In this special edition of BCRF’s podcast, listen as five preeminent breast cancer researchers talk about what’s exciting in the field now
Every October, the Breast Cancer Research Foundation (BCRF) celebrates the more than 260 investigators the Foundation supports at its annual Symposium and Awards Luncheon in New York City. These scientists are driving major advancements in breast cancer research, and during the inspiring event, the Foundation recognizes their achievements and devotion to ending breast cancer once and for all.
This year’s program included an informative symposium focused on breast cancer prevention and treatment featuring an expert panel of BCRF investigators. We’re proud to bring you that discussion here in this special bonus podcast.
This year’s symposium panelists included Dr. Abenaa Brewster, Dr. Lisa Carey, Dr. Robert Vonderheide, and BCRF Scientific Director Dr. Judy E. Garber, who received the Jill Rose Award for Scientific Excellence at the event. BCRF Founding Scientific Director Dr. Larry Norton moderated.
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Below is a transcript of their conversation.
Dr. Larry Norton: Thank you. Thank you all for being here. This is one of the great opportunities that BCRF has for all year, in terms of all the things that BCRF does, because our it’s contact with you on a one-to-one basis, so we can talk about our work so we can answer any questions that you may have, and just so that we can interact and so our colleagues here can interact in front of you. So it’s a great pleasure being here again. We have many of our grantees, we have 260 grantees, is that right? Is that right? That you supported maybe more than that now and a very high percentage of them are actually here arrayed around the room. So we’ve got extraordinary expertise in the room for any question that you may have and we’ll all be involved in this activity.
I would just want to introduce our panelists, Lisa Carey, sitting next to me, from the University of North Carolina. They’re all going to have a chance to talk about their work that’s funded by BCRF and anything else that they want to talk about and go forward. Bob Vonderheide, from UPenn, and Abenaa Brewster, I got it right? Yes, Yes. Yes.
Dr. Larry Norton: There’s controversy about the pronunciation, but I got it right, is from MD Anderson. Lisa’s an expert in everything breast cancer, she’ll talk about her work. Bob is an expert in everything immune therapy, immune oncology and immune things in breast cancer and other diseases. And Abenaa is an expert in very innovative work that she’ll talk about I’m sure, in terms of cancer early diagnosis. And she’s also written about doctor-patient interface and many other topics of importance. And last and certainly not least, we have Judy Garber, who’s the scientific director of the BCRF, and this year I am moderating instead of Judy, which is traditional, because she’s the winner of our Jill Rose Award. Jill, and I’ll have a few more sentences about her at the actual luncheon, was one of really the founders of BCRF, along with Evelyn Lauder, the very, very early days. And it’s BCRF’s highest honor and we’re very honored that Judy accepted the award this year, and she will talk about her work. So she’s not a moderator this year, although I’m going to lean on her a lot to be a moderator too, she’s a panelist as well as being a moderator.
So Lisa, take it away.
Dr. Lisa Carey: Hi everybody, I’m Lisa Carey. I’m the deputy director for clinical science at the University of North Carolina, where I’ve been for a number of years and where we have a fabulous breast program. Outside of UNC, I co-chair the executive committee of a thing called Translational Breast Cancer Research Consortium, which is a BCRF-supported group of academic centers doing clinical and what we call translational meaning scientific work, simultaneously. And I co-chair one of the National Cancer Institute Cooperative Group committees.
I have been blessed with sort of two generations of BCRF funding. My first generation wasn’t an award to me, it was an award that went to one of those National Cancer Institute cooperative groups, the clinical trials operations, they’re all across the country and they do some of the most practice-changing trials. I was the study chair and helped design a trial that had a very practical clinical question. It was in HER2-positive breast cancer, and it was basically, are two anti-HER2 drugs better than one anti-HER2 drug? Which is a very traditional way to do a trial. But what we wanted to also ask is, why do some cancers respond to therapy and others don’t, no matter what you give them? But of course the National Cancer Institute doesn’t fund that part of it, BCRF does. So BCRF provided funding, so that at the same time that we ran the trial, we also did biopsies on patients who are in the trial and gave the scientists samples and said, “Okay, this patient responded, this one didn’t, tell us why.” That turned out to be incredibly important stuff because it turns out there were features of the tumor that were responsible for response and non-response, and there were features of the immune system helping to create response to therapy.
That turned into a larger initiative, many people in this room had other trials of that type going on. And we pooled analyses together and worked together, another thing that BCRF is great at is convening people, and that’s turned into, actually there’s an assay that helps us tailor therapy, that one of the investigators here, Alex Pratt, Alex wave your hand, helped create. There he is. My second generation is my own award, and my own award is around, we’re trying to figure out what it is in metastatic biology that’s different from the original cancer. Because when women die of breast cancer, it’s not the cancer that was in the breast, it’s what the cancer turns into when it goes to other parts of the body, and unlocking that biology is crucial to understanding why it happened in the first place. And most of the time when we talk about tumor biology, it’s a lot of great science on the original cancer, it’s usually not on the lung, the liver, the bone metastases. And so I’ve been very involved with BCRF’s help in a number of initiatives, that are collecting the original cancer but also samples of the metastases, to see what happened, within the same patient, which is massively important to understanding this process.
Dr. Larry Norton: Enormous amount of really superb work that Lisa’s doing. And I’m sure there’s going to be questions, we’ll have more discussion of that going forward. Bob.
Dr. Robert Vonderheide: Well thanks Larry. I’m Bob Vonderheide, I’m the director of the Abramson Cancer Center at the University of Pennsylvania. It’s really great to be here and thanks everybody for being here. And I’m a BCRF grantee for many years and it’s been fundamental to the research that I’ve been doing. Today’s theme, as you can see, is preventing breast cancer and we know really driven in large part by investigators supported by BCRF, there’s been incredible progress and treating patients with breast cancer. A lot more work to do, but great progress. I’d like to put out for conversation today, the notion as we move into preventing breast cancer, in the first place, that to capitalize on that opportunity the most, we need to bring in the immune system. It’s what I work on and focus on in the laboratory and with patients. And I think we’re at a point of great excitement where we can take what we’ve learned, in the treatment setting, to help prevent breast cancer by using the immune system.
Why do I say that? Number one, being a proud fan of the immune system. It’s one of the one of the few systems in the body that remembers, it remembers, you can teach it something and it remembers. Tamoxifen doesn’t remember, you got to take it every day. I got a vaccine for mumps and rubella, when I was in probably grade school, it’s still in me. I didn’t get mumps and rubella, I’m not at risk for mumps or rubella. It’s amazing the power of the immune system. The second thing is it turns out that we’ve learned over the years in studying, that the immune system is actually really, really interested in cancer, because like an infectious disease, cancer is foreign, it arises from the human body, but it’s different, and the immune system can see that. And over the years, and it’s taken time, we’ve been able to fashion therapies that activate the immune system and kill cancer cells. And it’s taken time to get those drugs available for patients with breast cancer, but now they are. It’s amazing, Larry, 10 years ago we couldn’t say that an immune therapy is now standard therapy, for certain patients with breast cancer, but now it is FDA approved, you see it on TV.
