Q&A with Metastatic Researcher, Suzanne A W Fuqua, Ph.D.
As you may have heard, this month we are partnering with the Breast Cancer Research Foundation for our first research grant, a $250,000 donation named the Kendra Scott Award in Honor of Holley Rothell Kitchen. So we decided to chat with our grant recipient, Dr. Suzanne Fuqua, to learn more about the powerful impact she's making in breast cancer research. (Spoiler alert: You might have a girl crush on her after reading this!)
First off, can you tell us a bit about you?
I’m a homegrown, Texas-educated girl. I went to the University of Houston for both my Bachelor’s and Master’s, and then finished my PhD at MD Anderson in Cancer Biology in 1981. After I got my PhD, I moved to San Antonio to train with the best – the late Dr. William McGuire, who started the San Antonio Breast Cancer Symposium. He built the world’s largest tumor bank, donated by women with breast cancer from all over the United States. I learned from a man who said, “We’re going to conquer this disease if we study the cancers that we get from patients that allow us to research their tumors.” Essentially, after graduating with my PhD, I’ve dedicated my whole career to breast cancer. I’ve come to understand why some therapies work, why some therapies don’t work for certain women, and how we can prevent the critical problem of metastasis.
Why choose to focus on metastatic breast cancer?
It is my focus now because I’ve realized that, simply put, it is metastasis which kills patients. What we’ve learned in years of research is that the primary cancer, which we scientists have studied for so long, is not the same as the metastasis. The tumor changes. Once it gets out into the body, into the bloodstream, it changes in some very bad ways. The tumor acquires some really nasty tricks in trying to avoid therapy. We call that resisting to the therapy – it’s not responding to whatever drug we’re using. The cancer’s ability to change and our ability to understand those changes, that to me is the critical heart. I think if we can target those steps of cancer evolution, that will be the real cure for breast cancer.
We love the passion you have in your work. What inspires you every day?
I have seen too many of my friends, and friends of friends, battle breast cancer. I call cancer the enemy, and I feel like a solider … I really do. I go to work every day and I’m trying to find the right bullet – the right drugs, or combination of drugs – that will beat the enemy and stop the metastasis.
Have you had any breakthrough moments that stand out to you in your career?
I have a few. The experiment I did that was probably most life-changing for me, and now we know it’s been life-changing and treatment paradigm-changing, was in the early 90’s. I gathered up samples that showed metastasis from our tumor bank (there were only 30 out of 100,000 samples) to see if there were changes or mutations in a specific gene. The gene I was interested in is called the estrogen receptor. It acts like a receptacle for the hormone estrogen. I hypothesized that in these metastatic samples, we would find a mutation – something that went wrong in that gene which would prevent a patient from benefitting from the therapy that’s targeted to that gene.
I found 3 out of the 30 metastatic breast cancer samples had this mutation, which to me was groundbreaking. But for years our work wasn’t recognized because no one could repeat it. It wasn’t until 4 years ago, at the San Antonio Breast Cancer Symposium, that 5 papers came out that said my work was finally confirmed, that 40% of women with metastatic breast cancer have this mutation – and this mutation is the direct cause of why the drug doesn’t work.
The take home message of that “breakthrough moment” in my career is that I made a discovery that wasn’t really appreciated at the time. And I’ll be honest, it has formed the person I am today.
Tell us more about this “estrogen receptor” and the work you’re doing with BCRF.
Think of it like a lock and key. The estrogen receptor requires estrogen, which is its key, and the lock closes behind it to keep the estrogen contained. When this receptor mutates, the lock breaks and it doesn’t care about the key. It’s open all the time and estrogen is free-flowing out of it, actually causing the cancer to grow faster.
The work I’m doing with BCRF is studying estrogen and mutations in the estrogen receptor, which determines how estrogen works, to see how it not only evades cancer therapy but also how it’s driving metastasis. What we have learned is that this resistance to therapy is caused by a mutation, mutations that happen more frequently in metastatic breast cancer, and these mutations are the very root of the evil of why it spreads. Our goal is to find drugs that still work on this broken receptor and combine that with a drug that targets the metastasis it’s driving.
So you think a cure for cancer is within reach?
People love to use the word “cure.” But cancer, as the enemy, has so many ways it can change. I think of it like a chameleon - cancer can change that quickly. You give it a drug and it’s going to start picking up on the scent right away – it’s changing colors. And once it changes, you can’t go after the same color again. What I really see as the future of breast cancer is that we will understand what color that cancer will change into, anticipate it and stop it – before it changes.
We are on such a breakthrough track now, I think for the first time in my life I am able to say I see the end of the tunnel. I see us managing metastatic disease like we do diabetes, which I couldn’t have said 5 years ago. If the cancer is being controlled, I see that as a cure. And I think we’re getting close, and people like Kendra Scott who are able to help us, they are the reason we’re going to be successful.