We performed transplantation experiments using the bacTRAP system. Transplanted gliomas induced by hPDGFb-driven glioma cells in hosts with altered tumor suppressor function showed higher percentages of the overall recruitment than in the wild-type hosts, indicating that complete or partial tumor suppressor loss may enhance the ability of the cells to be 
recruited. Although gliomas induced by transplantation of non-fluorescent Pten-deleted Ras-driven murine glioma cells showed recruitment of proliferating host brain cells into the glioma mass, the overall amount of recruited cells into Ras-driven tumors and the number of tumors that showed large regions of recruitment was significantly less than that seen with the hPDGFb-induced gliomas. An unbiased way to define a cell population lies in Gomisin-D identification of its gene expression signature and subsequent comparison to gene expression signatures of known normal or cancer cells to define its position on the axis of tumorigenesis. To quantify similarities and differences in the expression profiles of recruited cells and tumor cells using microarray analysis, we used the bacTRAP technology that allows immunoprecipitation of polysomes from specific cell types in vivo. RCAS/tv-a system allows to closely model the biology and histopathology of human oligodendrogliomas; although we have not performed direct comparisons between our mouse model and human glioma classifications, in many ways, hPDGFb-driven murine gliomas may mimic the proneural subclass of human GBMs. Our data suggests that olig2-expressing cells recruited in PDGF-induced murine gliomas can have similar morphologic, proliferative and functional characteristics as olig2expressing tumor cells derived from the cell-of-origin, with the caveat that a part of the similarity between the recruited and tumor olig2 cells may stem from their proliferative behavior. Extensive similarities between polysome-associated transcriptome of recruited versus glioma olig2 cells call for further evaluation of the precise definitions and criteria applied to terms “tumor” and “normal”, and indicate similar gene expression character of these cells. Furthermore, tumor suppressor loss and acquisition of mutations typically found in human gliomas allow these murine recruited cells to occupy large areas of the tumor and at times become the predominant cellular component of the glioma mass, completely independent of the cell-of-origin. Thus, the clonal expansion that overtakes glioma bulk during tumor progression need not be derived from glioma cell-of-origin. Transformation is the process of self-autonomous acquisition of the sufficient oncogenic alterations that change a normal cell into the tumor cell. Unlike epithelial cancers, the “normal” or stromal component of a glioma is composed of cells of the same lineage as the tumor cells. The inherent implication of this observation is that extracellular factors that promote glioma tumor cell growth may similarly affect glioma stroma. In our glioma model, initially normal recruited cells not derived from the glioma-initiating cellof-origin can be stimulated by hyperproduction of a growth factor receptor ligand, induced to proliferate, and driven to acquire various genetic aberrations and Cinoxacin aberrant expression profiles as gliomas progress, presumably because of the tumor microenvironment created by the progeny of the cell-of-origin. The process of acquisition and selection for such genetic and/or epigenetic alterations due to the pressures of the glioma microenvironment may be better termed “corruption”.