Dr. Larry Norton: It’s got to be true because you see it on TV.
Dr. Robert Vonderheide: Got to be true, I’ve see it on TV. It’s now time to take those insights into prevention and we’re doing that, two reasons. And we’ve tried this for many years and haven’t had great success, I think now we see a new wave of this, and why? We’re really talking about vaccines now, because we’re not just talking about suppressing, suppression, but we’re talking about starting an immune response and fighting a nascent cancer, or giving protection to a patient, before they’re a patient. We can do this because there’s been incredible advances in technology. Gene therapy, for example, DNA technology, RNA technology, we all know about the power, Nobel Prize winning technology for RNA vaccines. These are now with us, those very drugs that we’re using to treat patients will be very helpful for vaccinating individuals. And so there’s just a great new technology.
The other opportunity is that we’ve actually opened our mind to this possibility of trying to prevent and using the immune system as a prevention. When we take this idea to our infectious disease colleagues, they say, “Where have you been? Because how we use vaccines for infectious disease, to prevent.” And we often use the term in cancer, interception, maybe we can get into that later. What are we doing at Penn, with BCRF funding? With Susan Domchek, we’ve brought in many stakeholders to develop a DNA vaccine, that it generates an immune response that protects against the development of breast cancer and other cancers, we hope. We’re in the early stages, we’ve been working on this for years, but it’s a real milestone to tell you about, that we’ve now begun over the last few months to vaccinate healthy individuals, who are at risk for breast cancer, not breast cancer patients, healthy individuals who are at risk on the basis of a germline mutation in BRCA1 and 2. And we’re vaccinating them and we can’t wait to see the results, we can talk more about it, Larry.
Dr. Larry Norton: Fantastic. Yes, I mean Bob really alluded to the dark humor joke for many, many years was that vaccines are the future of cancer medicine, and always will be. But the fact is that immunotherapy is really here, it actually does work. We could talk much more about that, and I think that this field has really just exploded.
Abenaa?
Dr. Abenaa Brewster: Good morning everyone. My name is Abenaa Brewster and I am a breast medical oncologist at MD Anderson, and also medical director of the breast center at MD Anderson. So I just want to take one moment to say that, the reason I am a breast medical oncologist is because of Judy Garber. I was a second year student at Harvard Medical School and I decided I wanted to take the year off to do research, and who takes on a second year medical student? But Judy did, she was a very junior, very, very junior assistant professor at the Dana-Farber. And I worked for a year with Judy and the late Jane Weeks, and after that experience I said to myself, “I’m going to be a breast medical oncologist.” So thank you Judy.
Dr. Judy Garber: You’re very welcome.
Dr. Abenaa Brewster: So I’m very new to BCRF funding. I had always heard about people who had this elusive funding, and never really could understand what it was all about and what this club was all about. And so it was such a great honor when I was invited to submit an application. And I have been doing prevention now, in addition to breast medical oncology for, gosh, 22 years, and I think this is the most exciting time in cancer prevention. And the reason why I say this is because I think we’re about to see a paradigm shift in our ability to screen for cancers that we’ve never been able to screen for. And particularly for breast cancer, maybe to use a blood test, which we call a liquid biopsy, that measures substances in the blood, that can indicate whether or not there’s a presence of cancer before a patient even has symptoms. And I think that this has the potential to revolutionize the early detection of breast cancer, because as you know to screen for breast cancer, women literally have to come in every single year for a mammogram, and if they’re at high risk, they do a mammogram and an MRI. And so this new technology has the ability to really revolutionize how we screen for all cancers, but specifically for breast cancer.
So as it happens, I was approached by a computer scientist at the University of Houston and a radiation oncologist at MD Anderson, and the radiation oncologist was actually doing lung cancer, and they had developed this new technology, which is called a panorama. And what this new technique allows is for the detection of nanoparticles in the blood, which can identify substances that we call exosomes that are released from cancer cells. And this technology was able to detect and measure these very, very tiny particles. And so like most scientists, they need human samples, and so they approached me and I happened to have a cohort of women that I’ve been running now for, gosh, about 10 years, where we collect blood samples of women at the time of enrollment in the cohort, and then some of these women go on to develop breast cancers and others do not. And so it was the perfect opportunity to have a collaboration to see whether or not we can measure these exosomes that might identify the presence of breast cancer, even before a woman actually is diagnosed with breast cancer with a mammogram or with an MRI.
And so this is the kind of really early collaboration that the BCRF is so amazing at funding, because it would be very difficult to get a grant to look at these very new technologies, without a lot of preliminary data. And so we were very generously funded through the BCRF to do this work and this is some of the work that we’re doing. But I think we all recognize that, especially with the COVID pandemic, that whenever there’s new technology scientists, we get really excited about new technology, but what we really learned from the COVID pandemic, is that we really have to understand patients’ perspectives about new technology. And so part of that work is also going to be surveying women, in the general population, who are undergoing screening, to really understand what are their preferences and perceptions about liquid biopsies for early detection? And so I’m happy to share the results of some of that work.
Dr. Larry Norton: Wow, fantastic. Judy, you’re on.
Dr. Judy Garber: Right? So I’m not on as the moderator. So-
Dr. Larry Norton: No, you’re a panelist at this moment.
Dr. Judy Garber: Right. So, I’m Judy Garber and I’m at the Dana-Farber in Boston, and I’ve been working in cancer genetics for a really long time, as Abenaa just said, since you can do the math. But I think when we started in cancer genetics, and I have many colleagues in the room who’ve worked with me, we were interested in trying to find women at highest risk. And part of that interest was because we thought perhaps if we could figure out how to reduce the risk of breast cancer in them, how to prevent breast cancer in them, we could extend that technology to all women whose risk wasn’t as high to begin with, that they would be interested in learning about their risk and in learning about what to do about it. And I think that part was true. Women have been incredibly participatory, leading the way, making breast cancer genetics the most frequently tested gene sets among genetics in the US, and around the world.
And over these years we’ve learned how to, in many ways, take care of our patients who are found to be high risk, how to screen them better with mammograms and MRIs, while we wait for better technologies to come along, how to treat them better when their tumors develop, the ones we haven’t been able to prevent. We haven’t done as well in prevention. But I think all of us work in all those areas and live in hope, that as we watch the technologies improve for detection, for treatment, as you’ve heard from Lisa, in breast cancer is not necessarily related to BRCA1 and 2, or any of the other genes that we’ve been talking about over the last day, but treatments have improved and the immunology has improved. So okay, great work, we’ve done all this in treatment and we need to do more, but now it’s time to try to bring that back toward prevention.
