I finally got to watch Nova’s documentary on ‘The Ghost in Your Genes’ last night and was very excited to learn about the progress that epigenetics research has made in the last few years. 
As a believer that most complex diseases arise from gene-environment interactions, epigenetics has fit perfectly into a model for explaining disease risk. The work on how one identical twin can develop later in life, while the other does not, is such a prime example of how the environment can make alterations to a person’s genome over time. Researchers have underestimated (and some still do) the effect of methylation of DNA and other alternative genetic mechanisms affecting DNA expression on the risk of complex disease. This is likely why geneticists have not found strong support for genetic variants (i.e. SNPs) in their genome-wide association studies. From the perspective of a genetic epidemiologist, I have long thought that in order to determine susceptibility genes for complex disease, researchers need to look at environment effects (i.e. epigenetic influences) in the genome simultaneously.
NIH is starting to recognize the importance of understanding the epigenome and its role in human disease and recently announced the funding of several grants on this topic. Much more complex modeling and research studies are going to have been undertaken in order to start piecing this puzzle together but it is a very exciting time to see how it will unfold.
Happy Gene Hunting!
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Ah! It always feels good to read something that supports a theory- particularly when it comes to learning something about cancer- such a ubiquitous and noxious disease. In the recent issue of The Scientist, there is an article suggesting the idea of a viral cause for prostate cancer. Viral origins for cancer is not a new concept, by any means, and some go so far as to believe that all cancer is due to viruses. Human papillomavirus is thought to cause some cervical cancers (and now we have Gardasil and GSK’s new Cervarix® to hopefully reduce that risk) so why should it come as a shock for a virus could cause prostate cancer?
I find this article particularly interesting because my master’s thesis examined a large dataset (SEER registry cases) of prostate cancer cases and controls for factors which interacted with an increased 3-fold risk of having a first degree relative with prostate cancer. While the results of this study did not find an association between an increased number of sexual partners and prostate cancer directly, it did find a highly significant association and interaction between a high number of lifetime sexual partners (20+) and men who had one first degree relative with prostate cancer (RR: 4.5, 95%C.I.2.4-8.5). Unfortunately, due to political reasons (a senior person at NCI wanted to publish his own analysis on family history risk), I was not permitted to publish this finding. I have always suspected that having a large number of sexual partners in a lifetime would be associated with increased risk of sexually transmitted organisms, which could easily be a virus similar to HPV. Since many of these viruses ubiquitously infect the majority of people are exposed to them, the rate limiting factor for how soon a man develops prostate cancer (and it is thought that most all men will develop this cancer if they live long enough) may depend on his personal genetic makeup and resistance to viral infection and/or viral mutation of somatic cells in the prostate.
So what do you think? Would love to hear any opinions on this!
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As a believer that most complex diseases arise from gene-environment interactions, epigenetics has fit perfectly into a model for explaining disease risk. The work on how one identical twin can develop later in life, while the other does not, is such a prime example of how the environment can make alterations to a person’s genome over time. Researchers have underestimated (and some still do) the effect of methylation of DNA and other alternative genetic mechanisms affecting DNA expression on the risk of complex disease. This is likely why geneticists have not found strong support for genetic variants (i.e. SNPs) in their genome-wide association studies. From the perspective of a genetic epidemiologist, I have long thought that in order to determine susceptibility genes for complex disease, researchers need to look at environment effects (i.e. epigenetic influences) in the genome simultaneously.
