Published on August 2, 2019
During session one of our recent chronic lymphocytic leukemia (CLL) Town Meeting in Cincinnati, Ohio, an esteemed panel of experts, including blood cancer specialist Dr. Edward Faber, community oncologist Dr. Mark Marinella, nurse navigator Amy Sheldrick and nurse practitioner Lisa Ovesen, break down the latest treatment research and discuss ways to access the best care available. Dedicated CLL expert Dr. Nicole Lamanna, from Columbia University Medical Center, also joins virtually to share exciting progress and data as the field continues to move forward. Watch as they share knowlege about CLL care.
This program is sponsored by AbbVie, Inc, Genentech, Inc and Adaptive Biotechnologies. These organizations have no editorial control. It is produced by Patient Power in partnership with The Leukemia & Lymphoma Society (LLS), CLL Society and OHC (Oncology Hematology Care). Patient Power is solely responsible for program content.
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Transcript | Morning Session: Accessing State-of-the-Art CLL Care
Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, contributors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you.
Welcome to our CLL Town Meeting in Cincinnati. We’re calling this “Accessing State-of-the-Art CLL Care: What’s Right for You?” I have a question. Does your loved one have CLL? Do you have CLL? Would you like to connect with others who have CLL and are dealing with it? You have come to the right place. That is what a town meeting is all about. It is very likely that this is the first time that you’ve ever been side-by-side with someone with CLL outside of a hospital setting. So, that’s cool; you have a chance to get to know each other.
We’ve got an exciting program for you. I know there’s going to be a lot of questions, a lot of questions that everyone here is going to want to have answered and that the folks online are going to want to have answered.
For you online, start sending in your questions to CLL@PatientPower.info, that’s PatientPower.info. We are going to do our very best to answer as many questions as we possibly can. Just a little bit about myself; my name is Jeff Folloder. I’m in year nine of my CLL journey, son in 2010 I was diagnosed after assuming that taking naps all the time was just part of getting older. I soon learned that I was trisomy 12 mutated, and my first doctor wanted to start me immediately on a chemotherapy regimen. I freaked out, as I’m sure most of you did when you got your diagnosis.
I freaked out to the point where the first thing that I did was get a second opinion. I wound up getting a second opinion at a cancer research institution by the name of MD Anderson in the Houston, Texas area. My second opinion said yes, you still have CLL, but I don’t think we need to do the FCR treatment program. I’m like; okay, so what are we going to do? Absolutely nothing. Great. I soon learned that this is what’s called “watch and wait,” or as our patients call it, “watch and worry.” I didn’t care for it that much.
After about two years of this watching and worrying I was enrolled in a clinical trial at MD Anderson. I went through the entire clinical trial where I participated in a novel treatment regimen using just the immunotherapy portion of the treatment. I received six and-a-half years of rock solid remission to the point where I was actually labeled as MRD-negative. Now, when I was going through these folders that you have in front of you, for all the folks here, I was reading through my bio. I noticed that I really do need to update my bio, because this bio says that I’m still in remission. That is no longer the case.
I relapsed about a year ago. My white blood cell count was going up, my absolute lymphocyte count is getting a little wonky, my platelets are misbehaving, and there’s stuff going on, but it’s not so bad or so fast that it’s time for treatment, so guess what I’m doing again? Watch and worry, yes that’s right where I am. Now, I’m very confident in what’s going to happen in my future. My doctors seem to have a good grip on things, and I’m living a great life. I was chatting with this medical experts up here on our panel earlier, and I told them that my mind knows that I have relapsed and my blood work knows that I have relapsed, but my body is not quite so certain of it yet.
I am a dedicated power walker. I try to get in 5K to 10K every morning, and this past November while relapsed with CLL I got in my first marathon, so 26.2 miles in one go at 14 minutes and 28 seconds a mile. Not bad, huh? I am one of those people that believe that patients who take an active role in their own care have better outcomes. That has been proven over and over and over again in just about every clinical setting. I have chosen to live the best possible life that I can. 15 years ago I was a couch potato. I’ve never been big, I never had to exercise, and I never had to worry about what I ate, but that has all changed.
Clinical researchers were able to get me into a good place and I felt like I kind of, sort of owed it to everyone to do something about that. So, I’ve begun eating healthier, and I’ve been exercising all the time, and I actually feel better. Go figure. One of the things that I’m sure that nurse practitioners deal with all the time is patients who come in and say, “I’m so fatigued,” and they are. When they say go exercise, how does that work? We’re going to talk about that in a little bit.
