SO3 EP08 RTAC – Dr. Heather Parsons & Dr. Nancy Lin
[00:00:00] Dr. Eric Winer: Our treatments for her two positive breast cancer have become so much better that the question that’s arising are some patients curable. There are clearly long term survivors, and there’s the thought that in particular patients who have never received any treatment before, because they’re, they’re coming in for a diagnosis and the cancer has already spread, but that those patients may have the ability to be cur of their cancer.
And so with all of these drugs, that that seem to be non-pro resistant or non overlapping in terms of their resistance, can we develop curative approaches? And what I can tell you is I can’t share any results, but what I can tell you is that we’re optimistic enough that this might be possible that other Parsons and Nancy lid and others of us have been involved in trying to put together a national study to, to deal with this question.
[00:01:02] Lisa Laudico: Welcome to the Our MBC life podcast from share cancer support, dedicated to exploring life with metastatic breast cancer. From the perspective of us, the people living with this disease and the experts who partner with us to help make our lives better. I’m Lisa Laudico and I’m so glad you’re here since no one should face NBC alone.
The road to a cure series continues today. As we head north from pod headquarters in New York city to Boston home to red Sox, nation, senior producer, Victoria Goldberg and guest. Co-host Dr. Paula Jayne have a conversation with Dr. Nancy Lin and Dr. Heather Parsons. If I wanted to build the perfect world series team of oncologist researchers, Dr. Lin and Dr. Parsons would be first round picks for me, for sure. This is the third stop in our series that will release a new interview on the concept of a cure every Monday until the beginning of the San Antonio breast cancer symposium in early December, the road to a cure team led by Victoria Goldberg is made up of Dr. Paula Jayne Dr. Ellen Landsberger and Kate Pfitzer. There is so much to unpack in this episode. So let’s get started. Here is Victoria.
[00:02:37] Victoria Goldberg: Hi friends. Welcome back as we continue on our journey today, we’re visiting the city of Boston and the whole of what rivals with the MD Anderson. As the most powerful cancer center in the world. On one side of the Charles river, you will find Dana Farber Beth Israel, and mass general hospitals. On the other side of the river, the Whitehead Institute, the broad Institute and the campuses of Harvard and MIT researches in these few square miles produce a staggering amount of knowledge about cancer in their search for finding a cure.
Like all of you, I have long ago accepted the fact that NBC is treatable, but not curable. But if you think about it, It’s not at all surprising that a possibility of a cure was raised at Dana Farber during the welcome remarks at the 2020 Dana Harbor cancer Institute, embrace and embrace stands for ending metastatic breast cancer.
For everyone. These remarks were made by Dr. Eric Winer, the president elect of the American society of clinical oncology. You probably recognize his voice and this episodes open my co-host Paula Jayne and I are here in . Dana Farber to talk to Dr. Nancy Lin and Dr. Heather Parsons about the concept of cure and the national study that Dr. Winer was referring to. But first, we asked our guests to tell us a little bit about themselves and what led . Them to become medical oncologists specializing in breast cancer.
[00:04:28] Dr. Heather Parsons: My name is Heather Parsons. I’m a medical . Oncologist at Dana Farber and I take care of breast cancer patients. And I also do a research and an understanding how we can identify biomarkers in the blood that can tell us information about a patient’s cancer.
Is it still there? And we can’t see it on a scan. Is it gone? Is it coming back? And it showing signs of resistance to certain drugs. We’re trying to understand those kinds of questions from tiny bits of the DNA that get out of the cancer and, and end up in the blood. I got interested in cancer in general when I was studying to be an internal medicine doctor and I wanted to, um, get to know patients and to be able to take care of them, not just see them one time.
And that was it. And general medicine is really important. You, you have to know a little bit about many things, and I wanted to know a lot about something. And so oncology seemed like a perfect fit because you got to know a lot about oncology as well as other parts of medicine, but also had this special relationship with patients over the long term and breast cancer seemed perfect to me because there were a lot of patients who did really well for a really long time.
A lot of whom could be cured. Some of whom might be living with their cancer for a long time, but you can develop they’re really special relationship with the patient with breast cancer.
[00:06:04] Dr. Nancy Lin: I’m Nancy Lin and my research initially started in running and designing clinical trials for patients with metastatic breast cancer, with a couple of different.
Focus areas, one being the problem of cancer that spreads to the brain. So brain metastases, but also really trying to develop treatments that overcome treatment resistance. So when a cancer becomes resistant to a specific treatment, how do we best develop new treatments that will still work despite the old treatments stopping, uh, to work.
And the way that I came to oncology was both personal and professional. Three out of my four grandparents died of cancer. So cancer has, you know, certainly been in our family, but also as with Dr. Parsons, I like the personal aspect of it. You get to know people over a long period of time. You care for people for a long period of time.
And the relationships are very, um, intense because of how much cancer becomes for better or worse. A part of people’s lives. A lot of chemotherapies that we have now didn’t exist either. So it’s really exciting to be in a field where things move at a pace that you can actually see.
[00:07:23] Dr. Paula Jayne: I really couldn’t agree more as from the patient side, we sometimes get tired of being told you’re lucky that you have breast cancer. Yeah. Having made friends among stage three and metastatic folks who have other types of cancers and having had multiple types of cancer myself, I can vouch that the level of research in MBC is lightyears ahead of so many others. And it’s both exciting and also humbling. This kind of research is happening, as you said in real time that we can see. So it is a good test case for this question about cure. We know that cure is a very. Loaded concept . And so we’re . Trying to start these, uh, interviews with just some basic discussion of language and kind of some overarching questions.
So we could spend just a few minutes talking about the concept more globally before delving deeper into the, uh, work that you are both doing. So this’s just the first baseline question to make sure that we’re on the same page. We would ask how you personally might define a cure within MBC specifically.
[00:08:34] Dr. Heather Parsons: So I think you’re right. Cure is a loaded term and. The most traditional understanding of cure in other diseases might be that you have a condition, a disease, and you get a treatment for it. And then it’s gone in earlier stage breast cancer. That is fortunately true for many people. And the goal of bone marrow transplants in breast cancer in the late 1990s was for getting rid of every last breast cancer Selma.
Unfortunately, that wasn’t successful. The thought that it just wasn’t possible came to be the standard idea in breast cancer. And our understanding of what cure might be is that either the diseases under control and without significant side effects and significant burden on the patient for an indefinite amount of time or that it is gone completely.
[00:09:27] Dr. Nancy Lin: Yeah. There’s total cure, which I think of as you receive some amount of treatment, you stop that treatment and the cancer never comes back for the rest of your life. Ultimately, that would be the, the best thing, right? If you think about other diseases like we don’t cure diabetes, we treat diabetes, we don’t cure HIV, we treat HIV.
