Investigaciones sobre el cáncer de mama (seno) en ASCO 2026

Welcome to The Breastcancer.org Podcast, the podcast that brings you the latest information on breast cancer research, treatments, side effects, and survivorship issues through expert interviews, as well as personal stories from people affected by breast cancer. Here's your host, Breastcancer.org Senior Editor, Jamie DePolo .

Jamie DePolo: Hi, I'm Jamie DePolo, senior editor at Breastcancer.org, and I'm podcasting live from the 2026 American Society of Clinical Oncology Annual Meeting. My guest is Dr. Eleonora Teplinsky, a board-certified medical oncologist who specializes in breast cancer and gynecologic oncology. She's the head of breast and gynecological medical oncology at Valley-Mount Sinai Comprehensive Cancer Center in Paramus, New Jersey, and a clinical assistant professor of medicine at the Icahn School of Medicine at Mount Sinai in New York.

She's also the host and creative force behind the INTERLUDE podcast, which shares the stories of women who've been affected by cancer. Dr. Teplinsky also serves as an ASCO expert. She's going to explain some of the most important breast cancer research presented at this year's conference.

Dr. Teplinsky, thanks for joining us. So, what caught your attention this year?

Dr. Eleonora Teplinsky: Thanks for having me. You know, there's been a lot of discussion here at ASCO, this year, about, kind of updating on studies that have been published. So sometimes, we see brand new studies and lots of ground-breaking things, and sometimes, in a year like this one, we are building on all the studies that have been presented to really understand longer-term follow-up, nuances in the population, and outcomes. So, I want to put that out there, that not every year is going to be the year in breast cancer, but one of the big studies that is new that did catch my attention is the OPTIMA trial.

And what that really looks to see is can we broaden the group of patients where we can omit chemotherapy in hormone receptor-positive, HER2-negative breast cancer. So, currently, if someone has more than three lymph nodes, we recommend chemotherapy, generally, and for pre-menopausal women who have lymph node-positive disease, the current data has shown a benefit to chemotherapy, and there are studies kind of looking into that more.

And the question really has been, in the pre-menopausal space is, is it the benefit of chemo, or is it that chemo makes someone menopausal, you know, induces ovarian suppression? So, which one really is it, right? Because these are very hormonally-driven cancers.

So, what they did in this study was they had two groups. One group received, so, you had to have 0 to 9 positive lymph nodes. And if you had negative or zero lymph nodes, you had to have a tumor size 3 centimeters or greater. So, one group received standard chemotherapy and endocrine therapy, and these were patients 40 years of age or older, and then, the other group received a molecular test-driven strategy. They used a test called Prosigna. Now, people may not be familiar with this test.

We typically use Oncotype or MammaPrint as our molecular test, but Prosigna is another one that was used, and if you had a low recurrence risk based on the Prosigna result, you received endocrine therapy alone, and if you had a high risk, you received chemotherapy and endocrine therapy.

And what they found was that there was no difference in these two arms, of the standard chemo and endocrine or that test-driven strategy of potentially de-escalating chemotherapy, and that benefit held up in patients with up to nine positive lymph nodes and in pre-menopausal women. So, very exciting.

A couple of caveats to the study that I think we have to keep in mind, and one, people are going to be listening to this and saying, well, I didn't get Prosigna, or I didn't get this, and I had to do chemo, and I want to acknowledge that as data comes out where we de-escalate treatment, that can be hard to hear if you had to do more intense therapy, but it's short-term follow-up.

So, we know our cancers can recur 10, 15, 20 years down the road, and they have not followed patients for long enough yet. So, we have to keep that in mind, number one. Number two, people are going to ask, well, I had five positive lymph nodes and my Oncotype score said this. Can I omit chemo? And we have to keep in mind that these are not the same tests.

And I would caution anyone about using a test that was not used in this study to omit chemotherapy. And then, lastly, we don't yet know about the endocrine therapy that was received. So, in this study, very important, all of the pre-menopausal patients had to receive ovarian suppression. So this really answers that question of, is it the chemo or is it the ovarian suppression? But they had to receive ovarian suppression. We don't know if they received tamoxifen or an aromatase inhibitor. We don't know how long they stayed on it.