And I have to say that having BCRF as a really willing partner in this is critical, because you can imagine this is not where pharma lives. It’s understandable, they are in drug development for treatment and they have to be our partners in that, we can’t do that work, that Lisa described, without the drugs themselves. But once the drug has been developed for treatment, prevention is really an afterthought and prevention is a liability, often, and it’s not where they spend most of their energy and their considerable efforts at drug development. So it’s up to us to take that forward, or backward if you want to think about it that way, to try for prevention or interception, to try to make a difference before cancer starts. So BCRF has been a great partner for that.
Dr. Larry Norton: And we’re covering a whole lot of territory here, there’s no question about it. You have in front of you or on your seat or something, places that you can actually write questions. I guess there’s some mechanism for collecting the questions, does that exist? Well, so hearing this, if things pop into your mind you want to hear more about, please write it down, we’ll try to get to it during this period of time.
Lisa, you work a whole lot on therapeutic trials, clinical trials, you mentioned TBCRC and that as well. A lot of them are involved with treatment of advanced disease, metastatic disease, metastasis where the cells have left, the cancers have left the breast, they’ve gone to a part of the body. That’s the serious part of breast cancer and we need therapies from that. What have we learned about the treatment of metastatic disease, you think might be relevant to earlier therapy and in particularly area prevention?
Dr. Lisa Carey: Well, I’ll state the obvious, which is, all the things we do in early breast cancer to prevent recurrence, we learned in the metastatic setting. I mean most of our drugs, including all the targeted therapies, start in the metastatic setting, that’s where we test them first. And then if they look promising and successful, then we see if they can help improve the cure rate, which is the goal of care in the early setting. So we’ll set that aside, I think in terms of biology, there’s a couple of really interesting things that are coming out of work that a number of people in this room have done.
The first is if you just think of the tumor cells, the tumor itself, it isn’t static, it changes. So the nature of the cancer itself can change over time and with treatment, which means it’s more fungible than we thought, and you may be able to identify the relevant biology, at a particular time point and intervene then. The second is the immune system, as Bob was just alluding, that itself varies a lot, it’s different in the beginning of a woman’s cancer journey, how her immune system is reacting or not to the cancer. And then over time it seems to change again, and it may be different in different parts of the body. And that may be why some people get cancer in the liver, their metastasis preferentially goes there, and another one it’s in the bone. And understanding that, and those, for want of a better word, microenvironmental influences on cancer behavior, may be crucial to us being more personalized in how we treat patients.
Dr. Larry Norton: Thoughts among the panelists about this?
Dr. Robert Vonderheide: Well, I agree with you-
Dr. Larry Norton: Bob, you were nodding very, very vigorously.
Dr. Robert Vonderheide: Well, because Lisa said phrases like immune system.
Dr. Abenaa Brewster: His ears went up.
Dr. Larry Norton: That always gets his attention.
Dr. Robert Vonderheide: It is so interesting that the immune system reacts as a cancer grows, and the immune system is wired to turn itself off, when it turns itself on, it’s so dangerous, it knows that. So if there’s an infection, it takes care of it, but it turns itself off, there’s many, many mechanisms. Cancer, somehow, particularly breast cancer, has come to understand what those mechanisms are. And when we look at patients with metastatic disease, we understand that their immune systems are pretty beaten up, chemotherapy beats it up and the tumor itself beats it up. And we’ve been thinking for years, is that because we always start with new drugs, with patients with metastatic disease, that’s where we start with immune drugs, but that’s the least likely scenario for them to work. And so it took us a decade to get out of that mindset, in fact, now the standard use of immune therapy, which many people in this audience help pioneer, is to give it even before you’ve had surgery for a local breast cancer, that’s where it’s working the best. Because likely the immune system is less beaten up, by the chemotherapy, and also the tumor is smaller. So that dynamic, to capitalize on immune therapy of what’s going on in the tumor, I totally agree with. That’s why I was nodding.
Dr. Larry Norton: Oh.
Dr. Lisa Carey: And can I just add one thing to what you just said? Because I think it’s really important to highlight, what Bob just said is so we see it play out in the clinic all the time. Because immunotherapy that we give for triple-negative breast cancer, in the metastatic setting, it only works in a subset of them, that can be selected as having activated and still functioning immune systems. If you give it preoperatively, to patients who haven’t gone through getting beat up and all that way, as far as we can tell, it has a chance of working in all of them. So it’s really a different scenario, depending on when you try the same intervention, same drug.
Dr. Larry Norton: It occurs to me when you’re talking, that really early diagnosis would make a whole lot of sense in this particular setting.
Abenaa, I’m going to direct this to you. Do you think that there’s a real connection between the work that you are doing, in terms of really early diagnosis, looking at exosomes, other people looking at circulating DNA? I love the exosome idea, I mean it’s a fascinating idea. I mean is, before cancer cell will metastasize the liver, often the liver is prepared to accept that cancer cell because exosomes have gotten there first and have prepared the way, that’s how important they are. And I think the idea of using that as detection method is just brilliant. But do you think that what’s going on now with really early detection may actually synergize with the things you’re hearing?
Dr. Abenaa Brewster: Well, when I think about early detection, I think of it more in terms of, how does that allow us to really intervene even earlier, in terms of prevention? So when we identify women who are at high risk of developing breast cancer, certain populations of women now have the opportunity to take medications, like Tamoxifen, Raloxifene, the aromatase inhibitors, which work to reduce risk. And so when we think about these early detection markers and what if you have a positive test that shows that you’re harboring a breast cancer, but you do a screening mammogram or an MRI, and there’s no evidence of cancer? Then isn’t that really perhaps the best opportunity to then prescribe preventive therapy for a patient, with the hopes of treating a cancer that is in its earliest stages of development and hopefully prevent a cancer from even developing clinically? And so I think that that’s really the exciting part.
And we know that adoption of preventive agents, like the ones that I’ve mentioned, have been very low, but a lot of that has been because women are like, “Why are you treating me for something that I don’t have, when you can’t even really very well predict whether or not I’m going to develop breast cancer or not? I’m high risk, but that risk is not a risk that is a certainty.” And so this is really a setting where you can say, “Well gosh, we know that there’s something there and could we potentially intervene before it becomes clinically symptomatic?” And I think that’s really what the power of these early detection tests can bring to us.
Dr. Larry Norton: Bob?
Dr. Robert Vonderheide: I just wanted to add something, as you said, that phrase before it becomes clinically. So we’re beginning to understand that there’s this smoldering portion in the life cycle, when the cell wants to become a cancer but it’s not a cancer yet. It hasn’t started invading quite yet. And so when we think about prevention in some cases we’re thinking about, very early on prevent the toxin that’s going to cause a cancer, like don’t smoke. But this opportunity, we’re starting to call and folks are starting to call, interception. There’s a pre-malignant lesion, there’s something there, you’re finding evidence. And it’s very vulnerable to therapy, it’s not so complex, it hasn’t metastasized, it’s in kindergarten of cancer school. Okay? I just made that up.