But the other way to think about cure, that’s perhaps more like long term disease control. Maybe we need to use a different word is that people live with their disease and it doesn’t affect their life expectancy. And it doesn’t affect their quality of life in a dramatic way. And in fact, that’s, what’s happened with HIV.
We don’t cure people with HIV, right. But in fact, somebody who’s 25 who has health insurance and lives in the United States actually has a completely normal life expectancy with HIV. They live the same amount of time as somebody without, and that’s with medication. So there’s ultimate cure, which I think of.
You get your course of equivalent of antibiotics and you’re done and you’re cured. And then there’s the, even if it’s not cured, it’s in long term remission, I guess is one. You could put it mm-hmm but really the idea that people could truly live a normal life expectancy. I. I personally don’t like referring to metastatic breast cancer as a chronic disease, cuz it, it underplays how serious it is and how it really does cut people’s lives short.
But our goal ultimately is for breast cancer, not to shorten someone’s life.
[00:10:59] Dr. Paula Jayne: That is a good point about, do we need more terminology? And can we draw from these adjacent fields of HIV research?
[00:11:07] Dr. Heather Parsons: Yeah, I think we actually lack language for that. We don’t often speak in stage, um, for breast cancer of remission exactly. I think cure is still a little bit of a, as we’ve all said a loaded term and breast cancer and so. It would be helpful to have some more language around that. I think that there’s some reluctance to think of in that way, even though all of us have at least some patients who are doing really well for a long period of time.
[00:11:33] Dr. Paula Jayne: Currently the paradigm within this field basically is for the vast majority of us, MBC is incurable and these kind of paradigms come together for multiple reasons. One is that hopefully they match the evidence that we have, which I think it is what’s happening, but sometimes there’s practical benefits that go along with that. And so I have a question that’s slightly coming at it sideways. And so we’ll see if it’s a useful question for discussion or not.
What are the benefits to both the science and to the patient’s lived experience of this current paradigm that NBC is incurable. Are there benefits that are practical to patients and looking at it this way? So thinking of it this way,
[00:12:13] Dr. Nancy Lin: as doctors we’ve been hesitant to use the word cure, because we certainly don’t wanna over promise. Um, in our practices, we lose people to breast cancer and we don’t wanna make promises that we can’t keep, you know, and the way I talk about it with patients is that I say that at the moment, we don’t have a way to eradicate the disease, meaning that we don’t have a way to say, I’m gonna give you four doses of this cocktail, and then you’re done, and your cancer will never bother you again.
I’d love to get to that point someday, but we’re certainly not there. And what I can say is that we’re gonna give the best possible treatment at this point in time. And when the next time something happens with the disease, we’re gonna get the best possible treatment. At that point in time, one of my patients actually just said that what keeps her going?
And she literally said this yesterday is you have to live to live. Like you gotta get to the new drugs that get you another year and then get to the drugs that get you another two years. I think that’s really true of metastatic breast cancer.
[00:13:16] Dr. Heather Parsons: Does the thinking of it as incurable help the science? I don’t know that it does.
I think that it actually is, uh, unhelpful in some ways, Nancy and I were very closely with more basic scientists at Dana Farber at the broad Institute at the medical school here being brave and thinking of it as potentially curable is actually an important thought exercise because it helps us be braver in what we wanna do.
On the other hand, we also wanna be mindful and very thoughtful about what the potential side effects are of those treatments. And so there’s a reason behind it, but it is helpful, I think, from a scientific point of view, to think of it as how could you cure this disease or these diseases, if you think of them as curable.
[00:14:01] Dr. Nancy Lin: I think also at what point do we feel like we have enough tools to ask whether we can cure metastatic breast cancer? And for a long time, the answer was, we don’t really have enough tools. We already showed, unfortunately, with a bone marrow transplant, for those who are not aware, what it really means is that people got really high doses of chemotherapy larger than you could normally give.
And the only way we could give them is by giving people bone marrow transplants afterwards, because otherwise we killed off all the bone marrow cells. And we learned from that set of clinical trials that if you just take okay chemotherapy and you blast people with high doses of everything you got, it’s still not enough.
You have to have much better drugs. You can’t just take okay. Drugs. And raise the doses and hope that that’s gonna be magically curative. But I think that what it did on the other hand is make people really skittish about even trying a curative intent clinical trial, because it was such a bomb, but we think that for her two positive breast cancer, we finally have drugs that are good enough to go for it.
And that’s really very different. Even from 10 years ago, 10 years ago. I don’t think any of us would’ve thought we had enough good drugs to quote go for it, but I’ll let Dr. Parsons explain.
[00:15:21] Dr. Paula Jayne: Yeah. So just to sum up briefly to make sure that I’m understanding what you’re saying is that the downside of potentially curative approaches from a patient perspective is the quality of life impact.
And when you don’t have targeted drugs or you don’t have drugs that have a favorable side effect profile, it, it may become a choice that needs to balance. Extension of life and quality of life. And I love this concept of being brave in the science and identifying those areas where the drugs are targeted enough or good enough that we might consider pushing that paradigm a little bit.
And so if you’re open to a Dr. Parsons, I’d love to move, um, into a discussion of your recently funded grant, which so many of us are very excited to see move forward your NIH grant, to look at whether or not a subgroup of her two. Patients may be able to, to stop treatment and see how we do. Would you mind giving us just a brief overview of that?
And then we can delve in a little deeper with some questions.
[00:16:24] Dr. Heather Parsons: Sure. Thank you so much. So I think one way that I’ve found about this is that we need exquisitely sensitive tools and paired with exquisitely effective therapies, to be able to really start to address this issue of, or this potential for cure.
And then we think that in. Her two positive metastatic breast cancer. For some patients we may be there and we at least need to test whether that’s true. And so the study that’s, uh, funded by this grant is called stop her two. And it is a study to look at whether for patients who have her two positive NBC and have been on anti her two therapy.
So some systemic therapy for at least three years. And. This is important desire to stop their therapy. They and their doctor agree that it’s okay for them to stop. They would stop their therapy. And we do this already in clinic. Uh, we don’t have any specific guidance on how to do that or in whom to do that, but to do it as part of a study and then to be monitored closely, both by conventional scans, which are what we would use now, but also by a test, looking at these circulating tumor DNA or little pieces of DNA in the blood sometimes also called minimal residual disease or MRD.
To look at whether that test can also ensure that a patient continues to have their cancer controlled and the patients are followed for, um, an extended period of time. And, and then at the end of the study, when the study is technically done, they can choose to go back on their therapy if they wanted to, or to continue off therapy patients who would like to be part of the study, but are not yet ready to stop their therapy.