So, I'm a little hesitant about kind of broadly applying it because let's say you have a hard time tolerating chemotherapy and endocrine therapy, and now, you've omitted chemo, where does that leave us? And again, patients 40 years or older, so, it's not going to be the younger, very young population. So, lots of questions, I think promising, you know, more data will emerge with time and will build on that.

Jamie DePolo: I'm glad you pointed out the under 40 because I feel like that was a question. What if somebody was 38, 39 diagnosed, but we can't really apply the results to them, can we?

Dr. Eleonora Teplinsky: No, we really can't, and I think sometimes we want to deescalate where we can, and so, there's like, oh, can we do it in a little bit younger? But I think, sometimes, you do have to be a little bit of a purist and follow the data. And I think the part that is also interesting is, you know, we've talked a lot recently about pregnancy-associated breast cancer and postpartum-associated breast cancer, and those cancers do tend to be more aggressive.

And so, it'd be interesting to see, and I don't know if we'll get that data, but how many of the patients in this group would fall into that category. So, I think I'm going to use it, but I'm not going to blanketly apply this. You know, I think that it's going to be a conversation because, again, we don't have that longer term follow-up just yet.

Jamie DePolo: And then, it seems, at this meeting, there's been a lot of discussion about new oral SERDs, selective estrogen receptor, either I've heard downgraders, or downgraders or degraders, one of the two Ds, and how that might work and where they fit in.

Dr. Eleonora Teplinsky: SERDs are definitely the hot topic. I mean, everyone's talking about SERDs. So, let's separate it. Let's talk about early-stage and metastatic. I'll start with metastatic because it's a little bit easier. So, for metastatic breast cancer, we have several SERDs approved. We have elacestrant, we have imlunestrant, we also have fulvestrant, but that's been around for a long time, so, and that's not oral, right? So, we're talking about oral SERDs.

The way that they work is that they're different than your aromatase inhibitor, which blocks estrogen production. These degrade and downregulate, so they do both, the estrogen receptor. And so, they're thought to be a little better-tolerated. And currently, in the metastatic setting, they are approved for patients who have an ESR1 mutation. So, an ESR1 mutation essentially is when the estrogen receptor is just turned on. It no longer, normally, you know, the aromatase inhibitor blocks estrogen production.

I think of this, and there's nothing to fuel the estrogen receptor, and it shuts off, you know, the cancer cell can die or slow down. With an ESR1 mutation, the estrogen receptor is always on. So, it no longer responds to that estrogen that's floating or being blocked. So, the door is always open, if you will, causing cell growth. And so, the drugs are currently approved for patients who have an ESR1 mutation. There was recently an approval for the drug vepdegestrant, which is a PROTAC, which works a little bit differently.

It actually kind of uses the body's degradation or garbage machinery to degrade the estrogen receptor. So, a little bit of a different way of blocking. So, that's in metastatic disease, and the approvals currently, again, are all in ESR1 mutations. We're seeing data with giredestrant that's going to be presented at this meeting with the evERA trial, which is also oral SERD in metastatic disease. So, more to come on that.

Now, in early-stage breast cancer, and I think this is where the big excitement is, at the San Antonio breast cancer meeting in 2025, we saw data from the lidERA trial, which looks at the oral SERD giredestrant, in early-stage breast cancer, and they found really important things.

They found that it reduced the risk of recurrence compared to standard endocrine therapy by about 30%, but also was better tolerated. There was less discontinuation, especially on the basis of joint pain. So, there's a lot of excitement about, when are we going to have it? And how are we going to use it? And notably, giredestrant, in this study was given with ovarian suppression.

So, a lot of excitement about, oh, can I avoid ovarian suppression? And probably not, and there was some data presented recently that showed that it was in the neoadjuvant setting where people who had not yet had surgery and showed that giredestrant didn't work as well without the ovarian suppression. So, more to come on that. And then, the other part is that in the lidERA trial, so far, they did not combine with the CDK4/6 inhibitor or present that data yet, like Kisqali or Verzenio, so, but right now, it's not yet approved in early-stage breast cancer.

