Introduction to Erg-Fusion Mutation Prostate Cancer

This figure from The Cancer Genome Atlas Research Network explains how the 333 different types of prostate cancers can be tied to different epigenetic, genetic, and protein expression changes. Additionally, it helps describe how the fusion mutation occurs and how it impacts different pathways.

“The Molecular Taxonomy of Primary Prostate Cancer.” 2015. Cell 163 (4): 1011–25. https://doi.org/10.1016/j.cell.2015.10.025.

 

Prostate cancer is one of the most common types of cancer for men in the world. In fact, only lung cancer, breast cancer, and colorectal cancer affect more people. With this being said, one out of seven cancer diagnoses in men is due to prostate cancer. It is clear to say that the 3.1 million new prostate cancer diagnoses and 307,000 deaths a year due to prostate cancer is a significant problem for society (Ferlay et al).

In addition to quantifying the amount of people impacted by prostate cancer, researchers have also started to determine all the factors that may increase or decrease the risk of getting prostate cancer. Al Olama et al. and their group completed a metanalysis to look at the risk factors of over 87,000 people. They were able to trace these risk factors such as race, age, and family historyand identify 23 new loci that impact the likelihood of developing cancer.

The mechanisms that cause prostate cancer include DNA hypermethylation, AR pathway activity, DNA repair defects, and PI3K/RAS/RAF pathway activation. Since these four broad categories make up 333 different ‘types’ of prostate cancer, it can be hard to determine what similarities these cancer cells have in common (“The Molecular Taxonomy of Primary Prostate Cancer“). With this being said, these broad classifications serve as a general reference for the type of mutation a prostate cancer cells may have. It would not be uncommon to see cancer cells with many additional mutations that increase the severity of the disease. In addition to the many mutations that may arise after the aforementioned mechanism, the field of prostate state cancer is immense since it covers a variety of disciplines. Since it is nearly impossible to summarize the whole field of prostate cancer in one document, I will focus on one mutation that leads to prostate cancer, the TMPRSS2-ERG fusion mutation.

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