They can also con participate by continuing their therapy, but undergoing the same monitoring protocol. That the other patients will do. It won’t be randomized in the usual way that a study would be where people get assigned to it. They’re choosing it. Mm-hmm , but they will be able to participate. And we’re really excited about it.
It’s gonna be done through the translational breast cancer research consortium, ort, CRC, which is a group of breast cancer programs throughout the country who all work together to do these kind of what we call translational studies, where there’s a lot of science involved. They’re usually on the somewhat smaller side, but we’re really excited about.
[00:18:54] Dr. Paula Jayne: I, you can’t see my face cuz it’s a podcast, but I’m just beaming because we’ve been hearing about the possibility of the study for a while and to see it actually get funded and be able to move forward is so exciting. so if we could geek out a little bit and get into the like nitty gritty, if we could just back up for a second and talk a little bit about Herceptin directed therapy and whether this functions as a type of immunotherapy and if so, why is Herceptin effective when so many other immune directed therapies in NBC have not been as effective?
[00:19:27] Dr. Heather Parsons: Herceptin is that monoclonal antibody and antibody made against the, her two protein. And it’s a really incredible science story where scientists worked for a long time, starting back in the late seventies and identified first this protein on cells that was really indicated that patients might not do very well if they had that marker.
Then other scientists, uh, work together to create an antibody that would target that. And then the drug was developed and the efficacy of trastuzumab of Herceptin is really phenomenal. Went from taking a disease that was very aggressive and lethal and not almost everybody. And to being a, a, a, a much more, um, treatable disease and, and curable disease.
For many patients, we thought that that probably worked by just targeting the cells and blocking the molecule. But in fact, it may be, and this data is there, but less well developed that the immune system is part of the reason why it works so well that the monoclonal antibody brings other, um, components of the immune system to those cancer cells and causes the immune system to actually attack the, the cancer cells.
And that may be why it is also so highly effective. And your question about the other immunotherapy, which we sort of call immunotherapy, but usually is targeted at one of PD one or PDL one molecules. And those are working a little bit differently. The Herceptin is targeted at these particular tumors, the PD one and PDL one are helping by unveiling the cancer cells that are from the immune system because of their activation of the molecule.
It it’s true. Those drugs have not been as nearly as effective in breast cancer as they have in some other kinds of cancer. Although in some subtypes like triple negative breast cancer, there is certainly some very good data that they’re effective.
[00:21:23] Dr. Paula Jayne: Right. When you were putting together this study, what level of evidence is out there that it might be safe for select populations of Her2 people to go off their therapy?
[00:21:37] Dr. Heather Parsons: Whenever we’re doing a study, we always wanna make sure it’s not just like a creative idea we have in our head or that we studied in a Petri, gets our or one mouse, and then we make it a good idea. So we need some patient evidence or some really strong rationale, and there’s a few different themes.
And if you look at the really seminal study called Cleopatra, which was done some years ago now, but studied how effective trastuzumab or Herceptin together together with Pertuzumab or Perjeta is in treating metastatic breast cancer. And it was compared to what was then the standard, which was . Just Herceptin alone.
We saw some interesting things. All the, the patients who got the Pertuzumab did much better. They lived longer and stayed on their therapy for a longer time than the patients who only got trastuzumab, which was great news. Cuz then that became the standard of care. But another interesting finding was that if you look at that same study, you can see that some patients maybe around 20% who got the Progeta stayed on that drug indefinitely, they continued to receive it on Kalan Myer, curve, flattens, and patients just continued to stay on it.
So that was a big hint that there’s something, um, going on here in terms of a long term, um, F efficacy of it. And that patients were doing really well on the drug. So that’s not off the drug, that’s on the drug. But the other thing that happens is there are a number of. Retrospective studies looking back at patients who have gone through therapy for, for her two positive NBC.
And there are some data from a few collections of patients that say that there are patients who do stop and seem to do well over a long period of time. When we talk to other, uh, colleagues at scientific conferences, everyone struggles with what do we do with a patient who’s been on this therapy for five years.
For six years, they have to come to clinic every three weeks. They can have side effects from the drugs they’re they are expensive drugs. And so copays can be an issue. They’re some people just decide, you know what, I’m gonna try and stop. And knowing that people do do that. And yet there’s no guidelines for this.
There’s no guidance from any scientific body or group or anything that says how to do it. And so we thought it was important to study.
[00:23:57] Dr. Paula Jayne: We all know about micro metastases and dormancy. So these people who do well for a long time off of treatment, does that suggest that her two directed therapies may be having an impact on either continuing dormancy or actually attacking at the micro metastases level?
[00:24:20] Dr. Heather Parsons: I think our evidence is pretty thin in some of these areas. There’s a, actually a paper from my mentor, Dr. Ben park, looking at a patient who stopped their two therapy and they actually. Looked at circulating tumor DNA over a long period of time and didn’t find it any longer. So that’s some evidence that at least there was an active disease in somebody who is continuing off of therapy for a long period of time.
But in terms of exactly how that’s working, whether they remain cancer cells that are just dormant, whether they’re totally gone. I don’t know that we know the answer to that.
[00:24:52] Dr. Paula Jayne: Sure. That makes sense. So speaking about minimal residual disease or micros, could you tell us a little bit more about the cell-free DNA and how that is going to help to drive this study?
[00:25:05] Dr. Heather Parsons: Sure. This is a really important part of the study, so. We want to be able to have very sensitive diagnostic tests in order to manipulate these very effective therapies. And so we have lacked this in cancer generally, but in breast cancer specifically for a long period of time, people have heard of tumor markers before, and lots of patients have those checked.
We now have the ability to look at tiny bits of cancer in the blood cell-free DNA. That’s coming from the tumor also called CT DNA or circulating tumor DNA. And there are a lot of studies, including from our own work, showing that even when somebody is thought to have their diseases absent from their body, you can detect bits of this cancer of CT, D a or Mr D.
And that does predict when cancer may return. And that also seems to predict when their cancer has gone away. So I think we, we can make this test more sensitive and that work is ongoing. This. Test can be studied in patients who would like to stop their anti her two therapy to see whether the absence of minimal residual disease, MRD predicts patients who will be able to stay off their therapy without recurrence, and whether the presence of it tells us that actually, that that person is cancer is coming back and we need to restart their therapy.
[00:26:33] Dr. Paula Jayne: That’s awesome. So can we talk a little bit about kind of the design and the research questions of your study? If I understand correctly, it’s gonna have two parts, the retrospective, and then the prospective. Do you mind just talking a little bit about those two parts and then especially the perspective. what sure. What will be done there?
[00:26:50] Dr. Heather Parsons: For sure. So the retrospective part is led by Dr. Lin the cohort of patients who have kindly signed up for and donated their blood specimens were part of our embrace program at, uh, Dana Farber. And we’ve been able to look back and see patients who have had this, what we sometimes call exceptional response.