Okay, so this is the town hall format, or town meeting. A couple of reminders; please remember that the opinions expressed during this program are not necessarily the views of the program sponsors or our partners. Our discussions and what you’re going to hear today is never a substitute for medical advice or care from your own doctor. Please, please, please talk to your doctor about what’s most appropriate for you. You can get ideas. You can get plans put together, but take this information back to your doctor.
I want to thank our partners. Let’s give a round of applause to Oncology Hematology Care, LLS and CLL Society. This town meeting is sponsored by ADVI, Genentech and Adaptive Biotechnologies. One of the things that I want everyone to know about those sponsorships is that there is no editorial oversight from these companies. These companies provide this generous support so that we can have an open dialog. This is not an advertisement for any one brand or type of medication. This is not a plug for any specific protocol. These companies are genuinely interested in improving your quality of life and getting the knowledge that is available to you, so thank you again to ADVI, Genentech and Adaptive Biotechnologies.
This program is produced by Patient Power in partnership with the U.S. Oncology Network, Oncology Hematology Care, The Leukemia & Lymphoma Society, and the CLL Society. I’ve got a couple of questions here. This is going to require a little audience participation. Survivorship for cancer is defined as anyone who has a diagnosis of cancer that’s still alive. Easy enough. So, with that said if you have survived one year please raise your hand. Outstanding. If you have survived two years raise your hand. Well done. We’re going to accelerate this just a little bit. If you have survived five years, raise your hand. Now, we’re going to get out there. If you’ve survived 10 years raise your hand. Tell you what; 10 years and up stand up. You get a round of applause too.
Thank you. Long-term survival is what we are after, and long-term survival with a quality of life.
Let’s get to the headlines and further break down the research and treatment news. We are going to be talking about accessing state-of-the-art CLL care. How do we actually get to the state-of-the-art stuff? We are going to break down the latest CLL research data so that you guys can hear what’s going on from conferences like ASH and ASCO. We’re going to talk about the impact of living with a chronic cancer diagnosis. Most importantly, we’re going to have a Q&A session. This is where you get to take what you’ve heard and take what you’ve been wanting to know and get answers from people who have been there, done that, and got that t-shirt.
We’re going to drill down to all of these hot topics with the experts including the expert information that some of you have sent in, but we’re going to encourage you to send those questions to CLL@PatientPower.info. So, we have our medical experts up here on the stage right now. We also have a panel that we’re going to be bringing on after our break. I’d like to do a brief introduction. First up, I’m going to ask Lynnda and Dave Kasanicky to stand up, wave and say hi.
Dave is one of those guys who raised his hand at the 10-year mark. It’s kind of a big deal. I mean CLL patients are living longer and longer, and he’s also got his wonderful care partner, Lynnda, here who is going to spill the beans on what you care partners really, really want to know. We’re going to do a little bit of “To Tell the Truth,” right? John Binz, please stand up and we’ll give you a round of applause. John was diagnosed in 2006 while caring for his wife. To say that John has been through a lot would be the largest understatement that I could make today, but the takeaway that I want you to hear from him is that you just keeping going, right? Just keep going.
Now, we have one more person sitting down here. Alison Mulholland is a financial navigator. Why is this important? Why do we have a financial navigator that’s going to be joining our panel later on? Let’s be blunt. These really cool, new—we call them novel—agents, these hotshot bills that everybody is talking about right now, they ain’t cheap. They’re really, really expensive, and sometimes figuring out a way to pay for these novel treatments is as important as getting access to them. That would be known in the trade as a tease. We’re going to be talking about that in a little bit.
Okay. I’m going to have a seat now. Could I ask our medical experts to tell a little bit about themselves, sort of an introduction to our online crowd and our in-house audience? Dr. Faber, you’re here at OHC. Tell us a little bit about yourself.
Thank you, Jeff. I’m originally from Pittsburgh, Pennsylvania. I had a mother and father each with a separate cancer, and as I was going through school and studying molecular biology I got a job at a bone marrow transplant unit in Pittsburgh and that started my interest and focus on blood cancers and learning how to do bone marrow transplants and treat patients with blood cancers.
Dr. Marinella, tell us a little bit about yourself, what you’re currently doing, and how you got here.
