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. Author manuscript; available in PMC: 2013 Jun 10.
Published in final edited form as: Cancer Res. 2011 May 24;71(11):3739–3744. doi: 10.1158/0008-5472.CAN-11-0342

Figure 2. Contrasting the Conventional Model for cancer initiation with Adaptive Oncogenesis.

Figure 2

A. For the Conventional Model, oncogenic events are generally advantageous, and thus cancer initiation is limited by the incidence of these events. B. For the Adaptive Oncogenesis Model, phenotype-altering epigenetic or genetic changes will rarely be advantageous within a population of healthy, well-adapted stem and progenitor cells. But following aging or damage-induced reductions in stem/progenitor pool fitness, oncogenic events that improve fitness should provide selective advantages. C. Proposed adaptive landscapes of stem cell populations within a healthy young individual or within an aged or carcinogen-exposed individual. The X and Y axes represent the potential genetic and epigenetic diversity. The Z axis represents fitness. Small arrows indicate mutational or epigenetic changes that could lead to cancer, which come with a high cost for cellular fitness for a young healthy stem cell population, but much less of a cost within a damaged stem cell pool.