten (f). (g) Quantification of number of transplanted gliomas (z-axis) containing various percentages of recruited cells (x-axis), induced by transplantation of non-fluorescent hPDGFb-driven or Ras-driven murine glioma cells into the wild-type or Ink4a/Arf+/- bacTRAP olig2 RP-eGFP hosts (y-axis). Note that significant recruitment occurs upon transplantation of either hPDGFb-driven and Ras-driven murine glioma cells into the Ink4a/Arf+/- hosts.