Winter 2025 Breast Cancer Research Round Up

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: Hello, as always, thanks for listening. My guest is Dr. Kevin Fox, professor emeritus of medicine at the University of Pennsylvania. Dr. Fox is a medical oncologist who specialized in the treatment of breast cancer during his 36 years on the medical faculty. He’s also a Breastcancer.org medical adviser. Dr. Fox is going to explain some of the most important breast cancer research that was published or presented from December 2024 to February 2025. 

Dr. Fox welcome to the podcast.

Dr. Kevin Fox: Good morning. Thank you, Jamie. I appreciate the invitation.

Jamie DePolo: Thank you for doing this. It’s always helpful to have an actual oncologist breakdown some of this research.

So, the first study I thought we’d discuss is called Young-PEARL and it found that Ibrance plus Aromasin, along with ovarian suppression, was better than Xeloda in stopping cancer growth in pre-menopausal women diagnosed with metastatic, hormone receptor-positive, HER2-negative breast cancer who had, and they previously received tamoxifen. And that is a lot of words, I realize, to say that Ibrance, which is a CDK4/6 inhibitor, offered better progression-free survival than the chemotherapy Xeloda. 

And it is worth noting, I feel like I have to point out, that after about six years of follow-up there was no improvement in overall survival. So, before we get into the details of the study, I was hoping you could explain the difference between progression-free survival and overall survival. Because I know both are used as study endpoints or outcomes and I know some patient advocates don’t really like progression-free survival, they’d rather have overall survival. So, if you could talk about those, the differences between the two to start.

Dr. Kevin Fox: Of course, sure. So, progression-free survival very basically is the time between the starting point when the patient that participates in the clinical trial is assigned their treatment, the day that they are assigned at random to receive one thing or another, is a starting point. Progression-free survival is the interval between that point and the first time when their cancer shows signs of any progression. So, basically it’s an indirect measurement of how long the therapy is effective.

Overall survival is the time interval between the same starting point when the patient receives their treatment assignment by random on the clinical trial until death, death from cancer progression, death from any cause. The reason that oncologists prefer the measurement of progression-free survival is that I think it’s an appropriate measurement of the time that one can expect to get benefit from the treatment. No treatment works forever, and so progression-free survival is simply a measure of the time during which, in essence, the treatment is doing the patient some good. And as long as the treatment is well tolerated, we feel that, that is a meaningful thing. 

The other thing to say, is that because patients with hormone receptor-positive, HER2-negative breast cancer live such a long time, and even if the therapy ceases to be effective, they can go on to get something different and continue to live and thrive. The overall survival endpoint turns out to be a little bit less important because everybody’s doing okay. And in hormone receptor-positive, HER2-negative, stage IV breast cancer, the natural history is so long in so many patients that we expect patients to live a long time. And when a treatment fails to demonstrate a survival advantage, part of that is because when that treatment has ceased to be effective, the patient goes on and gets something else and does just fine. 

So, to oncologists, progression-free survival will be always the, the more important endpoint, or measurement, in a clinical trial because it essentially says that whatever we’re doing is working for longer than what we used to be doing, which is part of the whole point.

Jamie DePolo: Sure. And I think too, overall survival can sometimes take, as you said, because people are living longer, it could be 20, 30 years, and the study may not have been set up to go that long. 

Dr. Kevin Fox: Correct.

Jamie DePolo: So, it can be hard to measure that way as well.

Dr. Kevin Fox: And if we waited to just report that, we may never — we could go a decade before we would be allowed to present any relevant clinical research, which is entirely too long. 

Jamie DePolo: Sure. Okay, so now let’s talk about the Young-PEARL study. Why was it important? It seems like the CDK4/6 inhibitors perhaps caused fewer or less severe side effects than chemotherapy, is that part of it?

Dr. Kevin Fox: I think that’s essentially it. And I think the Young-PEARL study, it does not teach us something new, necessarily, but it reinforces a trend in the way we treat breast cancer, which is now felt to be appropriate for young patients.

The reason this is important is really historical. And I’m, at the risk of giving too much ancient history, if you, if you look at the way that we have approached the treatment of this subtype of breast cancer, and you know this is the most common type, it’s 70% of all the patients that we see, and if you develop stage IV cancer, for a long time the choices that we had were basically some form of hormone or endocrine therapy or chemotherapy. It was A or B. 

