  This picture of cancer was pieced together over decades from various sources of evidence—from Virchow’s observations of chromosomal abnormalities in cancer cells, to epidemiological patterns of incidence in cancer, to the discovery of the “src” gene—one of the first mutations found to be associated with cancer.  This vision of cancer as the product of oncogenes replaced a “regulatory” view of cancer, according to which cancer was a “breakdown in normal constraints on growth” (for a history, see, e.g., Morange 1993, 1997, 2003). Not coincidentally, the “oncogene paradigm” arose at the same time that some of the first bioengineering technologies, which enabled early cancer researchers to use the techniques of molecular biology to study identify genes associated with cancer progression (Fujimura 1987). While this is a reductionist research program, in the sense that the aim is to decompose the system of interest and understand the parts in operation, not all early advocates of the multistage theory were cell and molecular biologists. Two of the first advocates of a multi-stage theory of carcinogenesis—Armitage and Doll—found that curves of average lifetime incidence of lung cancer in smokers appeared to have the same shape as that of nonsmokers, simply shifted to earlier ages. This suggested that cancer could arise from a rate-limited series of insults acquired over the life course. Since the 1980s, hundreds of genes have been identified, mutations to which are associated with the hallmarks of cancer. Carcinogenesis, on this view, results from damage to DNA, or errors in the process of cell division, as well as either endogenous factors (various hormonal or other factors that promote cell growth), or exogenous factors (infection, and inflammation), which over time can lead to dysregulated cell growth.