I’m Mark Marinella. I work with Dayton Physician’s Network in Dayton, Ohio. I’m a General Medical Oncologist in private practice, so I take care of everything. I’m from northeastern Ohio, from Wadsworth, Ohio. I went to Mount Union College, but I did not play football if you know those guys, and then I went to medical school in Dayton and did internal medicine. Then, I took a detour. I was an internal medicine specialist/hospitalist for 10 years but came back to what I really liked—loved actually—which was oncology. I did training a little later in life and that’s what I do now.
Excellent. Now, we have one picture up on the slides right now of Dr. Nicole Lamanna. Dr. Nicole Lamanna is not here physically with us. She will be here virtually with us in a little bit, so we will be hearing from her later. Lisa Ovesen, what do you do?
I’m a nurse practitioner for O.H.C. I see both patients with cancer and blood diseases. I work on the east side of Cincinnati here in our new office that we’ve just built. I’ve been with OHC for five years. Prior to that I worked at Cincinnati Children’s Hospital taking care of kids with cancer and blood diseases, but I fell into oncology. I’m actually a blood-and-guts trauma nurse, and I was recruited to Cincinnati Children’s Hospital just based on some skills that I had from the trauma units. I’ve been doing cancer and blood disease healing for about 13 or 14 years now and I love it.
Thank you. Amy Sheldrick, you are a nurse navigator. First of all, what is a nurse navigator?
We just help patients navigate their way through their cancer journey. I started with OHC almost 16 years ago, and back then we were called a clinician but the new word has been navigating or navigators. I’ve been in oncology for my whole nursing career, which is about 18 years, and it started when I was eight years old and had a playmate in our neighborhood that go leukemia, and since then I can tell you I’ve always wanted to be in oncology since then and got into nursing and have stayed in that since then.
Thank you for being here. We’re going to dive right into the meat of what’s going on. We’re going to talk about accessing state-of-the-art care for CLL. State of the art is a strange term, because the CLL field is moving so fast. State of the art today isn’t necessarily what state of the art even yesterday was. Dr. Faber, can you talk about potential treatment approaches for both frontline and secondary—topline of what the initial approaches look like?
Sure. When I meet patients with CLL, to me the work starts even before you see yourselves in the office. Many folks have different ages, and there are different types of CLL, and how do we arrange this barrage of new medicines that are coming onto the landscape? It’s really to me the art of how we treat our patients. As you say, watch and wait.
Watch and worry.
I was going to get to that, and so we, I think as physicians have a watch-and-worry, too because our chemotherapy agents despite what we can read on the internet and oral agents are much easier, more convenient, and the side effect profiles are different and better in some respects. Our agents and the treatments of CLL can also harm folks, so I have a watch-and-worry too sometimes when I treat our patients with CLL. I would really try to avoid creating something that we can’t treat later on like an acute leukemia. For me, the standard—you mentioned FCR and how that scared you—but there are obviously very smart people down at MD Anderson, and FCR has been around for 15 to 20 years. Probably some of our largest and longest survival data is from FCR in that particular patient population.
Moving beyond that, because of side effects and availability we do have new agents; new versions of rituximab (Rituxan), the ofatumumab (Arzerra) that you’ve mentioned, and we have obinutuzumab, (Gazyva) and alemtuzumab (Lemtrada) and so forth and so on. Now, we have these pills that you’ve talked about that can be easy like ibrutinib (Imbruvica) as we move forward in clinical trials. There are new versions to try to avoid, atrial fibrillation and bleeding risks and hurting the liver, so from here there are very nice directions and algorithms in the literature. We try to take this heterogeneity of CLL and try to make some sense of it and then assign these treatments to folks.
We have a fancy chart up on the screen that the folks are watching right now. It’s sort of a matrix. If you’re young and fit and IgVH mutated, FCR is a reasonable choice. Is that still state of the art?
When we talk about survival, if that’s our end point, I believe it still is because it offers a decade or more of outcomes. We have all of these new agents as you pointed out there, but long-term follow-up is ongoing, so it takes time. In oncology a success can sometimes be a hindrance because the better we do the longer we have to wait to see how the newer agents might be better.
Good point. The gentleman who founded Patient Power, Andrew Schorr; he was one of the original FCR patients and I think he’s going on 19 years now post FCR and living rather a great, globe-trotting life at this point. There are a lot more tools in your tool bag. Dr. Marinella, would you like to talk about some of those tools because we’ve got a bunch of things listed up here and most of them are difficult to pronounce.