And there was always a bias, especially going back 20 or 30 years, among oncologists that if a young person developed stage IV breast cancer of this type, there was always a tendency to favor chemotherapy first because of the sense that it would be more likely to work, that it would work faster, but of course, chemotherapy is inherently unpleasant. There was always a bias, though, among oncologists to be more aggressive, so to speak, with chemotherapy in younger patients, and this is the way it was for a long time. Then about 10 to 15 years ago these CDK inhibitors came along and many of the listeners are familiar with them, there are three and if those CDK inhibitors were combined with endocrine therapy it worked remarkably well. 

And so a new standard developed around 2011 or so, when the first CDK inhibitor was approved, that instead of just giving endocrine therapy, we’d give endocrine therapy plus a CDK inhibitor. The obligation we had at that point was to establish that this new form of treatment of combining those two things, was as good as or better than chemotherapy, so that we could justify using this in patients rather than chemotherapy. So, there have been several clinical trials already, which have clearly demonstrated that the combination of endocrine therapy plus a CDK inhibitor is as good as or better than conventional chemotherapy. Most of that research, however, was conducted in older patients. 

The Young-PEARL trial is the first to look specifically at young people that now can justifiably avoid chemotherapy as their first-line treatment. And so this is, it basically reinforces a, a trend which has been established, it reinforces the CDK inhibitors plus endocrine therapy as an appropriate care standard instead of chemotherapy. And now makes that very clear in people who are younger. So, the long-standing bias in favor of giving chemotherapy hopefully will gradually go away. Chemotherapy is still useful, but it probably should not be, necessarily, except in some special cases, it should not be the first thing that we do. 

Jamie DePolo: That’s great. And I think that’s good for, you know, people diagnosed with that type of breast cancer because, as I said, I believe from at least from what I’ve read, it seems like the CDK4/6 inhibitors while they still cause side effects, they’re not as severe as chemo side effects.

Dr. Kevin Fox: I think it, I think it’s very clear that, that this is an easier treatment. Chemotherapy affects people, of course, very differently, but if you look at the side effects in aggregate, I don’t think there’s any question whatsoever that the CDK inhibitors plus endocrine therapy are a better and easier treatment. 

Jamie DePolo: Okay, perfect. Now, the second study I want to talk about is the PATINA study, which made quite a splash at San Antonio last December. This study also looked at Ibrance and the results showed that adding Ibrance to the standard of care first treatments for metastatic, hormone receptor-positive, HER2-positive breast cancer — so basically metastatic triple-positive breast cancer — increased progression-free survival by more than a year, which everybody was like, whoa, that’s incredible. 

And I know that Ibrance isn’t yet approved by the FDA to be used in this way, but what the discussion was, it sounds like Pfizer is going to file an application for that use. So, could you break down this study for us?

Dr. Kevin Fox: Yes, I think it’s important to look at this in the context of how we have treated HER2-positive breast cancers. So, again, there’s a little bit of history here. As many of the listeners already know, HER2-positive breast cancers are a unique subset of breast cancers of which, which constitute about up to about 20% of all patients. The existence of the HER2-positive subset was recognized 40 years ago and what we knew at that time was that about 20% of patients with breast cancer had this excess of this HER2 receptor protein, and those cancers were notorious bad behavers.

So, a little over 25 years ago this stuff called trastuzumab, better known as Herceptin, was developed, which was a whole, a new thing. It was..it’s a monoclonal antibody. It was a new, a new concept in cancer treatment. And it was tested in patients with HER2-positive breast cancer and worked remarkably well. The only catch was it was, it worked best when given with chemotherapy. So, in 1998 was the year it actually happened, we, the whole treatment for HER2-positive breast cancer changed, and patients were given chemotherapy and this new stuff called trastuzumab, and it was a remarkable success. 

And a few years later, then this second antibody called pertuzumab, also known as Perjeta, was developed. So, the rigid care standard was if a patient was diagnosed with HER2-positive advanced breast cancer, she would be advised to get chemotherapy plus these two new, newer antibodies and the results were dramatic. And that’s all fine, except that it involves chemotherapy, which again is inherently unpleasant. So, now we, we fast forward to the fact that half of the patients with HER2-positive breast cancer are also estrogen receptor-positive, so that defines the patient who is triple-positive. 