So patients who have been able to stay on their therapy for a very long time and also patients who have had a more conventional response to their therapy and have had to switch. And so we’re gonna compare this test, this MRD test in those two groups of patients in blood samples, don’t via the embrace program and that’s.
One part of the study and, and that work is ongoing right now. And then the prospective study, which we’re hoping to submit to our IRB shortly is a non-randomized study. So it’s patients, um, entering the study have to have been on their therapy for at least three years. They can just choose to join the study if they will stop their therapy.
And they will be monitored every three months with scans and blood tests. Again, it won’t be the thing that. Guiding our therapy based on. So we’ll study that. And then patients who don’t want to stop therapy can join the study and continue on their therapy and just donate blood and undergo scans. At the end of the one year, we will compare patients who are in the continuation off therapy and how successful that is in patients who are in the stopping group.
So that’ll be the, the end point for the study.
[00:28:20] Dr. Paula Jayne: Okay. And so the people who are functioning as controls wouldn’t then switch,
[00:28:25] Dr. Heather Parsons: they sure could decide to do that if they wanted to, but they’re because they’re not randomized. We didn’t put a switch in there.
[00:28:33] Dr. Paula Jayne: I guess one question that Victoria and I would probably be very interested in because we’re both triple positive. Is, are you planning any subgroup analyses where you look at the impact of hormone status? And then of course with that I’m always interested in, do you have a hypotheses about the impact of crosstalk between the two on results and what would happen? Would those people drop out their hormone directed therapy or would they keep it and how would that impact, um, You’re both nodding, which none of our listeners. There you go.
[00:29:05] Dr. Heather Parsons: That, that is a great question. Um, and not a softball question. Um, we actually decided after talking with folks in the CRC and thinking also about the science as well, that patients who have triple positive disease would probably continue on their anti . Hormonal therapy, um, because there does seem to be some ongoing indolent disease related even in triple positive disease, but also in ER, positive her two negative disease that the hormonal therapy, we felt the, the benefits would outweigh the stopping.
So we decided to have . Patients continue on their anti hormonal therapy, but in terms of comparing the. Triple positive to patients who have just her two positive disease that’s year negative. We certainly will do that. It’s not a big enough study where we’ll have lots of subgroup analyses that we can do, but we will look at it for sure.
[00:29:57] Victoria Goldberg: So can I ask a question? I’m very practical. So when are you gonna start recruiting?
[00:30:03] Dr. Heather Parsons: That is a, a great question. The protocol is written and needs to be first approved by our TB CRC group. And then also, obviously by the IRB, and then we hope to start recruiting perhaps later this year.
[00:30:17] Victoria Goldberg: And how many sites and how many people?
[00:30:21] Dr. Heather Parsons: So this, so it depends on the budget somewhat. And the TB CRC, we will open it at somewhere between probably five and 10 sites. And it’s about 70 patients.
[00:30:32] Dr. Nancy Lin: The visits are every three months. So even if it’s not in Boston or near one of the TBCRC sites, hopefully it’s still possible for some people. Yeah. Yeah.
[00:30:43] Dr. Paula Jayne: I think people are gonna be highly motivated. So I think that there are ways to .
[00:30:48] Dr. Heather Parsons: That’s great to hear. Cause we’ve had a lot of input from our patient advocates, both as part of Liz, Frank who’s. We work very closely with here at Dana Farber, but also the advocate group through the, her two working group at T B CRC and the TB CRC overall have been really instrumental in designing the . Study.
But it’s always good to hear that there, beyond that too, that there’s enthusiasm for the study.
[00:31:11] Victoria Goldberg: Oh, absolutely. That’s great. I, I, I happen to be an administrator on one of the, uh, closed Facebook groups for her two positive metastatic breast cancer. That’s all they’ve been talking about for the last, for the last year.
[00:31:26] Dr. Paula Jayne: Yeah. We’re not kidding. Of course, for us it impacts every day of our lives. Herceptin is a very kind drug, but it’s not without side effects and it’s not without a cost beyond that or other directed therapies. So we’re excited.
[00:31:38] Dr. Heather Parsons: We work, especially in the days of zoom in something of a vacuum.
[00:31:41] Dr. Paula Jayne: Sure.
[00:31:42] Dr. Heather Parsons: The only, so it’s really good to hear that.
[00:31:45] Dr. Paula Jayne: I do wanna ask one final question on this, and I know that you’ve already looked at this in early stage hormone, positive people, because of course, those of us who are triple positive or her two positive in that small subgroup are, are super excited, but we’re not the majority of MBC patients. And so what is the hope that this research can broaden out to other subgroups?
[00:32:07] Dr. Heather Parsons: I, I wanna speak both as someone who believes in the science, but also if I wanna be sufficiently skeptical our hope with these Mr. D tests as if they can become paired again with effective therapies. Cause without that, they are just really a prognostic test, which isn’t very helpful, always. Um,
[00:32:25] Dr. Paula Jayne: oh, I don’t it truly, this is not something we plan to talk about, but I think one of the hardest things about living with MBC is the uncertainty. Yeah. And if we had a test that could tell us. It, the end is coming. It, it’s not something that’s easy to talk about. And I don’t know that we have specific timing. It, it seems from the preliminary research that you’re able to predict years in advance if I’m reading that correctly. And so I think anything that helps us direct how we live our everyday lives. Yeah. Even if it’s not as directive with specific treatments, it it’s helpful.
[00:33:01] Dr. Heather Parsons: That’s good to really good to know. Cuz I, I think sometimes we get as physicians, we become less excited about those kinds of tests, but to hear that it’s really important.
[00:33:09] Victoria Goldberg: Oh, it’s absolutely the uncertainty. And if you, yeah, that it’s gonna become resistant or it’s gonna flip is always with us
[00:33:18] Dr. Paula Jayne: and practical decisions. Do I cash in my life insurance policy? Do I take that big trip? It sounds silly, but it, these are the decisions that we live with in a vacuum of data and so any data becomes extraordinarily valuable, even if difficult.
[00:33:34] Dr. Heather Parsons: I do think that if these tests improve in prospective clinical studies, that they are even some fraction of as valuable as they seem to be in the early sort of retrospective.
Small studies. They could be really impactful in terms of both directing therapy in earlier stage disease, but also in, in MBC and in helping guide therapies in a more rational way than we currently do in both in terms of increasing therapy and helping patients who need more therapy, but also hopefully decreasing therapy for patients who don’t need it as much.
[00:34:13] Dr. Nancy Lin: Right now, we don’t have a great way of other than looking at the data look strong or not strong in a kind of general way. What’s a drug that’s good enough that we might try to aim for. right. So we look at the data and we see what’s the response rate and how long do people stay on the drug on average?