Yes, we do. As a generalist who takes care of everything, CLL has changed immensely in the last six months. If you look at all of the articles that have been published in the New England Journal alone in the last year—and even in the last three or four weeks there have been a couple—it is a whirlwind, and when you throw myeloma in there and immunotherapy it really is. To access state-of-the-art care in my opinion would be, if you’re seeing a general medical oncologist, which is really where most patients get their care; it’s that they’re up, they’re reading, and most of us are.
I think that’s a given in our specialty. Oncology is a specialty where people—you know there’s demand if you practice evidence-based, state-of-the-art care. As far as other tools, I will say for FCR I still believe in it. Again, as Dr. Faber said the MD Anderson data goes out 15 years or so and some of those patients, if you pick the right one and they need to be mutated—I think FCR still plays a role—now, with other tools as far as standard outside of trials, the biggest one that people talk about is ibrutinib, which is called a BTK inhibitor. It’s an oral drug that’s very effective, and it is effective in—if you look at the study called the Resonate Study and they’ve updated this and had some new ones—it’s effective in mutated and unmutated.
I’m sure we’ll talk about 17Ps and 11Qs; it’s effective there, too. Venetoclax (Venclexta) is the other one that is getting a lot of press and probably will change CLL treatment and as far as that, a toolbox, where that may come in handy—and it will be interesting to see what Dr. Faber says—that we might not be able to offer a fixed duration of therapy, which is good about FCR, because there’s some recent data on venetoclax combinations.
There are the PIC three kinase inhibitors, idelalisib (Zydelig), but there are a lot of ancillary tools when you take care of these patients and use these drugs because knowing how to use a drug and knowing a lot about the disease is one thing, but then the complications and the supplementary tools with the anti-infective prophylaxis. So, as the tool box gets bigger it does sometimes make it a little more confusing during the conversation with an individual patient.
It occurs to me that I may have been a little bit short in failing to ask you, Dr. Faber, what are these different things? What is the difference between a chemotherapy agent, an immunotherapy agent, and these novel inhibitors and small molecules? We probably should have started that at the beginning because they all work differently, don’t they?
Absolutely, Jeff. To me, state-of-the-art is a perspective, and what we have are general chemotherapy agents like fludarabines and cyclophosphamide that you see there. When I used to teach med students and residents we had an auditorium and how do our drugs work? I would say; imagine on the side doors that somebody came in with a hose and started spraying the room. A lot of you would get wet. Some of you are pretty quick, and you’d get behind the seat and you would stay dry. That’s kind of how our chemotherapy, like fludarabines (Fludara) and cyclophosphamide (Cytoxan); it’s not very directive. It’s general, and so now instead of trying to affect the cell from a general aspect a blood cell is a sphere and it has proteins and there are antibodies like rituximab and obinutuzumab, and it recognizes these proteins on the surface.
We had good success with the introduction of these monoclonal antibodies, and then as we learned more, when not everyone in a clinical trial responded the same way or in life; then we started to look inside the cell. Inside the cell we have a surface and we have another little sphere called a nucleus. There are pathways and the ways that cells communicate to live and die. Medicines like ibrutinib and idelalisib and venetoclax; the way that CLL cells have an advantage to grow after being signaled from the outside, these drugs address that and so to me, as I’ve said state-of-the-art is a perspective, because we still have older therapies that work extremely well. We have newer agents that come to the front and then we learn more about further science that helps.
To me, there’s this ebb and tide of; we have traditional chemotherapy, we have immunotherapy, we have targeted therapy, we have novel agents depending on how you think of that, and really we restructure and juggle those so to speak. If you look on clinicaltrials.gov today, you will see all versions of monoclonal antibodies and immunotherapies, and checkpoint inhibitors, which aren’t represented there, but and so really as you circulate and find these combinations, to me that’s exciting because as everyone in the room here and online, it really can be individualized care. How do we sequence and how do we combine these agents to maybe be as good as FCR?
It’s a great point to make, and the concept of this combination therapy is particularly attractive to me because like you said we’re juggling all these different components. Nine to 10 years ago when I started my journey chemo was, for all intents and purposes, the only avenue of treatment. In just that short period of time we’ve gone into these other modes and those modes have put us in a place where, when we start talking about personalized medicine we really are doing the juggling thing that you were talking about. It’s not just that you have CLL. It’s that you have this specific type of CLL, and you are reacting in this particular way to these particular treatment protocols and so two people who are trisomy 12 mutated may have vastly incomes. We’re learning why now. Is that fair?