Do we need to give those patients chemotherapy? Well, at the beginning we do, and we would normally give a patient chemotherapy, plus Herceptin and Perjeta, for a few months, make sure that it worked, which it almost always did, and then at that point we would stop the chemotherapy and replace it with some form of endocrine therapy. And the endocrine therapy could be whatever, whatever you hadn’t been exposed to before. In most cases, it was an aromatase inhibitor, but it took chemotherapy out of the equation and the patient could then go on and receive endocrine therapy, and Herceptin, and Perjeta and do just fine, and feel just fine. Taking chemotherapy out of the cocktail is always a good thing. So that’s the way things stood and have stood for a long time in this group of patients. 

And so, this PATINA trial now introduces a third component. We’ve already talked about the CDK inhibitors and they were approved for hormone receptive, hormone receptor-positive, HER2-negative patients, as we know. It’s already been almost 15 years that we’ve used them. And now this was the first experiment to look at giving it to patients who were HER2-positive, so it was an obvious important question to ask and there’s a whole scientific justification for this. So, this clinical trial addresses that issue. So, very simply, the patients when diagnosed would receive the standard treatment. 

They would get chemotherapy and Herceptin and Perjeta, most of the patients on the study got the Perjeta, and then they would get that for a few months. And if they had responded and things were getting better, or even if things were static, stable, then the chemotherapy would be dropped. And at that point, the patient was assigned, at random, to continue the Herceptin and Perjeta and endocrine therapy, or the experiment, which was Herceptin, Perjeta, endocrine therapy, and the CDK inhibitor, in this case palbociclib or Ibrance. Very simple and the results were, I think, striking. 

Again, this endpoint of progression-free survival was prolonged, as you said, by more than a year, which in studies like this is a dramatic difference. And the fundamental question is that’s all fine and good, but would it be tolerable? Well, of course, it appeared that the side effects of Ibrance, under these circumstances, were really no different than they are in all circumstances. A little bit of low white count, some patients had diarrhea, but by and large it, in the opinion of most oncologists, this was really a change in paradigm. We can now justify prescribing the CDK inhibitors to patients who are triple positive, in lieu of chemotherapy, and that’s the essence of it. Of course, the FDA approval is another matter. 

I think, my suspicion is, that many oncologists have already petitioned the patient’s insurance company to get approval for the coverage of Ibrance under these circumstances. How successful they’ve been, I don’t know, but you know the reality is, in many cases, this can be approved even before FDA approval, based on this evidence. It will be much easier to do it once this study is formally published and available for complete review. But anyway, this was, in our world this was a big deal. This was a change in the way we approach HER2-positive, estrogen receptor-positive breast cancer, plain and simple. 

Jamie DePolo: Okay. And thank you for sharing about how doctors may be using it because that’s always a question I have when, when we get results like this and they’re so, as you said, striking, but the drug isn’t officially approved by the FDA for that use. I know I talked to a couple of patient advocates when I was in San Antonio and one said, I am so excited about the PATINA study because that’s what I have. I have metastatic, triple-positive disease and I need to talk to my doctor about using Ibrance. So, I guess, the doctor could prescribe it essentially off-label, but it’s the question of insurance coverage, right? 

Dr. Kevin Fox: Correct. There’s nothing that says we cannot prescribe it, but the cost of these drugs can be formidable and you know the responsibility, I think, of the healthcare provider is to go through the necessary, albeit aggravating, process of trying to get approval, which is not always successful. But under circumstances like this it is, it does pave the way to doing the right thing. This isn’t the first time we’ve confronted this. When Herceptin was first demonstrated to be useful, you know, it didn’t get approved overnight, but we were able to, at least in some cases, acquire it for patients. Perjeta the same thing. 

So, you know, there’s always a process here, but I think there are, there are workarounds, which we can at least try. Hopefully, the FDA will be on board efficiently with this decision, which seems like a slam-dunk. I mean, there’s no reason I can think of that this would not be approved as part of routine therapy. 