Dr. Judy Garber: Yes, but I think that’s really important. So prevention seems permanent, if we could prevent something, we can keep it from happening forever. Interception at least means that we can redirect some of what’s happening, we can try to keep these things from happening, but we may have to do it again. That’s okay, we have a long lifetime. If your vaccine works, Bob and worked in patients who you could find who had risk that was really clear, either from risk like knowing they had a gene so very high risk or even better finding them in the very earliest stages, maybe that would be the timing of the vaccine. Unless you have something we can give everybody, like polio.
Dr. Robert Vonderheide: 100 percent, that’s why this notion of interception has to be partnered with risk assessment. And that’s the only way we’re going to know if these new interception approaches are effective, there has to be some rate of an event that we can measure that’s gone down. And so whether it’s genetic risk assessment, which is what we’re doing, that’s why we’ve partnered with individuals who have BRCA1 and 2 mutations, through the Basser Center at Penn, or some other biomarker test or a family history. This is what we need to understand. Those have to come together, as you’re saying.
Dr. Judy Garber: Right. And the audience knows that as hard as we’ve tried, we’re still looking for better ways to find who really is at high risk. We have the highest risk individuals, but most women get breast cancer and we didn’t really see it coming. So that’s still an area of active work.
Dr. Larry Norton: Yes, actually that’s something that I get asked about a lot actually. And I think we’ve defined certain things you can inherit from your mother or father that give you very high risk, but the things you can inherit that give you kind of an intermediate risk or a higher risk than the general population, but not so high that one would consider an extreme thing, I mean, what do we do about those cases? And that have had a genetic test, a hereditary genetic test, and they find that they’re carrying a gene with low penetrance, meaning that it’s not a super high risk of developing disease but a higher than baseline risk, what do we do about those kinds of cases?
Dr. Judy Garber: Well, I’ll start, but let’s see. How do we think about risk? Well, we all have risk obviously, and risk is something even that we had a very interesting lecture from Dame Leslie Fallowfield who’s here, who studies risk communication, how do we talk about risk? And it turns out we are not very numerate, we’re not very good with numbers, so risk is a challenging concept. That was true in all of her demonstrations of all the providers sitting in the room, not just our patients. But trying to think about assessing risk, communicating risk, so people are working on looking at our genes in a different way, not looking for a strong gene like BRCA1 or 2, or even a moderate gene like CHEK2, but looking for patterns in the genes that would help distinguish, who’s at higher and lower risk? And who by exposure to things like hormones in different ways over a lifetime, or carcinogens that we haven’t been so good at identifying, might we be able at least to figure out who’s at high, medium and low risk?
We’re all high enough to have mammograms, we’re just not all high enough to think about preventive therapies, unless we can make those therapies so nontoxic and so effective, that we’d all want to do them like we do other kinds of prevention. Yesterday there was a session on prevention at our research meeting, and there were people doing really amazing work in both of those directions and trying to make effective interception or prevention agents less toxic and more acceptable, and people working on ways to improve the immune system, and people working on ways to try to detect. So if Larry asked me, what do we do about people who we know have some increased risk? We have ways of modifying what we do for low risk or high risk. So, you’ll have to keep funding us so that we can make this work better. Because as I’ve worked in this area my whole life and as have Mary Beth Terry and other epidemiologists here, Christina Ambrosone, so many people, and we have improved things, but we haven’t really hit the home run yet. So stay tuned.
Dr. Abenaa Brewster: Judy, I just wanted to pick up on your point that, we do a really poor job of communicating risk. We do a really poor job of communicating a lot of information, treatment decisions, screening decisions, risk decisions. I mean, we struggle with the language in a way that really connects patients to the information. And I think that we also have to get really comfortable with recognizing that as our advances go up in treatment or prevention, we have to bring our colleagues along, we have to bring along our behavioral scientists, we have to bring along our decision scientists, to help us with the messaging to patients. So that we don’t end up widening disparities with groups of patients who understand it, they’re very educated and they get it, and other groups of patients who don’t really know what we’re talking about, and therefore don’t adopt some of these developments that we’re making. So just getting back to some of the work that I’ve done with BCRF, in the survey that we did with, we’ve now got almost a thousand women who’ve responded to the survey, 25 percent African-American, 55 percent white and 15 percent Hispanic women. And what we found is that when you look at the level of interest in new technologies, like liquid biopsies, there was no difference by race. But when we looked at the level of interest by educational status, that was when we saw huge disparity. So women who had a college or graduate school education, 50 percent to 60 percent of them said that they would be extremely likely to use liquid biopsies for early detection, if they became available, while only 25 percent of women with a high school education felt the same way. And so these are disparities that we’ve got to investigate. And now when we think about, “Okay, what is the next step?” The next step has to be, how do we message to women who may not have a college or graduates level education and really explain to them the benefit of these technologies, what they could potentially do, so that we don’t create even wider disparities in the adoption of our care?
Dr. Larry Norton: Because we’ve started talking about this topic and I think it’s again, a question that we always have to deal with. I personally don’t like to use the word race because I can’t define it from a genetic point of view, even though it is a social construct, and we could talk a lot about that. But there is such a thing as ancestry and that people can trace their genes to parts of Asia, many different parts of Asia, they’re all different, Pacific Islands, Northern Europe, Southern Europe, Africa, whatever. Do we have enough information to know how that genetic ancestry, DNA ancestry, interplays with some of the things that we’re talking about? And I think Lisa, you’ve done work in this regard as well, so maybe Lisa, you start, in terms of the North Carolina studies.
Dr. Lisa Carey: Yes, well, and thanks for bringing that up because I wanted to give a shout-out to something that BCRF is doing, that’s hugely important in this particular realm, the Health Equity Initiative. So the Health Equity Initiative is a BCRF funded convening, I mentioned this is what BCRF is really good at, taking people who have done amazing things and partnering them with each other so they have more power to answer fundamental questions. So Melissa Troester, Julie Palmer, and Christine Ambrosone, please stand up.
Dr. Abenaa Brewster: And Lisa, can I add Melissa Davis and Lori Pierce.
Dr. Larry Norton: Lisa Newman.
Dr. Lisa Carey: Lori Pierce Is the chair of this initiative. I was calling out those three because they are merging these very, very powerful data sets from Black populations, and looking at, within Black populations, what can we learn about why Black women, self-identified Black women, have worse survival? Because it’s not true of all of them, it’s general thing. So one of the things that they have found, and this gets back to Abenaa’s comment before, one of the strongest predictors of having a stage three or four versus a stage one, whether or not you’re getting mammograms. So the communication of how important it is to have mammography, it’s a basic thing that we all know about, but that message isn’t getting through and it’s having a real consequence, in terms of the nature of the tumors that people are getting.