Yep, and I think two examples, as Dr. Marinella brought up with the drug venetoclax and even bendamustine; those drugs have been around for quite some time. Bendamustine got dusted off the shelf, so to speak, about a decade or more ago and now it’s a very important component of treating CLL and other non-Hodgkin’s lymphomas. When I was starting out in research in the ‘90s, anti-sense gene therapy was very fashionable and Bcl-2 was a big target. Here, now comes along venetoclax that inhibits that protein that gives survival advantages. Just because therapies may have failed in the past it doesn’t necessarily mean they don’t have a role. That’s the neat thing about how these drugs and these combinations are coming into the landscape.
Dr. Marinella, I’m going to ask the million-dollar question here. I’m also going to drop the C-word into this question. The million-dollar question is what is the goal of treatment for a CLL patient? For some of us, any of us, none of us, or all of us is it reasonable to consider the word, “cure” in the landscape at this point? I think I told you that hard questions go to you.
Historically for CLL there’s a general statement. People have always asked, “Is this curable?” The answer typically has been no. CLL often is an indolent disease. I have, and I’m sure Dr. Faber does too, lots of patients in our practice that come in once a year. They’ve had this for 10 years, some 15, and some 20, and some people never need to be treated. Again, that goes back to biology, but historically CLL has been considered just a low-grade cancer. You might treat it, back off, treat it, back off, and it’s not curable. There’s a wide spectrum, too because there are patients that need to be treated the minute they walk in the door so to speak and other patients that you don’t treat.
The word cure for CLL, I think at least the way I interpret things has been raised by the folks at MD Anderson. With the FCR regimen and mutated, especially if you’re at 13—not necessarily, but if you’re mutated and they treat it with FCR there are people that achieve minimal residual disease. I think their latest data probably has maybe half of those patients are doing well, with 10, 15, and 19 years in Sweden that probably are cured. People might argue that. The other thing, though that could potentially lead to a cure is now the combinations of drugs. There are numerous clinical trials and I can’t comment on all of them, but they’re looking at combos.
The one, and I don’t know about CAR-T therapy, but CAR-T therapy may also be something in the future that, depending on where it’s put into the treatment logarithm could change the paradigm. There’s a disease called CML, chronic myeloid leukemia that was a different disease but is an analogy. It was considered fatal, and untreated it is fatal and there are oral drugs for that. Now, with some of the potent oral drugs for that after three or four years of remission we’re thinking of taking some patients off. Some of those patients may not relapse, so I have asked in my mind what would be most likely; venetoclax, ibrutinib and now newer, with the second, third and fourth generations of these. Will we obtain a similar thing with CLL as we did with CML?
Granted, it’s a different disease but I think the answer is perhaps, and then the CAR-T. I think people are starting to think about that word now.
Let me follow up just a little bit. I mentioned earlier when I was introducing myself that after my clinical trial I achieved MRD negative status. Can you explain to our audience what MRD is, negative or positive and why it’s important? Is this actually a goal?
MRD is tough even for me to understand. It stands for minimal residual disease. There are different ways of detecting the amount of cancer cells in general in the blood. One is under the microscope, where you look and you see all these cells. That’s the most rudimentary method. Step and bleed would be in the bone marrow under the microscope, if can still see cells. Even if you treat somebody and a couple of months later look under the microscope and don’t see any cells floating around they’re still there probably. Then, you dig a little deeper. That would be with the bone marrow, and you may still see some cancer cells there but not in the blood, because the bone marrow is a more sensitive test.
In some cases. you don’t see any cancer cells in the bone marrow, and then you drill a little further to detect MRD. In general practice outside of a research institution we typically do it with something called flow cytometry, which I cannot explain very well. It’s very complicated, but they take the bone marrow and they put it in a machine. It looks for markers and proteins and spits out a bunch of information and can tell you down to one in 10,000 in most labs if there’s disease there, so it’s even more sensitive. There are more sensitive, like 10 to the eighth, but MRD if attained is associated with a better prognosis.
So, is MRD negative a goal of treatment?