And are there people out at five years and eight years and 10 years. And that’s how Dr. Parsons has come up with this study. But if you were to look at other subtypes, well, how do you know if immunotherapy and triple negative breast cancer for a group of patients who are doing really well is good enough that we might think about stopping.
If it turns out that the MRD test predicts what treatments are, it’s not gonna tell you which treatments are definitely good enough, but if it turns out that you have to have MRD clearance to be able to stop treatment safely, because that’s one of the things the study tell us is, is it, do you need to have that or not?
It turns out you do need to have it. You could imagine that you could look at other studies and say, what’s the proportion of people who clear their MRD with treatment X, and it might be zero. It might be that 30% of patients respond, but no one clears the MRD and then you wouldn’t be so excited about testing a curative approach with that treatment.
This is a very small step and there’s a lot of steps in between what I just said and where we are now. But I think it’s really trying to find a way to evaluate. That is really different than what we do now. Right now we consider it good. If a patient has stable disease and it is good. People can survive a long time with stable disease BEC, but that’s partly because our goal is not to cure metastatic breast cancer.
If it turns out that MRD predicts who we can potentially cure and which drugs might actually be effective, I think that’ll be really big.
[00:36:09] Dr. Heather Parsons: One, one last thing I wanted to say about the study too, because it’s an important part about it. And Dr. Lin just alluded to it. This kind of study has been done in a disease called CML, which is a chronic leukemia and they use a different kind of drug, which we don’t think has immunotherapy type activity, but it did have side effects and they tried stopping.
And in this early studies, they stopped. Some patients have to go back on about half of the patients had to go back on. But the important part was that of those patients who went back on all of them, their disease was re controled. We wanna make sure that we’re taking good care of people.
[00:36:53] Dr. Paula Jayne: We’ve talked about groups where the question of cure is close enough that we now have a trial that’s exploring it. Unfortunately, we know that there are many types of MBC or areas of disease where have a much longer road to go. And that’s either because of particularly aggressive disease or lack of targeted treatments, or simply because, as we survive longer, we run up against these barriers of drug resistance or brain mets or leptomenengial
[00:37:17] Victoria Goldberg: so maybe we can talk about brain mets as you alluded to that, there is some stuff is going on in the Her2 space and not as much in other subtypes, but the reality is that of, of the three subtypes, the, her two is the subtype that gets the highest risk of.
Brain mets I’ve looked at some statistics. It is quite old. That’s probably around 10 years old. They do side 25 to 50%. That’s right. Risk of brain mets in her two, a little less in, uh, triple negative and quite a bit less in ER, positive. So why is it people who are living with the, her two disease have a high risk of brain mets?
[00:37:59] Dr. Nancy Lin: We think there are two things going on and they conspire to increase their risk. One is that people are living longer with her two positive metastatic breast cancer. So it’s actually not uncommon for somebody to live 5, 6, 7, 8, 9, 10 years with her two positive metastatic breast cancer. It’s not everybody obviously, but it’s not rare, but many of the drugs that we give don’t get into the brain very well.
And so if there’s a little speck of cells that travel to the brain randomly over time, It can set up shop there and over time people can develop brain metastases. So one part of it we think is just simply that people are living longer. There’s more time at risk for brain metastases, cuz the risk in any one year is still relatively low.
If we look at other factors, it turns out that her two probably in some way. Allows or encourages breast cancer to travel and set up metastases in the brain. And we know that cuz there have been some experiments done where people either turn on or off the, her two expression and inject cells and animal models into the heart or into the, uh, carotid arteries in the neck to see whether turning on and off certain genes increases the likelihood that cancer is able to go to the brain.
And it turns out that her two is one of those genes and there have no experiments where if you treat these mice with various anti her two types of treatments that the rate of cancer going to the brain goes down. So these two related things, her two on its own increases the risk of cancer going to the brain.
And then people are living longer such that if even if any one year the risk is low in that one specific year, if you spread the risk over 10 years, it turns out to add up to quite a high risk.
[00:39:57] Victoria Goldberg: Let me ask you again because I’m not sure I understood. So for you as an individual, your risk of, uh, getting brain Mets increases the longer you live with this disease,
[00:40:12] Dr. Nancy Lin: let’s suppose it’s 10% in the first year and eight or five or 10% in the second year, five or 10% in the third year and five to 10% in the fourth year that ultimately adds up over time.
Oh, it’s not that when you’re diagnosed with metastatic breast cancer, there’s a 50% chance, or you have brain meds in six months. The longer we follow people, we see that even if somebody is six years out or seven years out, there is still a risk of developing brain metastasis. Even that far out from diagnosis.
[00:40:45] Victoria Goldberg: I have a couple of questions that I think a lot of us are interested in.
And even those of us who don’t know much about science, we know enough buzzwords to be scared. So we’ve all heard about blood brain barrier and how it’s a good thing because. Protects the brain from the toxins, but it’s a bad thing when it comes to cancer because the blood brain barrier doesn’t let systemic treatments get through and penetrate the, the barrier.
But I have seen a lot of discussions that seem to say that given the fact that there is a mat in your brain, it indicates the blood brain barrier is less protected. And does that mean that having a less protected blood brain barrier help with treatments?
[00:41:38] Dr. Nancy Lin: Yes. That’s a good question. So we know that in brain Mets, there is a leakiness of the blood vessels that feed the brain metastasis, and that leakiness is very different from the normal blood brain barrier.
and part of the way we know this is that when we send people for an MRI scan, we put in an IV and we put in the special gadolinium tracer dye. And the way that we find the brain Mets is that the dye actually gets into the brain Mets and it doesn’t get into the normal brain. And so you see a contrast there, and that’s what allows us to see the brain Mets.
So we’ve known for a long time that brain Mets have a leaky blood brain barrier. But the way that drug development has happened was normally what you do is you take a drug, you put it in mice or rats or some animal, and then you see like, where does the drug go? Mm-hmm does it go to the brain? And most cancer drugs, don’t go to the normal brain.
The blood brain barrier keeps out toxins and those drugs don’t get in. And so what it has been assumed without any testing in people is, oh, it’s not gonna work in the brain. As it turns out, we have actually a lot of examples now of drugs that don’t get into the intact blood brain barrier, but actually do work in the brain.
And they include medicines like Lapatinib, which actually doesn’t cross the intact blood brain barrier, but it gets into the brain TM one or sella again, doesn’t cross the blood brain barrier, but it turns out that between 30 and 50% of people who get sella have tumor shrink kitchen in their brain, if they’re given that treatment and the list goes on.
