The XXXX microenvironment.

@entity5 @entity11 @entity463 @entity1313
High-grade @entity1313 are heterogeneous with respect to the composition of bona fide @entity5 cells and with respect to a range of intermingling parenchymal cells. @entity463 harbor multiple cell types, some with increased tumorigenicity and stem cell-like capacity. The stem-like cells may be the cells of origin for @entity5 relapse. However, the @entity5 -associated parenchymal cells-such as vascular cells, microglia, peripheral immune cells, and neural precursor cells-also play a vital role in controlling the course of pathology. In this review, we describe the multiple interactions of bulk @entity11 cells and @entity11 stem cells with parenchymal cell populations and highlight the pathological impact and signaling pathways known for these types of cell-cell communication. The @entity5 not only nourishes @entity463 , but also provides a specialized niche for these stem-like cells. In addition, microglial cells, which can contribute up to 30% of a @entity1313 mass, play a role in @entity463 cell invasion. Moreover, non-neoplastic astrocytes can be converted into a reactive phenotype by the @entity11 microenvironment and can then secrete a number of factors which influences @entity5 biology. The young brain may have the capacity to inhibit gliomagenesis by the endogenous neural stem and progenitor cells, which secrete @entity5 suppressive factors. The factors, pathways, and interactions described in this review provide a new prospective on the cell biology of primary @entity1313 , which may ultimately generate new treatment modalities. However, our picture of the multiple interactions between parenchymal and @entity5 cells is still incomplete.    2011 Wiley-Liss, Inc.