We don't know when it's going to be approved yet, hopefully in the next six-plus, 12 months, but you know, these things take time, unfortunately, and I think that's always a concern for all of us. But they did present an update from the lidERA trial at ASCO, this week, and what they found was that the benefit of giredestrant was there, regardless of pre-menopausal or post-menopausal, because that's important, right?

Again, we think of our premenopausal women as sometimes having a little bit more aggressive disease, and so, we want to make sure that we're adequately, if we're switching therapy, that it's effective. So, that's what we received, you know, with lidERA, but we're still waiting for that FDA approval.

Jamie DePolo: And then, I want to ask you, too, there were a couple of presentations that talked about PFS2, progression-free survival 2, which I had to look up a couple of times. It seems very complicated to understand, and I'm wondering if you could explain that and then talk a little bit about the one study, the ASCENT-04 trial that made kind of a big splash.

Dr. Eleonora Teplinsky: PFS2, also a hot topic for so many reasons, and it's a hard concept. I think I even have a hard time understanding PFS2, but basically, when you think about, first, let's understand what PFS is, so, progression-free survival. So, if we give someone a treatment, and we say that it improves progression-free survival, meaning it reduces the time until…while they remain alive until their disease progresses.

So, if something has an average PFS of 12 months, that means, on average, people will have stable or improved disease for 12 months before they develop disease progression. PFS2 looks at that next line of progression with the next treatment. So, let's say someone is on an aromatase inhibitor, okay? And at 12 months, they progress, and then they're switched to a SERD, for example.

And then, in six months, they develop disease progression, right? PFS2 is that 12 months and six months added together. There's going to be 18 months. So, some people will measure it from, you know, there's different ways of measuring it, and maybe report it a little differently. But think of PFS2 as that time to the subsequent progression after that next line of therapy. And why is it important?

Well, the question becomes if you did an aromatase inhibitor and a SERD versus giving a SERD in the first line setting, if the PFS2 is equivalent, right? So, whether you do AI and then SERD, or SERD then AI, and the PFS2 is equivalent, that tells you there's no difference as long as you give them both. But if PFS2 is greater with AI than SERD, for example, that tells you that the sequence becomes important.

So, it really helps us think about sequencing. So, hard concept, but think about it basically in what happens after there's disease progression and in the next line of therapy that you give, right? And it helps us, again, think through what is more beneficial to give first, what is more beneficial to give second, and so forth.

So, now, we have the ASCENT-04 trial. So, ASCENT-04 is patients with metastatic triple-negative breast cancer who have never been treated for metastatic disease, and they also are PD-L1 positive, okay? And the standard has been chemotherapy with the immune checkpoint inhibitor pembrolizumab or Keytruda. That's the standard of care. ASCENT04 looked at instead of giving chemo with pembrolizumab, what if you gave sacituzumab govitecan, which is an antibody drug conjugate?

This is Trodelvy. What if you gave sacituzumab govitecan with pembrolizumab versus chemotherapy plus pembrolizumab? And so, the original results showed an improvement in progression-free survival. So, meaning if you give Trodelvy first with Keytruda, you have a longer time until someone develops disease progression.

But then, what if they got chemo, and you gave them Trodelvy afterwards, right? Does it matter? Does the sequencing matter, right? So, now we have at ASCO the PFS2 benefit, okay? And what we see with the PFS2 benefit is that yes, people who received Trodelvy first have the greater benefit in further reducing disease progression than if they received chemo first.

And in a lot of the group that received chemo first, many of them went on to get Trodelvy afterwards, and so, it tells us that, yes, we should be thinking about Trodelvy first and then chemo rather than the other way around. So, I think that this, in particular, here reinforces what we are hoping will become the next standard of care, which is an antibody-drug conjugate with sacituzumab govitecan and pembrolizumab rather than chemo and pembrolizumab.

Notably, this doesn't yet have an FDA approval, but we're hoping that these kind of endpoints will help with further supporting FDA approval. And I think it's particularly relevant because we know with metastatic triple-negative breast cancer, there is a number of patients who are not able to receive subsequent lines of therapy, just due to how quickly the disease grows and progresses.

And so, we want to give our best drugs up front, right? To allow patients to hopefully stay on them for as long as possible and then have the opportunity to get next lines of therapy. So, hard concept, but think through of, like, is there sustained progression and does the sequencing matter?

