While adult body mass is approximately the same for the dinosaur and the elephant, duck-billed dinosaurs are thought to have had a shorter lifespan. Metastatic cancer was found in a duck-billed dinosaur, suggesting cancer was common enough in that lineage to be preserved in the fossil record, but not in other species of large dinosaurs. In contrast, cancer risk was estimated to be 5% in elephants. For instance, cancer risk, which is 11–25% in the human population, is not vastly different between mice and humans. The solid blue line represents the observation that there is no relationship between cancer risk and (body mass)*(lifespan). The solid red line indicates a linear relationship between cancer rate and (body mass)*(lifespan) and the dashed red line represents an approximation of the expected cancer rate assuming a model describing the probability of an individual developing colorectal cancer after a given number of cell divisions. Thus, the expected cancer rate for large and/or long-lived species is higher than for smaller short-lived ones. Cancer is a disease of uncontrolled cell growth and division, and the risk of developing cancer increases with the number of cell divisions during the lifetime of an organism.
This has profound implications for our understanding of how nature has solved the cancer problem over the course of evolution.Īn illustration of Peto’s Paradox. In fact, the evidence suggested that larger long-lived mammals actually get less cancer. However, a 2015 study that compared cancer incidence from zoo necropsy data for 36 mammals found that a higher risk of cancer does not correlate with increased body mass or lifespan. Therefore, large bodied and long-lived organisms should face a higher lifetime risk of cancer simply due to the fact that their bodies contain more cells and will undergo more cell divisions over the course of their lifespan (Fig. If every cell division carries a certain chance that a cancer-causing somatic mutation could occur, then the risk of developing cancer should be a function of the number of cell divisions in an organism’s lifetime. Some somatic mutations may occur in genetic pathways that control cell proliferation, DNA repair, apoptosis, telomere erosion, and growth of new blood vessels, disrupting the normal checks on carcinogenesis. These mistakes are called somatic mutations. Every time a human cell divides, it must copy its six billion base pairs of DNA, and it inevitably makes some mistakes. In a multicellular organism, cells must go through a cell cycle that includes growth and division.
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