The Mutations Cancer Avoids

As a final blog, I came across something interesting on the internet. Usually we equate cancer proliferation with a mutation that results in a loss of function and the cell begins to replicate uncontrollably. However, a study published online today showed that while nuclear DNA of cancer cells has many mutations, the same is not the case for mitochodrial DNA (here). In fact, the scientists found that colorectal cancer cells has three times fewer new mutations than normal colon cells. The type of mutations found in normal colon cells were typical mutations in response to oxidative damage: C:G to T:A transitions. When you consider that cancer cells rely more on anaerobic glycolysis for energy as opposed to oxidative phosphorylation, the contrast becomes clearer. The scientists speculate that with fewer mutations, the cancer cell mitochondria function better, thus the cancer cells have a better metabolism and can live longer, if not forever.


This finding was interesting to me for two reasons. The most obvious is that it identifies cancer cell mitochondria as an important target for drugs. The more stress that chemicals can induce on the cancer cell mitochondria, the more it can impair the cell's metabolism and ability to survive. The second, and more philosophically-altering finding, is that instead of focusing largely on the mutations cancer cell's accrue, perhaps we should also pay attention to the ones they do not. Based on the decades of research, this approach may seem counterintuitive, but nonetheless this study sheds light on the possible importance of this approach. Perhaps the cancer cell's ability to resist mutation is a result of its internal wiring to find the most optimal condition.

It may be possible to study the cancer cell's lifespan and understand what mutations it undergoes and which ones it does not, but studying both sides of the fence will surely give scientists a greater insight. Along the lines of studying resistance to mutations, if the mechanism through which this is done is identified, it would provide another degree of drug targeting.

All things considered, I think the approach to studying which mutations cancer resists will provide a new element of understanding the genius that is cancer. Aside from the philosophical shift that this study suggests, what major differences are there between nuclear DNA and mitochondrial DNA? How does the environment of the two DNA affect their susceptibility to mutation? In which type of DNA does a mutation have a greater effect?

There obviously are a million different paths to take from this, and each seems to entail a greater discovery on the other end. A lot of the time we get caught up in trying to identify all of the ways in which cancer cells mutate that we sometimes forget that its mortality could be due to its ability to stay "normal". I think if we shifted the theoretical approach to understanding the genius that is cancer we may find a whole new world of treating it.