Jamie DePolo: Thank you so much for explaining that. That was very helpful. I understand it much better. And I guess one quick question about that. If somebody did progress, if they received Trodelvy and Keytruda, is chemotherapy then the next treatment they would get?

Dr. Eleonora Teplinsky: Generally, yes. I mean, some people are using other antibody-drug conjugates. For example, trastuzumab deruxtecan is approved if you're HER2-low, and so, yes, I think that there's a little bit of not entirely clear. You know, there's a lot, there's several choices, but I will say that in metastatic triple-negative breast cancer, this isn't like a hormone receptor-positive breast cancer. We don't have as many options. So, one, we need more options, but yes, generally, then after that first antibody-drug conjugate, most people are going to probably go to chemotherapy at that point.

Jamie DePolo: Okay, thank you, and then, finally, the other thing that seems to be swirling around this meeting are GLP-1s and cancer. And to me, it seems like a lot of the studies are retrospective. So, I'm not sure how applicable they are, but what is your take on all that?

Dr. Eleonora Teplinsky: GLPs are definitely very…everyone's interested in the GLPs, for so many reasons. But one of the things we saw at this meeting is, again, a lot of retrospective studies where people are going and using large electronic health records or databases to pull diagnoses codes or billing codes, you know, for patients on a GLP-1 and look to see how does that impact in terms of cancer?

So, one of the big studies that we saw, again, one of these retrospective studies showing that the use of GLP-1 medications reduce the risk of disease progression or recurrence in several cancers, including breast. And there's some other studies about looking at potentially lymphedema reduction and other things, reduced cancer incidence. So, there's a lot of benefits, and I think it raises a number of questions that the community has, right?

We have to keep in mind that these are retrospective studies, number one. And we don't have the information about what type of cancer, what treatment did they get, right? We don't know any of that, number one. Number two, generally, these medications are being prescribed for FDA-approved indications. So, that is based on weight. That is based on diabetes, right?

We can agree or disagree on that, but that is currently what these medications are approved for. So, we do not know, because I've been getting asked a lot of questions, should I just go on a GLP-1, right? We don't have that answer yet. And so, we don't know if someone does not have diabetes or whatever their BMI is, if they don't meet those criteria, and we recognize BMI is not the perfect measure of health, but it's easy to abstract from, you know, and use.

Then would they have the same benefit in outcomes? And the reason we don't know this is because we don't entirely know yet what is the mechanism by which GLP-1s are reducing cancer risk? So, is it through weight loss? Is it through impact in metabolic health, right? And so, should we be thinking about metabolic syndrome, right, and all of these? Is it an insulin resistance?

Or is there an actual mechanism of the GLP-1 medication? And so, that's different, number one. Microdosing, lower doses, we have no data on that. And notably, many of these studies are using older GLP-1 medications. So, we don't know how this reflects current-day GLP-1 medications. So, my takeaway on it, and we do think, though, that it can be used with endocrine therapy — with aromatase inhibitors, tamoxifen — it can be used in metastatic disease.

There's some interesting, some very questionable, you know, things about, like, there's one study that showed maybe a concerning signal when using with chemotherapy, but it's all poorly defined, right now. And so, I think what's important is to think about it, you know, to talk to your doctor, right? You're seeing all these GLP-1 headlines. Ask your doctor, do you think this makes sense for me? Am I eligible for it?

But I want to stress that there are two, at least two that I know of, probably more, prospective trials going on where they're putting patients on a GLP-1 and following them. So, that will help us figure out benefits. 

But number two, we can't forget the foundational pieces of lifestyle medicine, right? So, the GLP-1s are one part of it, but we want to make sure that we're still prioritizing movement, and diet, and sleep, and stress management, and social connection, and all of these things that help us, too. So, I think more to come, but I do think there's been a little bit of hesitation or fear of, like, can I use these medications together? And I think, although, again, retrospective, we're comfortable with using the medications on endocrine therapy.

Jamie DePolo Dr. Teplinsky, thank you so much. That was so helpful. Always appreciate your insights.

Dr. Eleonora Teplinsky: Thank you for having me.

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