Jamie DePolo: Okay. Okay, thank you for that. The third study I want to talk about looked at imlunestrant, which is an oral SERD, selective estrogen receptor degrader, that’s a type of hormonal therapy. It’s similar to Orserdu, which was just approved, and the EMBER-3 study found that among people diagnosed with estrogen receptor-positive, HER2-negative advanced-stage breast cancer, imlunestrant led to longer progression-free survival than standard therapy, standard treatments, if the cancer had an ESR1 mutation. 

And then when the researchers added Verzenio to imlunestrant it improved progression-free survival compared to imlunestrant alone, whether or not the cancer had an ESR1 mutation. And so why is this important? I know at several of the conferences I’ve been to there has been a lot of focus on ESR1 mutations and my understanding is that when that happens the cancer stops responding to hormonal therapy, am I right?

Dr. Kevin Fox: That’s exactly right, somewhere around a third, up to maybe 40%, of all patients. Again, we’re talking about breast cancer that is hormone receptor-positive and HER2-negative, again, the most common type. When we are dealing with patients with stage IV cancer of that type, we have discovered that about a third, up to 40% of patients will have this thing called an ESR1 mutation. ESR1 is the gene that controls the existence and structure of the estrogen receptor, and if it’s mutated it implies that the patient will become, will be more likely to become resistant to standard hormone therapies, such as aromatase inhibitors. 

So, we need obviously better therapies to confront patients with those mutations and thus far only, only one, which you mentioned is elacestrant, which was specifically approved for treatment in patients with that mutation.

This particular study of imlunestrant brings a new, a new compound of the same type into the picture, but it adds on the, the added feature of giving it with a CDK inhibitor, which is something that has not been explored yet. But I think to put this in some kind of context we have to stop for a minute and ask, who were these people that were in this trial? 

These were patients, all of whom, virtually all of whom, had had prior exposure to an aromatase inhibitor and a CDK inhibitor. So, the reason I bring this is up is because this study is a, sort of a real-life depiction of the kinds of patients with stage IV cancer who have received aromatase inhibitors already and in many cases were also receiving a CDK inhibitor. In situations like that, what are our options? Well, the standard option for years and years was this stuff called fulvestrant or Faslodex, which is an estrogen receptor downgrader or SERD, like this new drug we’re talking about today. But as many patients that are listening know, fulvestrant has to be given by injection, it’s annoying and uncomfortable.

Jamie DePolo: Two injections, right?

Dr. Kevin Fox: Yeah, right, exactly. Yeah, two, right.

Jamie DePolo: One in each cheek.

Dr. Kevin Fox: One in each check, every month, like religion and it’s really annoying. And to be honest, it isn’t, also isn’t terribly effective. So, there has been a great movement to, to come up with other SERDs, especially ones that can be taken by mouth, and that’s what brought about the approval of elacestrant.

Now, we have imlunestrant, which appears to be, you know, very similar, but at least in this context, we learn those two things exactly as you presented them at the beginning. In these patients, all of whom had received conventional treatment already, and many of whom had already received a CDK inhibitor, were now assigned at random. 

You know, one group got just the imlunestrant, the pill by itself, one group got imlunestrant plus abemaciclib, and one group got so-called standard of care, which in more 90% of patients, the standard of care was fulvestrant, or Faslodex, the injectable one. So, that was the sort of control group and they showed exactly what you described.

If you look at comparing imlunestrant to fulvestrant in patients who have an ESR1 mutation, which is again about a third to 40% of the entire study population, it worked better, which is great, because we now have a substitute. But I think more importantly, now, when you look at the group that got both the imlunestrant and the abemaciclib together, they, no matter whether they had an ESR1 mutation or not, they also did better. 

And remember, that abemaciclib, also called Verzenio, was used here in patients, many of whom had already gotten a CDK inhibitor, and most of those patients had gotten the other two CDK inhibitors. So, it’s also a demonstration of the usefulness of giving a CDK inhibitor of a different type, when one has failed to be effective. So, I think there are two takeaways from this study.

So, we have a new, a new oral SERD, which I think just like elacestrant has proven out to be very tolerable, and when combined with a CDK inhibitor, in this case abemaciclib, it was even more effective. So, there are two takeaways from this study, which I think will also change the approach to patients with stage IV hormone receptor-positive, HER2-negative breast cancer. 