Dr. Larry Norton: Abenna, your comments about the exosomes, are you actually looking at people with diverse hereditary background, in that regard?
Dr. Abenaa Brewster: Well, of course when investigators say, “We’ve got this test.” My first question is, “Okay, so we’ve got to test this on a diverse population, right?” And so that’s exactly what we’ve done. So it’s not just samples of white women, we’ve included an equivalent amount of blood samples from African-American women, from Hispanic women, because I think these questions have to be asked, in diverse populations from the beginning. We’ve done a lot of testing of things on very homogeneous populations and then say, “Okay, how does it fit with this group and how does it fit with that group?” And for everything, AI algorithms, everything that we’re looking at right now, I think there’s a better understanding that, at the inception we have to ensure that we have diverse race and ethnicities, in order to really develop the best test that will then be applicable to the population in general. And so yes, that work is being done with the blood samples, so we don’t have results as yet with small sample size, in terms of looking at differences, but I think the development is really so important to be able to do it in a way that will be quickly generalizable.
Dr. Larry Norton: Fantastic insights into this area. Judy, let’s imagine that I’m an older person, I’ve developed breast cancer, I don’t have any offspring, all right, is there any value to me therapeutically, for knowing my genetic status? To know whether I’m BRCA1 or BAC2 mutant, for example, does this of any value to me or therapeutically, in any decisions I have to make?
Dr. Judy Garber: So I would say, excuse me, yes, there is, for many women with breast cancer, treatment with standard therapies will be perfectly effective. But, excuse me, there are other decisions to be made, even in women who don’t have children. First, those women may have other relatives, siblings, cousins, nieces and nephews, but for themselves, there are data that, especially for BRCA1, BRCA2, PALB2, that the tumors have a different biology, a different, and that different drugs can be, not only effective but effective in improving survival. So we do test more women, there are some women who have a very low risk, they’re even older than I am, let’s say, or they have a very little family history, or the tumor as it appears does not look like a tumor that has much chance of having this biology. But testing is largely inexpensive and hopefully widely available, not as widely available as we would like, like most things, but much better access. And yes, it can change treatment, and that work in fact began often in BCRF, but has taken place now in definitive trials. So we know that it can make a difference, at the time of diagnosis, and unfortunately if tumor occurs, there as well.
Dr. Larry Norton: Bobby, you talked about your vaccine being in early stages of development earlier, actually starting to accrue patients at the very beginning, who don’t have a disease, but maybe are particularly high risk. What would be the ideal time? Let’s say that somebody is a candidate for testing, which I think probably should be pretty much everybody, Mary Claire King here has championed that thought for many years and I’m totally supportive of that, but you get a BRCA test, when should you get vaccinated, if this vaccine ever becomes available?
Dr. Robert Vonderheide: So of course we’re not even close to being there yet, Larry, but we’ve begun to think about that. There are things we have to understand about these vaccines to make sure that they don’t somehow have a side effect that you wouldn’t want to introduce in an individual, maybe before they’ve had their children. But you could imagine in a person who is in their 40s, 50s, to be eligible for such a prevention vaccine, perhaps younger, if the data and the safety data is there, we truly want to prevent. And so we would partner and we are partnering with folks who are making very precise estimations of, when is a person at risk as they get older based on who they are? And we already use that to say, when should you start MRI screening? When should you start this type of screening? And we would follow that pattern, when the risk becomes significant enough that you might want to start screening an individual for these cancers, that would be an appropriate time to start the immune response. To Judy’s point, you could vaccinate and then stop, and then intermittently vaccinate as the individual gets older and older, it’s not necessarily a one-time thing.
The notion is that you can start the immune response and if you’re intercepting, you get an immune response to do its thing, get the weeds out of the lawn. And then once the weeds are gone, you don’t need to have a super active immune system constantly, and we would actually probably let it wane. So there’s memory this high, but it can come down and it’s lurking. When you revaccinate, as we sometimes do with infectious disease vaccines the response is even higher, and it’s very quick too, it happens just within days. So this intermittent reawakening of the immune system, rather than a constant, always on, always on always on, is the difference between a cancer prevention vaccine and an infectious disease vaccine. I have to have a constant on to protect myself against an infectious disease that could come at any time. But these slow growing pre-malignant cancers actually take a long time. So you can find a way to make the vaccines more tolerable, safer, have a lower risk of toxicity, by not having capital M memory, but lowercase m memory, by this intermittent approach. Total hypothesis.
Dr. Larry Norton: There’s been a lot of press lately about the fact that breast cancer seems to be occurring younger, and there are a lot of young people who are getting breast cancer at a higher rate perhaps than before. And I think that’s generally an important topic, and I think relevant to the question of how early you’re going to intervene. Is Dr. Partridge here somewhere?
Dr. Ann Partridge: Yes.
Dr. Larry Norton: I’m going to ask you the question, we’re going to get to the mic over to you. All right, what are we doing about cancer in younger people? I know this is a particular area of focus and interest for you.
Dr. Ann Partridge: Hi. Thank you for the question. So I’m Ann Partridge, I’m a medical oncologist at Dana-Farber, in Boston, where I work for Judy most of the time.
And so the question is about young onset breast cancer, which as you may have seen in the press, is actually growing unfortunately, and there’s lots of things we can talk about that. But the question was, what are we doing for young women? And I think some of the most important things are that young women are more likely to get more aggressive types of breast cancer. So all of the breakthroughs recently, particularly for triple negative breast cancer, as you heard about using the immune system to treat the cancer, as well as for diseases like HER2- positive breast cancer, all of those benefits are especially benefiting young women, who tend to present with the bigger tumors because they’re not being screened, and therefore we’ll get the preoperative therapy before surgery treatments. And we can use their responses now to even tailor their therapy out back after surgery. So that’s a huge advance for all patients, but with particular nuance for our youngest patients.
The other major area for our younger patients is around the genetics, and not just treating the first cancer, but a young person has a long survivorship time, by definition, assuming they do well with their first cancer, which of course most women do. And so we’ve gotten so much smarter and now we routinely test all of our young patients coming in for the known hereditary predisposing genes, and that really has opened the door for a lot fewer cancers and being more selective about who gets what, as we hone our testing and try and get the testing for all of our patients for whom it may benefit them. It’s been great, in that regard. Still a lot of work though.
Dr. Larry Norton: Judy?
