In clinical trials available today, patients with ER-positive breast cancer were randomized to endocrine therapy with or without PI3K inhibitors or mTOR inhibitors. In some trials, particularly with the mTOR inhibitor Afinitor (everolimus), for example, PI3K
mutations were prognostic, but not very predictive of response to the mTOR inhibitor. With PI3K inhibitors, there is a study that showed that those patients may respond better to a PI3K inhibitor in addition to the endocrine therapy. However, that inhibitor was too toxic. Therefore, we are now looking at more selective inhibitors, such as PI3K inhibitors.
We need to continue to test those. I don’t think we are at the point to be able to personalize and use this information in the clinic—to select one therapy versus the other.
Is there anything else you would like to add?
Over the last 15 years or so, we have been focused on protein coding genes. We even tend to focus on larger genomic testing, but each human cell has 20,000 genes—making it a large and complex system. There are thousands more noncoding genes, which we don’t know much about, and that is another area where we are trained to focus on if they are expressed, what they regulate, and what they do.
Additionally, we have the microenvironment, which relates to the immune system and many other things that are not directly in the cancer cell. We need to be able to understand all of this to truly develop personalized medicine in the future.