Jamie DePolo: Do you think, given the results of this study, do you think anybody would go back and do a similar study with Orserdu? And maybe not, maybe similar isn’t the right word, but look at Orserdu combined with a CDK4/6 inhibitor to see if the results were the same? 

Dr. Kevin Fox: Yeah, it would be very nice if that were to be done, but I think, and I guess, honestly, I think that’s probably more, at this point, a business decision than a scientific one, doing a study like this. This was an enormous clinical trial, it had lots of people on it, it was an enormous effort, and it involved, you know, many, many different centers. A tremendous piece of work and whether it would be necessary to prove the same point with the other SERD would be, in a perfect world, ideal. Whether it’s practical to try to do that over again, I don’t know. 

Jamie DePolo: Okay. Okay, I just wondered because I know, and I also, I also wonder, I guess, too, if somebody might try and do this with a different CDK4/6 inhibitor. Because I know, while they’re similar, they’re not identical and some have worked in some situations and some have not. So, I think extrapolating that this would work with any of the three isn’t accurate. That research would have to be done. 

Dr. Kevin Fox: Correct, we can’t assume that they’re equivalent. And the thing about this study that I found the most interesting was the simple fact that the treatment with abemaciclib was, was more effective than without it in patients, many of whom had already been exposed to that class of drug. And I think that’s, that’s a very interesting aspect of this study, which merits further discussion. 

Jamie DePolo: Okay. And then finally, we have the COMET study, which I know is a little bit controversial. It compared active monitoring to standard of care, which in this case was surgery with or without radiation therapy, for people diagnosed with low-risk, hormone receptor-positive DCIS. So, the researchers wanted to see if one group had more diagnoses of invasive breast cancer during this study than the other. So, could we just monitor and not treat or should we treat?

And as I said, the study was controversial, and I think part of it was because people in either group could decide to take hormonal therapy, which to me seems like it would skew the findings, so I’m going to ask you your thoughts about this study.

Dr. Kevin Fox: Yeah, there are lots of reasons that I, this clinical trial when reported, I guess, I’ll get to the, I’ll be honest, this, I found this unsettling and I, and I think I want to try to construct my argument in a, in a way that makes sense, but in the context of, you know, DCIS.

You know, ever since we started doing mass mammographic screening in the 19, especially in the early 1980s, what we learned is that mammograms were a very good diagnostic tool and they did what they were supposed to. They detected breast cancers at an earlier stage and suddenly fully one-fifth of all women in this country who were diagnosed with breast cancer had this thing called DCIS, which is non-invasive cancer, which poses no, no immediate threat whatsoever. And the standard of care was to do a simple surgical removal of, of the DCIS and that was good enough. 

If you look at it, surgery alone was probably a perfectly adequate treatment in 90% of the people who underwent the operation, and it could be a simple procedure, a lumpectomy, so to speak. And you know we’re always trying to find ways to make it better, so then after that, then we decided that we should see if radiation improved things, and it did a little bit. And we never leave well enough alone, and then we decided we needed to find out if hormonal therapy improved things even more, which it did. So, it got to the point where patients with DCIS were, in many cases, being advised to do surgery and then radiation therapy and take hormonal therapy as well, which seemed to many of us like a bit of overkill. 

And to take it one step further, then, I guess, mostly surgeons began to wonder if we need to operate on these patients at all, and so the COMET trial was done. And the problems with this are many. The concept was simple: one group gets surgery, they could get radiation therapy if the doctor felt that they should, some of them did, and the other group didn’t do anything surgically. They didn’t have an operation. What the second group did was, one, they got mammograms twice as often, that is twice per year, and second, they were allowed to take hormonal therapy, if they wanted to, and 70% of them did. And the problem I have there is if we’re doing, if we, if we hypothesize that doing nothing is okay, then we should do nothing. 

Because to me trading off a small, relatively small, operation for five years of hormonal therapy is not a legitimate trade-off, taking medications, the value of which are probably good, but completely uncertain in the long run. Medications which cost money, medications which have side effects, and many patients in the audience know, know them full well, and have consequences for long-term health with respect to bone density, blood clotting, cancer of the uterus, in the case of tamoxifen. Small problems, maybe statistically, but not if you’re one of the people who suffers one of those consequences. 