Dr. Judy Garber: Okay-
Dr. Robert Vonderheide: I wanted to weigh in on, so early onset young adult cancer, now I’m not an immunologist anymore, now I’m a cancer center director. We got to do something about this. It’s not just breast cancer, it’s 17 cancers, rising, we have 30-year olds with colon cancer, we have 40-year olds with lung cancer who don’t smoke. There are genetic reasons for this, but maybe the minority of patients, we’re learning more, I know we talked yesterday about some subtleties there. I think one of the things we need to do, Larry, is as cancer centers, as research foundations dedicated to cancer patients, to start interacting more and more with the general population, with our primary care doctors, our emergency room doctors, and say, it’s no longer acceptable to say a woman who has a complaint in her 30s cannot possibly have breast cancer. We got to stop that. And we need to educate folks that we maybe are not interacting with so much as cancer researchers, that this is a huge problem and we need to get a handle on it. It starts with educating and taking those symptoms and signs of our youngest patients, as seriously as an older patient.
Dr. Larry Norton: That’s really an excellent, excellent point. And the whole notion of how doctors healthcare systems have to listen more to people and respond to them in a productive way, is actually an active area of investigation now, communications, physician-patient communications. And not to dismiss complaint, as not being appropriate, I think is very much an important part of that.
Judy?
Dr. Judy Garber: So was just going to say we have to make sure those vaccines come before surgery. So right now surgeries work to lower risk, but you have to make us immune before that happens. So Lisa, and then maybe we could ask Ayan Croft to comment as well from the audience. Let’s hear a little bit about progress in metastatic disease, how have our treatments improved?
Dr. Lisa Carey: Well, I think we all want to not have to treat metastatic disease. The whole point of what we do in the early breast cancer setting is to prevent recurrence. That said, we have 43,000 women per year in the US die of metastatic breast cancer, so we’ve had a more than 40 percent decrease in that mortality, but we have a long way to go. Part of that decrease is better treatment in the metastatic setting. And even if we were to cure everybody who was diagnosed with stage one through three, we would still have 20,000, 25,000 women, who are stage four from the very beginning. So this is not going away, so we have to attend to that. A couple of things. The first is the goals of therapy for metastatic disease are fundamentally different than it is in early cancer, because we don’t think of it. God willing, that it will be, in the future, we will have things that we can say, this will cure metastatic disease, but at the moment it is considered incurable. So it is a disease where you are trying to control the cancer and the patient’s quality of life is as high as it possibly can be, and those two are equally valuable end points. And we ignore that at our own peril because we can certainly hurt our patients.
The truth is that with that paradigm in mind, women are living longer, with metastatic breast cancer, now than ever before. And that’s accelerated enormously over the last few years, partly because of really great treatments that are targeted and less toxic, and they’re living better, so it’s not just longer, but it’s better. The truth is that, so in HER2-positive breast cancer, and these are old data, if you were to actually capture it right now, some of the things, the advances that have happened in the last two years, are not yet reflected in our numbers, our survival numbers, but we’ve gone from maybe 18 months survival from the diagnosis of metastatic disease and HER2-positive disease, to more than five years. In hormone receptor driven cancers, it’s now four or five years, from, again, around 18 months. And even in triple negative, it’s getting over two years, it’s about doubled. And so that one’s still our thorniest, but a lot of advances coming in. And I can promise you that right now with the things that have happened in the last couple of years, all those numbers are already outdated. So you wanted to talk to Ayan about this.
Dr. Judy Garber: I’m just going to give Ayan a chance to comment, because I think all of us would say that, as happy as we are about all of the new drugs and all of the progress, that those numbers are really sobering.
But Ayan, here you are.
Dr. Ayan Croft: Yes, no, thanks for the question because it builds on what Lisa was just mentioning. We throw around the term targeted therapy, and what we mean by that is, instead of using drugs that just kill all fast-growing tumors, which is basically what chemotherapy is and which had been the mainstay of our treatment for metastatic disease for many years, for decades, we now are learning through the kind of science that BCRF supports, understanding what is driving a particular kind of cancer, and then developing drugs that block, that target, that driver of the cancer. And of course that means treatment is more complicated because different kinds of cancer have different drivers. So Lisa mentioned HER2-positive disease, we call it HER2-positive because it’s driven by an abnormal protein called HER2. But once it was learned that the reason these cancers behave the way they do, which is very aggressive, it was because of this HER2 protein, it led to the development of many drugs that block that HER2 protein. And as Lisa said, the prognosis for HER-II-positive disease, which used to be our worst outcomes, and we always dreaded finding patients who had HER2-positive disease, now those patients do better than all the other kinds of cancer because we’ve learned what’s driving those cancers’ behavior, and we can now block it.
And just to kind of show you how far we’ve come, for example, in HER2-positive disease, we actually have two trials that are being supported by BCRF, in this group of cancer centers called the Translational Breast Cancer Resource Consortium, or TBCRC, that are just getting underway, in HER2-positive disease. One of them is taking advantage of the fact that some of our HER2 drugs work so well that patients are probably cured, that they’ve been on treatment for many years and their cancer seems to have gone away. And we don’t know what to tell those patients, they’re always worried, we say, “Hey, maybe we can stop the treatment because probably the cancer’s all gone and it’s probably completely gone.” So we have a trial that’s underway now that’s being led by a physician named Heather Parsons at Dana-Farber, where we’re actually stopping their treatment and watching them, and checking with these blood biomarkers that Abenaa talked about, to make sure that the cancer’s not sneaking back up.
So that’s a group that we think already are cured with treatment, even though they started with metastatic disease. And then we have another trial that’s actually taking advantage of the fact that we now have not just one drug blocking HER2, but multiple drugs blocking HER2, each one working slightly differently. And we’re taking newly diagnosed metastatic patients and treating them, not just with one treatment, waiting for their cancer to grow back and then treating with another drug and just keeping their cancer as controlled as long as possible, we’re using all of our good drugs one after another with the idea of potentially curing their cancer by attacking the cancer in multiple different ways. The same thing we do for treating tuberculosis with multiple drugs and the way we treat HIV with multiple drugs, as a way to get rid of each, to try to block all the ways that cancers become resistant. And so that’s a trial that it may not work, it’s outside the box, but it’s the kind of thing that we really could completely change the paradigm of metastatic disease. So that’s just an example of, by understanding the science, understanding what’s causing each individual type of metastatic disease, that we’ve really changed the outcomes. And I think that’s just a paradigm for what we’re going to see more and more, in breast cancer and other cancers.
Dr. Abenaa Brewster: High risk, high reward. Let’s hope so.
Dr. Judy Garber: Can I make just one quick comment about what Ayan just said? And I think it’s really important to recognize, we all see the heterogeneity in the behavior of this disease, in clinic all the time. Every provider in this room, including me, has patients with metastatic disease, where the cancer just went quiet, and years, and years and years. And sometimes for one reason or the other, the patient comes off therapy, and I’ve had patients where I say, “Well, it’s going to come back and when that happens, we’ll start therapy again.” And then it never came back. I had a patient who used to taunt me, she would come in and she’d go, “Huh, let me guess the scan didn’t show anything, did it?” I was like, “Really?” So it’s incredibly important. The problem that we have is we all have these patients, so this does happen, we don’t know why, and this is where we need our scientist colleagues to help us, how do we make all of them like that patient? And the trial that Ayan was just alluding to, I think is a really great start.
