The cancer stem cell hypothesis postulates that only a subpopulation of cancer cells in a tumor is capable of initiating, sustaining, and reinitiating tumors, while the bulk of the population comprises non-stem cancer cells that lack tumor initiation potential. The interactions of these two phenotypically distinct populations can provoke various nonlinear growth kinetics in the emerging tumor. An environmentally independent, intrinsic dormant state is an inevitable early tumor progression bottleneck within a range of biologically realistic cell kinetic parameters. In certain conditions, cell kinetics can combine to enable escape to tumor progression, yielding morphologically distinct self-metastatic expansion of multiple self-limiting tumor clones.