So, doing nothing was not the case here because the patients who were assigned to do nothing actually took medication, in most cases, which I have never found personally to be a, an appealing choice. So, anyway, the experiment was not pure, so that’s problem number one.

Problem number two, is that the patients who were assigned to one group or another didn’t always do what they were assigned to do. I think the paper quoted that the number of patients who were assigned to have surgery, so-called standard of care, more than 40% of them didn’t do the operation. So, in the group that we’re tracking for the success of surgery versus no surgery, well, nearly half of those patients didn’t do the operation to begin with. 

And that’s… a standard part of clinical trials is that when you assign patients at random to do A or B, many patients will decline. And in the group that was assigned to just be monitored, 14% of them didn’t do their monitoring, they went on and had surgery. So, there’s, and there’s always going to be this problem in all randomized clinical trials, but in this case the problem was, was, in my opinion, enormous.

The third problem is that these patients were followed for a median of about three years and the information reported was the two-year rate of developing invasive breast cancer. In a study that involves the tracking of the natural history of DCIS, you need way more than two years before you can draw any legitimate conclusions, you need five or 10. 

So, I think although this study was done in earnest to answer an important question, I suppose, do we need to operate on patients at all, which is a legitimate scientific question, it is much too early to make any assumptions that, that is a proper thing to do. I think the standard of care has always been to surgically remove DCIS and I think for the moment, until we have much more information, the standard of care should remain to do just that. 

Jamie DePolo: Do we know, I don’t remember from the paper, is there going to be longer follow-up? Do we know how long this study is supposed to go on? 

Dr. Kevin Fox: So, I’d have to look back and see if they have prespecified. You know, these studies are usually reported after these prespecified time intervals or after a certain number of patients have had a recurrence. I am absolutely sure that they have mandated for their follow-up, they have to, two years is not enough time. Following patients with DCIS for two years wouldn’t convince any oncologist, surgeon, or radiation oncologist that that’s sufficient time to establish a new standard of care. So, I certainly hope so. I think it’ll be interesting to see how this plays out, but at this point it is, it would be premature, very premature to consider not doing surgery in patients at this point with DCIS. 

Jamie DePolo: Okay, I have one final question about that study. Do you think, and I realize you weren’t involved with the study, but I can’t help but wonder if it was difficult to recruit people into the study because DCIS, hearing you have cancer is scary. And being told we’re, you can join this study and you get nothing or you get this, you know, you get treatment if you want it. And I feel like it might’ve been hard to recruit people into the monitoring arm. 

Dr. Kevin Fox: You know, you’re absolutely right, convincing patients to choose this, to participate in this kind of experiment would be very difficult, thus I think they had to provide the patient the safety net, you don’t have to do surgery, but you can take this pill if you want to. And we can see from how this played out that the majority of patients who were given the opportunity to not do surgery and take the pill, took the pill, 70% of them did. And so giving patients that so-called, if you will, comfort, of taking a medication was a way, I think, to, I’ll say encourage participation.

Jamie DePolo: Sort of entice them to, yeah.

Dr. Kevin Fox: And I think, and the thing that I found astounding, and this involved almost 1,000 participants, which is considerable. What I found astounding was that the group who was assigned to surgery, as I said before, you know, a significant minority of those patients elected not to have the operation, they too could take a medication, and in that case, approximately two-thirds of them did as well. So, anyway, I think, you know, what, what rankles me is that, you know, doing, doing no surgery is an interesting concept, but it has to be done in the context of trying to do as, you know, do as little as possible if we, if we’re trying to “do no harm” by removing surgery from the equation. 

Then I would argue that doing no harm also perhaps should involve being reluctant to prescribe a medication, which can be unpleasant, and may not necessarily be known to accomplish what you want. So, anyway, that’s sort of my take on it now. Interesting concept, but it’s, it’s not ready for, this cannot be taken seriously at this point, such that we across the board stop telling patients to have surgery. We’re not ready for that yet. 

Jamie DePolo: Okay. Dr. Fox, thank you so much. This has been really helpful. I appreciate all your insights. 

Dr. Kevin Fox: Thank you, Jamie, appreciate it very much.

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