So I think it’s important to distinguish just because a drug can’t get through the normal blood brain barrier does not mean that it would not work in the brain. It doesn’t guarantee that it obviously works in the brain, but you can’t go from it. Doesn’t cross the blood brain barrier to there’s no use in trying in people with brain metastasis, because in fact, there’s so many examples now where that’s not true.
Why do we still wanna develop drugs that get through the blood brain barrier? The reason is not so much, it’s a little bit the treatment of the actual brain metastasis. But the big reason is that we think that that’s probably necessary to have any chance to prevent brain metastases, cuz in the end I’d rather prevent brain metastases than treat brain metastases.
And if you imagine like a little spec of cancer cells getting into the brain, passing the blood brain barrier and sitting there for a while before it does anything, if you could develop a drug that gets in at that time before the blood brain barrier is disrupted by the cancer, maybe you could prevent the brain.
Metastasis is from actually appearing in the first place. And for that, you probably do need drugs cross the blood brain barrier. So even though we have drugs that work in the brain, we don’t have great drugs to prevent brain metastases. And I think to me, that’s the most important reason that. We don’t just say, well, you know, any drug is fine, but we really make a deliberate effort to develop drugs that cross the blood brain barrier.
Cuz I think that’s the only way that we’re going to really have a chance to prevent brain metastasis.
[00:45:00] Victoria Goldberg: I have to tell you, I have heard this term many times and listen to conferences after conference talking about this, but this has been the best explanation that I’ve ever heard. So thank you so much.
But now I have to ask you another practical question. Yeah, though. How about to nib as a prevent drug for people who have Her2+ disease?
[00:45:25] Dr. Nancy Lin: Yeah. So in the, her two climb trial, that was the randomized trial that led to the FDA approval of Tucatinib. And the way the trial was designed was that some people got Tucatinib and some people didn’t, but everybody got IV Herceptin and everybody got oral chemotherapy.
And what was seen is that if you look at patients with brain metastases, as we now know, adding Tucatinib increased the chance of tumor shrinkage and the tumors remain outta control for longer. But one of the things that was done in the study, what we call post talk, meaning study, wasn’t designed to . Look at this, but now that you have the data, let’s look and see whether there’s any signal there.
And so one of the analyses was done was looking at all patients, whether they had brain Mets from the beginning or not. And in this study, everyone had to have a brain MRI when they started the study, even patients without known brain metastases. So everyone’s brain met status was known for sure at the beginning of the study.
And then what we did is actually look to see, well, what’s the rate of people developing new brain Mets. So not. Old brain Mets getting worse. What’s the chance is somebody who have a new spot appear.. And it actually looks like it’s lowered by about half with Tucatinib. This is not a definitive analysis because the definitive analysis are the ones that are planned from the very get go.
The statistics are done to make it all work. Right. Um, but it’s intriguing. And so there is a current study for early stage breast cancer patients that is open now in the us, through the cooperative groups and this study enrolls patients who get chemotherapy and Herceptin still have cancer when they have their surgery for their early stage breast cancer normally would get KET cell or TDM one.
But in this study, half the patients also get Tucatinib. . and we know from a previous study of this strategy, that about 6% of patients will have a relapse of cancer in their brain. And 6% doesn’t sound like a lot, but overall only about 10% of patients had to relapse anywhere in their body. So half the patients who relapse relapsed in their brain for early stage breast cancer, if we don’t prevent brain metastases, we’ll never cure everybody with early stage breast cancers.
One of the questions the study is asking is. Is there a low rate of brain Mets happening in patients who get the tatin and we won’t know that answer for years cuz that’s what the timeline is for these studies. But it, it will be looked at in a related way. Dr. Kerry and, and Dr. Sarah salmons at duke university have been trying to work out a study where for patients who have radiation for brain metastasis, normally we just leave them on their same treatment.
So if you’re on Herceptin and you have a brain metastasis, you might get stereotactic radiosurgery or gamma knife or CyberKnife like to those little spots. And then your oncologist will tell you, we’re just gonna continue, you know, your Herceptin and that’s a standard of care. But of course, everybody wants to know if you add Tucatinib, are you gonna delay the time to the next.
Problem in your, in the brain. So she’s hoping to have a study put together to actually ask that question. Studies are never guaranteed that there’s a lot of steps to get a study approved, see what happens. But I think that would be one way to try to get at this question. Can we start to design trials to prevent brain metastasis?
[00:48:53] Victoria Goldberg: You know what? They, what’s interesting though. It seems from what you just said. There is one group. Is excluded from this, the group of, uh, people like me and Paula are people living with the metastatic disease, but not having brain mets. Yeah. So in that way, we similar to the early stage population. So why wouldn’t they extend the trial to include us as well?
[00:49:19] Dr. Nancy Lin: I always think of these things as happening in steps, steps that feel and are very slow, but at least scientifically makes sense, even if they’re very painful from a patient perspective and a doctor perspective, to be honest, the patients who have brain metastasis already, we know they’re very high risk over the next year, developing something else in their brain.
And so if we wanna design a trial that gets at an answer, the quickest, that’s how you design a trial. If it doesn’t succeed in those patients, it probably will not succeed in patients who don’t have brain beds. If it does succeed in patients with brain Mets, then you could say, okay, well what about from the get go?
What about like, when you start Herceptin Projeta Tucatinib, you’re finished with your Taxol part of the treatment. What if you just throw to tib in there? Right? Mm-hmm that’s a good question to ask scientifically these questions. Take a while to answer. So before you embark in something very big, you oftentimes wanna do something a little smaller, but I think you’re right.
Ultimately what you’d like to do is find some regimen that is tolerable, that people could start. When they have a diagnosis of metastatic breast cancer, that’s gonna prevent the cancer from going to their brain. We’re not there. Whereas 20 years ago there was like nothing. Now we have some ideas and Heather actually is designing this other study in patients with newly diagnosed her two positive metastatic breast cancer, where in fact, the regimens are designed in hopes that they would help to treat both.
That disease outside of the brain and also have some potential to prevent cancer from going to the brain. So maybe
[00:51:02] Victoria Goldberg: Dr. Parsons will have to have you to talk about that. Two more questions, because I know the time is getting there. This is something that I just learned, uh, about, and it scared me a little bit.
So I thought I would ask you to ease my mind. We interviewed Dr. Cardoso a couple of weeks ago, and she talked about the micro environment in the brain. She alluded to the fact that the brain micro environment is different than the, the tumor micro environment outside mm-hmm . That is something we don’t know . How to address yet.
That I would really love to hear what your thoughts are,
[00:51:46] Dr. Nancy Lin: even if you don’t limit it to the brain. If you just think about all the different parts of the body, that breast cancer can go. We often see what’s called a mixed response, meaning that you have your scan and some areas look the same and some areas look better and maybe some areas look worse and it’s the same cancer sort of, and you given the same drug.
