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The evolution of p 53 network behavior

A major cause for the emergence of tumors is genetic mutations that occur when the cellular DNA is damaged and not repaired to its original state. When the mutations interfere with the normal regulation of cell division, then cell proliferation could cause the tumor to become cancerous [1]. While there is abundant evidence that exposure to chemical carcinogens and radiation has had an impact on cancer rates [2], there is also evidence that cancer is a general feature of multi-cellular organisms that has presented a long-standing evolutionary challenge [3]. A key component of the DNA damage response mechanism is the T P 53 gene which expresses the p53 tumor suppressor protein, the so-called "guardian of the genome" [4]. p53 and its ancestors have been protecting metazoans from mutations arising from DNA damage for over one billion years [5]. Recent research has shown that p53 plays this role by first sensing DNA damage, and then mediating various downstream processes in response. p53 can promote cell survival by upregulating genes that bring about cell-cycle arrest or DNA repair. However, p53 can also promote cell inactivation or death by bringing about permanent cell-cycle arrest or cell death [6–9]. How p53 levels and dynamics determine different cell fates in response to DNA damage is a crucial component of an organism’s tumor suppression mechanism [10–13]. It is therefore no surprise that a mutation in p53 is implicated in over 50% of human cancers [14]. One of the oldest known mechanisms cells employ in response to DNA damage is programmed cell death, also known as apoptosis [15]. Cells with DNA that is damaged above some "apoptotic threshold" level generally display sustained high levels of p53 [13, 16, 17], inducing the expression of proelimination genes [12, 16–18] that bring about apoptosis, thus limiting the risk that a cell lineage will become cancerous. The underlying behavior can be understood in the context of Statistical Decision Theory by imagining that cells attempt to decide on the truthfulness of the statistical hypothesis: "The damaged DNA can be repaired to its original form". It is clear that setting a low apoptotic threshold minimizes the risk of cancer since a cell that experiences potentially cancer-causing DNA damage would go to apoptosis. A feature of such networks is that they abet Type 1 errors. Such errors happen when the statistical null hypothesis is true (i.e., DNA can be repaired to its original form), but the cell is killed anyway. While not ideal, Type 1 errors would still be preferable to Type 2 errors, where a cell carrying a cancer-causing mutation could be allowed to live. A single Type 2 error could lead to lethal cancer, and this is in fact known to be one of the "hallmarks" of cancerous clones [2, 19]. That said, overly responsive networks with a low apoptotic threshold may result in developmental defects, reduced tissue growth, or high metabolic costs to replace the dead cells. A major task for p53 and the DNA damage response mechanism is therefore to effectively suppress the onset of tumors by selecting different cell fates that would increase whole organism fitness. This is achieved by trading-off between minimizing the number of Type 1 errors that take place, while also trying to suppress all Type 2 errors. While p53 is a vital component of the damage response network, it acts as part of a network of interacting genes that