The Cure for Cancer

Yes, I love comics. Especially when they prove a point I'm trying to make, which phdcomics often do.

The last paper we studied this quarter in the RSP journal club was one about prostate cancer. Surprisingly enough, it was my turn to select a paper and this was the one I came up with. And prostate cancer and/or genomics isn't something Environmental Scientists normally deal with.

But I chose this paper because it made no sense to me when I first read it. Normally, I don't go into papers involving intense genetics, but for once it really bothered me that I couldn't understand this paper's contents. And my best chance of understanding this paper was through the RSP journal club, and that turned out to work fine.

So cancer and it's complexities is something that noone fully understands, as we had discussed last week (refer: comic posted above). Prostate cancer, in particular (which this paper studied) causes 32,000 deaths annually, and over 200,000 new prostate cancer cases are reported each year, and most of these patients die because of it. Therefore, understanding the genetics of prostate cancer is of vital importance. That is exactly what this study tried to do.

They conducted pair-end, massively parallel sequencing on the tumor and compared the DNA from the tumors of of seven patients with compared it with  'normal' DNA. Now, this method of sequencing, can safely be called the newest and most amazing technology in genetic analysis. It is computationally heavy, and comparatively much faster than 'regular' sequencing. It's almost like sequencing thousands of strands at the same time! And to process that amount of information is even harder than running the analysis. So it's no wonder that this study was the first whole genome sequencing analysis of prostate cancer.

And the researchers came up with interesting results. I was recently discovered that chromosomal rearrangements, particularly recurrent gene fusions occurs in prostate cancer cells, which led to the idea that other genomic rearrangements may also play a more important role in the development of prostate cancer.

And the researchers were right in believing so. Here's what they found:

• 3 tumors with rearrangements that led to the disruption of CADM2 (I'll be honest: I have no idea what the role of CADM2 is, but I'm working on trying to find that out. I'll update this post when I do!)
• 4 mutations that resulted in disruption of either PTEN, a prostate tumor suppressor, or MAGI2, which plays an important role in the formation of tight junctions (read previous post on cervical cancer)
• A median of 3866 somatic base mutations per tumor (that's a lot!), which is similar to those in breast cancer.

While we were discussing the paper, I remember someone suggesting that some of these mutations might be the effect, rather than the cause of prostate cancer, because there wasn't a distinct pattern in the mutations of these seven tumors. I think that's an interesting theory, and something for scientists to definitely think about over the next several years. If anything has been made clear because of this fantastic study, it's the fact that cancer is probably even more complex than we had imagined, which is certainly saying something!


 Link to paper: I don't have it! I'm sorry. But I'm still looking. Here it is: http://www.nature.com/nature/journal/v470/n7333/full/nature09744.html#/landscape-of-genomic-alterations

Also, take a look at this:

And this: