Breast cancer experts gathered at the 2017 American Society of Clinical Oncology meeting to discuss developments in research and treatment. Patient Power founder, Andrew Schorr, was on-site in Chicago and interviewed Dr. Julie Gralow, Director of Breast Medical Oncology at the Seattle Cancer Care Alliance. Dr. Gralow shares highlights from the conference, including an update on immunotherapy and targeted therapy approaches. She explains what emerging research could mean for people with triple-negative, HER2-positive or BRCA-positive breast cancer.
Hello and welcome to Patient Power. I'm Andrew Schorr. We're in Chicago. I'm standing with an old friend, Dr. Julie Gralow, who is a world-famous breast cancer specialist at the Seattle Cancer Care Alliance and the University of Washington. We're at the American Society of Clinical Oncology meeting, the ASCO meeting, and there's news that happens here, and some of it is significant for women with more advanced breast cancer. So, first of all, Julie, thanks for being with us.
Thanks for having me. It's good to see you again, Andrew.
Good to see you. So tell us what seems to be significant that women with some types of breast cancer should pay attention to.
I think the most important breast cancer presentation which is going to impact clinical care when we go back to the clinic tomorrow is related to the PARP inhibitors. This is a class of drugs that is already approved in ovarian cancer in women who have a BRCA1 or 2 gene mutation. So we've got four or five of these drugs available in ovarian cancer, and what we saw at this meeting was the first presentation of a PARP inhibitor, olaparib (Lynparza), for metastatic BRCA1 or 2 positive breast cancer.
Now, that might only be 5 to 10 percent of breast cancer patients, but these drugs work very well with low toxicity relatively in this population. The study, the OlympiAD study, was a study of women with known inherited mutations in the BRCA1 and 2 gene, and they were randomized to kind of standard of care, whatever would be typical that they would be treated with versus a single agent oral pill, olaparib, whose main side effect is probably nausea, a bit of nausea.
And what we found was a superior time until the tumor started growing again from this oral agent. It works on DNA repair. The BRCA1 and 2 genes are involved in DNA repair. So when you have a mutation in one of them, you can't repair the tumor's DNA as well. So this is a really important finding, a new drug that will be available for a small subset of breast cancer patients tomorrow.
On the other hand, however, we are looking at this in a broader population, so while I think we'll be using it pretty quickly in clinic to treat BRCA1 and 2 mutation carriers, I think that we're studying are there other subtypes of breast cancer that kind of also have DNA repair inabilities that are part of what cause them to be cancer and would they also benefit? We have an ongoing SWOG trial looking at triple-negative breast cancer patients getting chemo, randomizing them to one of these PARP inhibitors or not to see if it actually accentuates the benefit of chemotherapy. And so we're trying to expand these drugs into a much broader population.
You brought up triple negative. We actually have someone who works with Patient Power who is dealing with that, and so there hasn't been that much. So is there the hope for that other population as well if they're not BRCA1 and 2 positive?
Right. Well, a subset of triple-negative breast cancer also acts, it has what we call BRCA-ness, and it has problems built into it based on the genes that cause the cancer in terms of repairing DNA, and that might only be a quarter of triple-negative breast cancer patients. That's just a guess. We don't really know. We don't know the right assays for picking out that group, although there are some out there now, and we're hoping that we'll find at least a subset of triple-negative breast cancer that benefits from these PARP inhibitors.
I mean, after all, I think we're understanding triple-negative breast cancers, multiple subsets, you know. There was a good study out of Vanderbilt a few years ago suggesting that just triple-negative breast cancer, which is about 18 percent of breast cancer, is seven subsets in and of itself.
The one triple-negative abstract that we saw that offers maybe some promise is one of the immunotherapies, pembrolizumab (Keytruda). It's an immune checkpoint inhibitor that you probably talked a lot about, because it's approved in a lot of other types of cancer, hasn't been a home run in breast cancer to date. None of these nonspecific immunotherapies that just kind of rev up the immune system have been a home run in breast cancer, but maybe in a subset of triple?negative we're seeing hints of activity. It would be great to have a therapy for triple-negative breast cancer that wasn't just chemo.
Okay. And HER2-positive women, you have had different medicines available now for a while. Many of them are doing quite well.
That's true, and we have four FDA-approved HER2 targeted drugs, probably a fifth on the way, neratinib, for kind of the extended early-stage setting. Is just was in front of ODAK and got a positive vote, so we'll see what the FDA says.
There were several abstracts here related to HER2-targeted therapies. The big one just from about an hour ago was a trial called the INFINITI trial. It was a trial on early stage breast cancer patients getting chemo and trastuzumab or Herceptin, and randomizing to get pembrolizumab, Perjeta or not. And while it was a positive trial, so women who got both of those HER2 antibodies did better statistically than women who only got the one antibody, trastuzumab or Herceptin, it was a tiny difference. For the whole population it was a less than 1 percent difference.
So—and it's expensive. It adds toxicity like diarrhea and rash, so I think we're going to have to figure out how—who needs these, you know, who is likely to still have a relapse with the standard chemo and trastuzumab and who needs more. I think one of the most important points of that whole presentation and what I was staring at when I looked at the slides was all women in the trial were doing really well. I mean, less than 5 percent of women in that trial had relapsed at five years. That's pretty good.
So I think that's the good news, and I don't think we need to keep adding more and more and more HER2 agents to the same population who's already likely to do very well. We need to focus our efforts on who is relapsing after the standard therapy, who is that small minority, and what can we do to change that.
So, Julie, with all you've talked about and looking at the broader population of women where breast cancer has spread, what do you want to say to them now with what you know, you see patients day in, day out, you're involved in all this research, that would them hope? We see different groups, subgroups, we talked about the BRCA1 and 2 groups, triple?negative subsets, so it seems like people need to know what they're dealing with their doctor, but overall it seems like a much more hopeful picture than ever before.
Well, there's a lot more hope, and women with recurrent or metastatic breast cancer are in general living a lot longer with therapies that in a lot of ways are less and less toxic. You know, we're giving less chemo up front in the majority of settings or maybe just a short course of chemo to overlap a HER2 drug and then stopping it, and we have a lot more women who are alive years and years and years.
I think we have some cures in the metastatic setting. I'm pretty sure I do in my clinic, but of course we don't know. We have to watch over time, but we've got so many goods drugs. We're subsetting breast cancer. Instead of a one-size-fits-all approach, we're subsetting—even ER-positive breast cancer is being subset into, you know, we call them the Luminal A and the Luminal B, one that responds a bit better to certain types of agents, the other that does just fine with the antiestrogen therapy. So we're subsetting and subsetting, we're individualizing, we're personalizing, and we're trying to decrease the toxicity of our therapies at the same time that we're increasing the efficacy, the benefit of our therapies.
Wow. I think it's a great story. So I guess, confirm for me, but I believe it's true, you and your doctor need to know what is your version of breast cancer that's become more advanced, and how do you get the least treatment that's most effective and on target for you. Am I right?
Okay. There we are with our friend, Julie Gralow, from the Seattle Cancer Care Alliance, University of Washington in Chicago, giving I think real encouragement to women even when breast cancer has spread or when it's come back. So we wish you all the best.
On location in Chicago, I'm Andrew Schorr. Remember, knowledge can be the best medicine of all.
Published By :
Jul 05, 2017
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