Dr. Larry Norton: It just reminds me of really the formative concept behind BCRF from the very, very beginning, from Evelyn Lauder’s idea in the discussion is, to bring together basic scientists who have a commitment to helping people with their science, and great clinicians and great, great clinical investigators together in one place, in one room, the first room was her dining room, and then it grew to this, to discuss these issues and to see what we could learn from each other and move things forward. And it really has been working. I mean, the kinds of observations that are being made, clinically translated to the kinds of things with the enormous power of modern contemporary science to address, really is making enormous progress. And it really is one of the things that’s intrinsic to the BCRF model, and something that we’ve championed and obviously built this wonderful organization around, and you have been supporting for all these years. And I hope there’s some new supporters out there as well, because that’s really where we’re going to make a lot of progress.
I’ve gotten a lot of questions from the audience because we’re talking about prevention as a general theme, about screening also, and about what’s happening in the area of actually anatomic screening, imaging screening. And the word mammography is thrown around, but there’s a lot of other techniques now that we’re applying in this direction. And one particular person who’s had a lot of biopsies for benign disease, they have fat necrosis, they feel lumps, they do biopsies. And obviously this is not something that people want go through, but how are we doing in the area of imaging? We have some terrific experts in the group, and I hope they’re in the room.
Connie, I’m throwing it to you with AI. Where are you
Dr. Connie Lehman: So, I love this question because one thing that we know is one size doesn’t fit all. So we have the false positives, the women that have biopsy after biopsy after biopsy, and it’s not malignancy. So Chris is going to talk, I know about some better ways to image to be more specific. I’m also incredibly excited that as radiologists, Chris and I have been working on new technology for a long time, but with artificial intelligence, we can go back to Imaging tests that we have and apply computer vision and apply AI, to extract more accurate data, from the imaging. So there are things on the mammogram, for example, to distinguish fat necrosis, calcifications from a malignant recurrent calcification, that my human eyes, even with all the experience in reading, is not going to be able to distinguish, but our very smart computers can.
So we’re starting to apply this more and more, and it’s basically saying, all the technology we have in imaging has been very exciting, we’ve made good progress, but we need to do two things better. We need to use AI and AI risk models to be better targeted, in who benefits from which test at which time, we’re making a lot of inroads, thanks to BCRF with that. And the second thing is, how can we extract more of the information that this advanced imaging has provided to us? How can we go beyond the human eye and the human brain to extract more accurate information? So, I’m going to turn it over here to Dr. Comstock.
Dr. Chris Comstock: So as a radiologist and as a breast imager, since the 1990s and mammography has been around since the 50s, I’ve always felt it’s time for a new product, a new screening tool, and we have those tools. I think our biggest problem with screening is under diagnosis. As we’ve heard, over 40,000 women still die every year of breast cancer, our biggest problem is we don’t find enough early breast cancers. And people probably don’t know this, but if I ask most people, what’s the sensitivity of mammography for breast cancer? You’re lucky if it’s 25 percent, we know that through the studies. Larry’s been a big believer since he’s seen the benefits of the new screening, I think screening 2.0, is vascular based screening. And just with contrast mammography and MRI, it’s a two to two and a half fold increase in sensitivity.
I think combining that with Connie’s work of targeting women with dense breast tissue, so using AI and breast density and history, we could really target these tools to find more cancers early. And I think a whole network of screening information, particularly with MRI, there is so much information there combined with AI, that if you had a ten-year cooperative group of data from MR-diagnosed breast cancers with their genetic profiling, with their treatments and their outcomes, we would have a wealth of knowledge to really figure out, “Hey, with AI, because there’s patterns there that we can’t recognize, we could really advance finding cancers earlier and reducing mortality.” It’s my opinion.
Dr. Judy Garber: I’ll add the applications of AI are so huge in the imaging thing, it’s also in pathology. So there’s the whole effort to try and take the slide, which we have slides on every cancer, and to use machine learning on that simple slide, in trying to improve risk assessment, and prognosis and things like that. And there’s some real opportunities there, particularly if you can get as much information out of that slide, as out of a $3,500 genomic test, right? We have a lot of trouble with access to care and cost of care in this country, and if we can do things as well in a more accessible way, then we all win. And imaging is going to be part of that, so these are complex.
Dr. Larry Norton: Yes, I mean I think you’re going to address this as well, I mean, but this is one of the questions, whatever you’re going to say, please say, but also address this, which is that, can you see the day where you go in for a blood test and then on the base of the blood test they say you don’t need breast imaging? Is that what you’re going to talk about?
Dr. Judy Garber: And Abenaa, wait a second, there’s somebody who asked for a definition of a liquid biopsy, so let’s make sure we’re not too jargony. Ai, artificial intelligence. Thank you.
Dr. Abenaa Brewster: So I just wanted to get back to the issue about new developments and screening. And I think many of you in the audience probably know that, who are getting mammograms, that now the FDA requirement is that when you get a mammogram and you have dense breast tissue, that you’re notified that you have dense breast tissue and to discuss it with your physician. And so I think that this issue, in terms of how accurate mammograms are, is probably going to be a real shock to a lot of women who think, “Gosh, I’ve been doing the right thing. I’m coming in every year for my mammogram. What are you talking about with dense breast tissue, and I need to discuss it with my physician?” And so I think that these again are opportunities for us to be able to educate, to message, because what we don’t want to women to interpret it as saying, is that you shouldn’t get a mammogram, that it’s no point in getting a mammogram. And so really being able to extend some of these new technologies, a contrast-enhanced mammography, for women who have dense breast tissue, to have better accuracy is going to be really important.
So the definition of a liquid biopsy, and I’m so sorry if I didn’t make that clear, so when I think about the definition of a liquid biopsy, it’s simply a blood test that’s looking for some marker in the blood, that can identify the presence of cancer. And there are different types of markers in the blood that individuals have been looking at, they’ve been looking at DNA from the tumor, they’ve been looking at DNA that has been shed from the tumor and there’s no actually tumor cells, their liquid biopsy could be looking at certain proteins in the blood that are associated with cancer, or these nanoparticles called exosomes. So it’s essentially using a blood sample to identify whether or not there’s a substance in that blood sample, that identifies the presence of a cancer cell.