So why should you see different results in different parts of the body? One possibility is that the different tumors in the brain or the liver or the lung have evolved over time so that they have subtle differences that you, we don’t measure routinely, but are there so one possibility is that there’s a difference in the response because the tumors are actually different.
The other possibility is that in order for cancer cells to grow, they have to co-op their environment. So they have to get blood supply, they have to get oxygen, they have to get nutrients and that the way they do it is different in different parts of the body. And because of that, it is either more or less resistant to treatment based on where it lives.
And one kind of way that we indirectly have an idea that this is true is that over the years we’ve had 30, some people who’ve volunteered when they went to surgery for their brain metastasis that at the time of surgery, when a surgeon cuts out the tumor, a piece of that tumor will be given to the lab and it will be grown in mice to be able to do mouse clinical trials so we can test different things and try to figure out what’s the right combination to bring to a clinical trial in people.
And it turns out that if you take the tumor from the human brain and you put it into the mouse brain, that 70 to 80% of the time it will grow there. It, it grows very well. If you take the same tumor and you put it into the equivalent of the mouse breast, it won’t grow, uh, only about 10 or 15% of the time.
Does it grow there? There’s something permissive about the brain so-called micro environment that allows the cancer to grow. We’re not really sure what it is. And some of the experiments that are being done by my collaborator, genes out who has developed these models over time is trying to tease out like what is going on that cause.
Tumors to behave differently. So what she’s found in the mouse models is that many different drug combinations of work in the tumors that are implanted in the breast, but not so many of them work in the tumors implanted in . The brain. And so now that you have this. Lab model, you can try to sort out, well, why is that?
I don’t have an answer yet, but hopefully there will be answer someday
[00:54:43] Victoria Goldberg: Alright. So now we’ll have you, well, this, this is a question I really ask both of you. What excites you? If you look around in what is happening in the breast cancer research here in the US and outside, what are the areas that excite you?
[00:55:07] Dr. Nancy Lin: we’re both looking at each other like who’s gonna go first?
[00:55:11] Victoria Goldberg: Go together!
[00:55:13] Dr. Nancy Lin: To me just to pick something from each subtype. So for estrogen receptor positive breast cancer, to me, what is really exciting is that we have not yet. Sort it out all the ways that we can target the estrogen receptor. If the estrogen receptor remains really important in this type of cancer, we have aromatase inhibitors, we have Tamoxifen, but there’s a whole bunch of new hormonal therapies or anti hormonal therapies that are in development.
And I think that they can potentially really extend the lives of people with metastatic disease and that subtype and some of those trials are already in phase three. So we’ll have some answers hopefully pretty soon for triple negative breast cancer. What is exciting is that for such a long time, there was no hook.
All you have is chemotherapy. That’s very hard to hear is patients hard to say as a doctor and, uh, now there’s immunotherapy and it’s not perfect and it can be improved upon, but at least there’s a stepping stone to start from there’s Trudel V not perfect drug, but again, a stepping stone to start from.
And it’s hopefully gonna turn into something that’s not. There’s nothing to target, but actually a disease where we do have targets. And in her two, we talked about a lot, but I think really, to me, the challenge in her two is how do you put all the treatments that we have together to give people the longest possible lives?
Cuz now we have a lot of tools and we gotta figure out how we use ’em the best.
[00:56:45] Dr. Heather Parsons: This might be cheating a little bit. I agree with all the things that Nancy said, but I’ll take a little different direction and say that I think one other area that’s exciting is even in the, the time that I’ve been a medical oncologist, it’s so quickly have we seen so much and I think is particularly in her two positive disease, but in general, it’s question of how much treatment to give or the right sequence to give it in.
And how much is too much for some people, how much is too little. And even aside from the biomarkers we discussed, there’s even right now in our clinics, we’re using things like the pathologic complete response to preoperative therapy, as a way to guide how we do treatment, those kinds of tools to guide each individual’s treatment, both in the earlier stage setting and in MBC, all of those and everything in between is really exciting because of the efficacy of these treatments.
We’ve really moved away from, um, giving everybody chemotherapy.
[00:57:44] Victoria Goldberg: Thank you so much. I promise this is the last question I wanted to ask you. And because in the field that you work in, the, the way the clinical trials are usually designed and, um, Dr. Stephanie Graff gave me a very good explanation, why brain mets patients are excluded from her trial.
I would like your opinion. What, what could be changed in the immediate future about how the trials are designed, how the, uh, brain Mets patients are excluded from most of them.
[00:58:21] Dr. Nancy Lin: Yeah. So I have had the privilege to work on this, both with the FDA and also with ASCO and this organization called friends of cancer research to try to promote guidelines, to increase the participation of patients with brain metastases in clinical trials.
So one important output was to say, if somebody has stable treated brain metastases in general, they should be included in trials. No questions asked and you might think that’s pretty obvious. And now it’s mostly done. In fact, that’s mostly how trials are written nowadays, but there was a group that had looked back and they did a literature search of every trial was 1400 trials plus published.
Until 2016 phase one or two trials in metastatic breast cancer. And they looked at I 160 or so early phase trials just for her positive breast cancer and half the trials excluded anyone who ever had a brain metastasis ever. Um, and so we have to get rid of that and I think actually most trials have gotten rid of that.
So I do think that there is at least that progress that if somebody has a brain metastasis is treated with radiation, for the most part, there’s almost no trial that excludes that patient nowadays, the part that’s harder is what about patients where. They have active or their cancer is worse in the brain when they enter the trial.
And the point of the trial treatment is to see whether the treatment will work in the brain. That’s harder because that’s obviously riskier from the standpoint of the person running the trial. And a lot of times there’s not a lot of data. So to me, I think there’s a couple ways to try to make this better.
One is that when people develop or design new drugs, Instead of only doing experiments where you see it as it get into the brain or not. And if it doesn’t, everyone’s gonna be excluded from here on out instead do the experiment where you put the cancer in the brain and you see if it works in the brain, cuz it turns out that we have pretty good data, that that’s fairly predictive of response in people.
So one possibility would be to say, it’s always standard. We look to see whether it works in tumors, implanted in the breast or tumors implanted in the liver. That’s just the standard, um, way that preclinical testing is done. Why not make it standard as part of the preclinical package to look, to see whether it works in the brain?
Not that it gets in the brain, but it works in the brain. Yes or no. And then the other idea would be to include patients with active brain metastases during the phase one clinical trials. Because you don’t really know something works till you try it. Somebody has to volunteer for better or worse for the trials for Tucatinib.
The phase one trials included patients both with stable and active brain metastases from the very get go. So the phase one trials included it low and behold. There were patients who had tumor shrinkage in their brain and because that they had that data and they had the laboratory data, then they felt comfortable taking the risk to allow patients with active brain mets onto the trials.
