Figure 1.

Cellular heterogeneity of RTK aberrations in glioblastoma: implications for appropriate drug targeting (adapted from Francis et al. [30]). Dynamics of the glioblastoma genome may generate or select for subclonal populations of tumor cells that are highly resistant to treatment, overall suggesting that comprehensive characterization of tumor heterogeneity is a prerequisite for the success of pharmacological inhibition of RTK alterations. Left, multiple amplifications of distinct RTK genes can be observed in non-overlapping subclonal populations from individual tumors, or within individual tumor cells. In other cases (right), tumor heterogeneity may exist as multiple alterations within a single RTK gene.