And what we really need these markers to be is very specific, in terms of what kind of cancer, it’s not very helpful to just be told you’ve got cancer. So these markers are needing to be very specific, in terms of saying what type of cancer that might be in the blood. But these markers have to be really accurate, because what’s the point of a blood test that’s positive in some individuals who have cancer but then is negative and the individual actually has cancer? And so what we’re really looking for is accuracy in terms of the blood tests, really being able to identify those women who have cancer and accurately identify when you don’t have cancer. And so to Larry’s point, if we could get to a very high level of accuracy, then that would lend to the ability to say, “Okay, if it’s positive, it’s positive,” You now would have some sort of screening in order to identify what type of cancer you have, where it is. But if it’s negative, it truly is negative and you don’t need to have screening, or at least not that year. So that’s really kind of where we are. Thank you.
Dr. Larry Norton: There’s a lot of questions about specific tests that are being marketed now. All right, and probably we ought to hold that because it’s such a complicated area, we probably ought to hold that to another time. I think that the point that all of us would make is that much more research needs to be done to know how to use those tests and other tests that are being developed, before we actually commit people to therapeutic decisions, for example, on the basis of the tests that are currently out there. We are a science organization, we believe very strongly in conducting the appropriate clinical trials, which often requires control groups to be able to answer these important questions. And there’s so many that we can’t go to each and every one in this regard, but it’s a very active area of investigation within the BCRF now. So basically just stay tuned as we learn more. We’re very much aware of this.
There’s one question that came up that I think is a very interesting one because it relates to everything that we’re doing, which is that there seemed to be a lot of people doing cancer research, breast cancer research out there in the world, and there’s a lot of different organizations doing it. Is BCRF doing anything to make sure that we have complementary research and not necessarily doing the same thing, replicating things? I’m seeing a lot of heads shake, I think a lot of people are interested in this. I’m going to actually pass this question over to Dorraya El-Ashry, who’s BCRF’s chief scientific officer, because she’s really totally on top of that question.
Dorraya, please stand.
Dr. Dorraya El-Ashry: Thank you, Larry.
So BCRF does a lot in this area and there are a number of breast cancer research foundations that look at very specific things. BCRF is the largest private non-funder of breast cancer research, and one of the things that BCRF has done from its inception is to focus on the entire spectrum of breast cancer. Many of the other breast cancer research foundations look at very specific aspects. METAvivor, for example, only looks at women who already have metastatic cancer and for research that will come up with new treatments for that. The Inflammatory Breast Cancer Foundation, only focuses, and they’re very small, on inflammatory breast cancer, which is a very rare, aggressive subtype of cancer, for example. And Komen, over the years has changed their focuses and now focuses mainly on early investigators and supporting them for their role.
BCRF focuses on the entire spectrum, from the most foundational biology to bringing that into clinical trials, and from prevention to metastasis, from treatments to survivorship, that entire spectrum. And BCRF, within the BCRF staff has a very strong marketing and communications team that we all work in collaboration with to get out the communication of the work that we do, the impact of that work that we do. And we communicate with these other breast cancer research foundations as well. And many of our investigators are funded by multiple of these research foundations as well, and so there is a tremendous amount of communication going on between them.
Dr. Larry Norton: Great. Thank you. And it ties together with one of the most frequent questions that I get with an audience, what’s the most important thing that we should be studying right now in cancer? And I say, “I will answer that if you tell me what’s the most important part of the airplane. Is it the left wing? Is it the right wing? Is it the landing apparatus?” And the fact is it is all got to work and it’s all got to work together. And so it’s not just this enormous collection of brilliant minds that are working on this topic, it’s also working with other organizations, it’s working with the big picture, that I think is very important. It’s all important, and there’s no specific topic that’s more important than others.
We’ve touched on a number of critically important topics, already, obviously we’re doing a much wider selection of research. Our website has actually got some excellent writing on it, that the wonderful team at BCRF has organized, that talks about the individual researchers. And I’ve got some comments about the individual researchers and I think we’ll bring them up here next year, the ones that were mentioned, because I think they’re very important. That work is very important as well. So just stay tuned and stay connected. I mean, I frequently say, in addition to everything else we’re talking about, staying informed, and staying connected and staying enthusiastic, is a very important thing that the public can do, to help us along for our mutual mission, which is the health really of all of us. We are in the very, very final throes of the session, I’m about to have something thrown at me if we don’t close up soon. So I’m going to ask all the speakers, ending up with Judy, our Jill Rose award winner, just for any final closing comments that they want to make, about their work or about the field in general.
I’ll start with you, Lisa.
Dr. Lisa Carey: Sure. It’s not an accident that breast cancer has more research funding than other tumor types, and breast cancer has had a nearly 45 percent decrease in mortality. Those two things are actually associated with each other. And, another statistic, more than 40 percent of funding for breast cancer research, does not come from the NCI. National Cancer Institute. It’s from you all. And that’s where the good ideas get started, and they get nucleated and they grow. And so thank you.
Dr. Robert Vonderheide: I should say I agree with Lisa as my closing comment. Listen, we know research cures cancer, and I just want to add to that concept that in order to do that, you need researchers, the people who do it. It’s no longer a solo person late at night with a bare light bulb, this is not how cancer research is done. But it’s still up and down, it’s difficult, a lot of failures before there’s success. And I just want to say to our BCRF supporters, that the researchers feel your support. At the time when it’s like, “This is never going to work.” There you are continuing to support, “The grant is there, I’ll get it done. If it takes me an extra two months, okay.” That is the role that you’re playing to put wind in the sails of the researchers, who do the research that cures cancer.
Dr. Larry Norton: Abenaa?
Dr. Abenaa Brewster: So those are hard acts to follow. But just to build on Bob’s, it’s not just the breast cancer researchers, it’s the big tent. And the ability to have funding that brings individuals together who look at things from different perspectives, is really where we’re going to get the breakthroughs. And so, as I said, remembering the computer engineer, remembering the decision scientists, remembering the psychologists, remembering the behavioral scientists, the ability to do research and interact in a multidisciplinary fashion, to bring those different perspectives together, I think is really where we have the best opportunities to make huge developments in curing breast cancer.
Dr. Judy Garber: And I have to follow all three of them. And I would just say, how can you not be optimistic at a time like this? There has been so much progress, there continues to be progress. Not every day, some things don’t work, some things are hard, but if you don’t take on the hard things, you’ll never make those different. Some things we’ve done in breast cancer have benefited other cancers, BRCA1 and 2, ovarian cancers, even pancreatic cancers, prostate cancers, you don’t always know where the next benefits will be or where you will learn. And I just cannot imagine a better time and a more productive time. Look, we’re talking about taking all of this amazing things we’ve learned about tumors, for prevention, when I’m finished, I would like that to be the priority because we’ve solved the cure problem. But I’ll settle for progress in both. Thank you for making this possible.
Dr. Larry Norton: Thank you all. Thank you all. I’m blown away by the erudition on the stage and in the audience. Thank you all for being here. Bye-bye.
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