They hoped would lead to FDA, you know, approval. They wouldn’t have done that if they hadn’t done their, the laboratory experiments or if they hadn’t included patients in the phase one study, cuz it would be too risky. I get it. You don’t wanna risk your FDA trial on patients that you don’t have any idea whether a drug’s gonna work or.
Um, and IRBs also, I think would have some difficulty with that, but hopefully one success story begets more interest in an approach like this. And I do think more companies are exploring this avenue. I do see phase one trials opening up a little. It’s not as much as you know, we’d all, but they are definitely opening up a little bit.
[01:01:58] Victoria Goldberg: That’s very promising. So I have lots and lots more questions, but I’m gonna keep them till the next time we meet hopefully soon. And I just want to thank you for being here and
[01:02:14] Dr. Paula Jayne: thank you so much for your generosity of time for being willing to sit with us for the work that you’re doing for the care that you show for metastatic patients, both for our quality of life.
Caring for people along with the science is a really nice matching of interest. And we’re so thankful to have oncologists who do both and thank you to, for your research translation skills or science translation skills, cuz that is distinct skill set and it makes it possible for metastatic patients to understand the science and have some more knowledge as we advocate for ourselves and try to understand what’s happening to us.
[01:02:47] Victoria Goldberg: Thank you so very much.
[01:02:49] Dr. Heather Parsons: You’re welcome. Thanks for having us.
[01:02:51] Victoria Goldberg: Podcast format gives us the power of controlling the narrative, and I will use it now and tell you a story over failed attempt to cure breast cancer with a bone marrow transplant in the early nineties, right around the time when the FDA pro tax or as a new treatment for breast cancer.
Another trend was taking hold. Oncologists decided that they had found a way to cure even the most dying cases of breast cancer without any new drugs at all. The chemotherapies of the past. And today are systemic treatments designed to kill rapidly dividing cells. In addition to cancer cells, it included the GI cells, hair follicles, and most importantly, bone marrow cells.
Bone marrow is vital to life. It produces red blood cells and platelets as well as white blood cells giving more than the standard dose of chemotherapy to a cancer patient might kill cancer once and for all, but it would wipe out bone marrow and kill a patient in the process. This idea, however, was not at all ridiculous.
There was a successful precedent in the treatments of block cancers and lymphomas there. The doctors had a successful protocol that is still in use today in delivering high doses of chemotherapy, bringing patients to the brink of. And following with a transplantation of a healthy bone marrow from a donor or a patient himself extracted before chemotherapy oncologists had wondered where the solid tumors like breast cancer had remained resistant to chemotherapy, simply because the strength of drugs used for these cancers was not powerful enough at Dana Harbor.
The solid tumor autologous bar program also known as stem regimen was first tried on a breast cancer patient, a 30 year old truck driver for Massachusetts. Her case was considered so terminal that she had been written off from every other experiment protocol. The patient survived the procedure, but died.
Unfortunately within a year still Boston doctors were not discouraged and tried. The procedure on more patients with seemingly more promising results word spread in 1993, duke university released the study of 85 breast cancer patients who underwent high dose chemotherapy followed by bone marrow transplantation between 1987 and 1991.
And the researchers found that these patients had a lower chance of recurrence than women who had undergone traditional chemotherapy. Even though researchers tried to caution against overinterpreting the trial results, the follow up period had been short and rather than randomized trial, the study had merely looked at a high dose group of patients.
10 women had died of complications caused by the treatment. but many oncologist had long assumed that the regimen was so obviously effective that no trial could possibly be needed after all, if the bone marrow could be obliterated by the searing doses of drugs, how could cancer possibly resist the news?
The doctors had discovered a possible cure for some of the country’s most hopeless breast cancer cases had already reached not just oncologists, but patients as well by the late 1980s, hospitals and private clinics offering marrow transplantation for breast cancer had sprouted up all around America, great Britain and France with waiting lists that stretched into several hundreds of women, even breast cancer patients whose disease was not advanced were demanding the treatment.
Many insurance companies refused to cover the procedure, which cost more than a hundred thousand dollars. And sometimes up to $500,000 arguing that it was simply experimental, but the public had lost patients. Patients did not want trials. They wanted drugs and they wanted cures for years. There was bitter fighting on both sides and the number of researchers who were beginning to doubt the results without randomized clinical trials was steadily growing.
The litany of complications was green infections, heart failure, scarring of lungs and so on. And fertility was often permanent. Patients were confined to the hospital for weeks and most ominous, perhaps between five and 10% of women. Ran the risk of developing a second cancer. Upper cancer is lesion as a result of the treatment between 1991 and 1999, roughly 40,000 women around the world.
Underwent marrow transplantation for breast cancer at an estimated course between 2 billion and 4 billion. Finally, after five years, four trials from American and European research groups had collected enough patients and data to determine whether high dose chemotherapy was superior to standard regimens.
The results were to be announced at the 1999 ESCO symposium. The day came for the studies to be presented at the society’s meeting in Atlanta where some 20,000 cancer experts from around the world had gathered to hear the latest in oncology.
A large room at the Georgia world. Congress center had been set aside for the presentation, but even that wasn’t large enough, two additional conference hall held an overflow crowd that watched the presentations via be B seat in the American and European trials.
Data showed that breast cancer patients who underwent high dose chemotherapy fared no better than those who were treated with standard chemotherapy. Patients relapsed at about the same rate in the summer of 1999. A final trial was designed to examine whether stamp might increase survival about among women with breast cancer that had spread to multiple lymph nodes.
Four years later, the answer was clear. There was no discernible benefit. It was over the last trial was the final nail in the CIN of step for breast cancer
in June, 2018. Researchers at the NIH who reported that metastatic breast cancer patient, whose name was Judy Perkins appeared to have been cured of her disease through an experimental immunotherapy treatment. Judy is a good friend and one of the nicest people I. Next Monday, she, I will travel to possess the Maryland, the home national Institute of health to check in with Dr.
Stephanie Goff, the leading investigator on this ongoing trial about neuro research in immunotherapy.
[01:11:10] Lisa Laudico: This podcast is produced by me. Lisa Laudico and the road to a cure series is produced and edited by our amazing and brilliant senior producer Victoria goldberg. In addition, the road to a cure series team includes Dr. Paula Jayne Dr. Ellen Landsberger and Kate Pfitzer expert sound designed by Samantha Silverstein, original music from Konner Kienzle and guest research by Cindy Frempong
our executive producer is Christine Benjamin senior director of patient services and education at share cancer support. You can find more episodes of our MBC life, wherever you get your podcasts. Be sure to subscribe to our news blast. Rate and review us and look for a new episode every Monday. Check out our blog and full episode notes on our email@example.com.
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