  As mentioned above, for most of the last twenty or so years of the 20th Century and the first decades of the 21st, the central concern of the majority of cancer researchers seems to have been identification of mechanisms at the cell and molecular level that regulate cell birth and death. Two characteristic features of cancer cells are their uncontrolled growth, and failure to undergo cell death.  This is often accomplished via changes to the “cellular machinery,” or mutations and associated disruption of pathways associated with regulation of cell division or cell death (Hanahan &amp; Weinberg 2001). So, it is natural to assume that explaining cancer requires identifying the chromosomal alterations, mutations, and epigenetic changes to cells that give them distinctive capacities of a cancer cell, as well as describe the ways in which these mutations systematically yield these effects. This framework for explaining cancer has been characterized as “somatic mutation theory,” insofar as cancer is viewed as a product of a series of mutations to cells during somatic cell division. Onset of cancer, on this view, may be accelerated either by inheritance of “oncogenes” or “tumor suppressors,” or by damage to DNA, for instance, due to smoking or UV radiation.