When it comes to cancer, tumor cells are constantly changing. Equipped with a dangerous advantage of genetic fluidity, these cells evolve to increase their chances of resisting drugs and immune system defenses.
The unfortunate fact that cancer cells are always evolving by highly sophisticated mechanisms makes it very difficult to predict how tumor cells will be affected by treatment. This often leads to patients receiving treatment and not responding to it, or responding only until their cancer comes back with improved defenses.
Researchers in the realm of precision medicine are continuously learning how cancer cells evolve, and it is becoming clear that mutation mechanisms in tumor cells are not completely random. In fact, a recent study led by researchers at the SIB Swiss Institute of Bioinformatics, University of Lausanne and EPFL, data was developed on how certain cancer cell mutations co-occur and work together.
Predicting Mutations to Advance Treatment
This theoretical framework, recently published in Cancer Cell, can predict the co-occurrence of about 500 known tumor alterations, and how these alterations can affect response to over 200 commonly used cancer treatments. The most comprehensive collection of molecular data from the Cancer Genome Atlas (TCGA) international consortium was used to reach these findings. This data includes 6,456 human tumor samples from 23 tumor types.
“Genetic alterations associated with the disease are not randomly picked based exclusively on their single effect, but combined and matched by evolution to maximize their synergy,” stated Giovanni Ciriello, Group Leader at SIB and at the University of Lausanne. Understanding this can allow predictions of which mutations are most likely to occur together, and to predict how the overall effect of these mutations can confer cancer cell resistance, or sometimes an increased sensitivity, to certain drugs.
Efforts to understand the evolutionary mechanisms of cancer is not new. In fact, researchers have been trying to understand how to approach the evolution of cancer cells for decades. In a 1976 article, esteemed cancer researcher Peter Norwell wrote that “more research should be directed towards understanding and controlling the evolutionary process in tumors before it reaches late stage seen in clinical cancer.”
After over 40 years, this statement is still true, as drug resistance continues to be a major clinical problem, not just in oncology.
And while evolution patterns in oncology are still far from understood, this framework of cancer cell dependencies can serve as a reference for functional and pre-clinical studies, and it is a crucial step in improving approaches for personalized therapies.
Last editorial review: August 17, 2017
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