When you’re MRD negative—and I’m asking this for me, personally, which I was—they did the bone marrow biopsy and we’re going to talk about the bone marrow biopsy in just a second; when they did the analysis of the bone marrow biopsy they said less than two intact cells out of 100,000 could be detected. That was pretty reasonable. My doctor looked at me and said, “Your disease is not here.” How did it come back?
We get asked that a lot. It did not come back. It was there and it’s the sensitivity of the test. If they have a test that can go down to two in one million or two in 10 million they probably would have found something. It’s a similar concept when you’re treating breast cancer and the surgeon said; I got it all. Sometimes we use chemo and sometimes we don’t. We’re giving chemotherapy to treat straggler cells that have escaped and are sitting somewhere else that we can’t detect. Maybe someday like on “Star Trek” they’ll hold the tricorder over but we can’t detect that. It’s a similar situation here. It’s the degree of the sensitivity of the test is what I would say.
So, MRD negative is a reasonable goal of treatment, but it’s not a definitive endpoint. Would that be a fair statement?
Yeah, I think so. I think your definitive endpoint is time.
You mentioned examining this tissue from the bone marrow. Most everyone in this room and online knows what a bone marrow biopsy is, but just for my own personal identification I do this at just about every town meeting. If you had one bone marrow biopsy please raise your hand. There you go. If you’ve had two, three, four, five, six clinical trials? I was on a clinical trial. I kind of broke the mold. We’ve had patients in town meetings who have had more than a dozen bone marrow biopsies. Dr. Faber, I’m going to ask this question directly to you. Why do you need to perform what many patients consider a very uncomfortable and medieval tissue extraction to do this test? Why can’t you get this stuff from the blood?
I like to think that I’m sensitive about this because I’ve had two myself to give normal samples when I was in research in the lab. I had one really good experience. I still remember her name, Debbie Davison. She’s a wonderful nurse practitioner, and I had a terrible experience the second time, so to me we do bone marrows when, or I believe they should be done when they’re going to change the management of your care. You’re correct. There are times that your white cell count is 50 or 100 or 400. The pathology that we need to help manage your care is there, and for many times maybe a marrow is not necessary.
If we take this a little bit back to the discussion about MRD, why does CLL happen? We have these neat things like these gene testing, trisomy 13, 12, and 11 and 17Ps, but as we’re learning there are changes in the genes that are associative with your blood cancer. They’re not causative because we have targets for these. If P53—I still remember the article in Nature in 1992—it was going to revolutionize cancer care. We have had targeted therapy against P53 for 25 or more years now and no one has been cured with a P53 inhibitor yet. So, as we try to find the information on where the cells float at and the lymph nodes that they involve sometimes people do have versions of CLL called SLL, which is like a lymphoma.
As I explain to patients, if your lymphocytes are floating in the blood we call that leukemia. If they decide to aggregate in a lymph node or your bone marrow we call that lymphoma. And so, to me bone marrows are necessary when we can’t learn as much in the blood. There are staging systems, and if adalimumab (Humira) is involved you are stage IV and there are outcomes associated with that, but for many folks I don’t know that the outcomes terribly differ between stage III and IV, so I don’t know that we always need a marrow to tell you that.
I’m going to write that down. You think we don’t always need a marrow, so the next time they want to drill a hole in my hip I can say; slow your roll, right?
Yes, you can.
It’s nice to have that card to play. Lisa, all of this stuff that we’re talking about; we haven’t even gotten to the new stuff like clinical trials and all that stuff. This is mind-boggling stuff. This is overwhelming stuff for a patient. We have this thing that most of us are aware of called Dr. Google.
I deal with Dr. Google a lot.
I suspected you might. We have access to all of this fantastic knowledge here and all of us with our Smartphones and our laptops and our MacBook’s and all of that good stuff; we can access all that information almost instantly. Talk about how your patients deal with that onslaught because it’s overwhelming. We’ve gone through words that hardly anyone can pronounce. We’ve talked about treatment options in chemo and patients have got to be overwhelmed. I’m interested to hear your take on how you guide patients through this little matrix here.
Well, many of my patients have gotten their medical degree from Google, so I deal with it a lot. I think it’s really hard for patients because there is such an onslaught of information. You just put CLL into your browser and you click and all of this stuff hits you.
I think what I try to talk to my patients about is; please come to us with questions that you have. Write it down. Bring it in. We’ll talk it through. I also tend to find just in general that people are really going to tell you their horror story and they’re a little less likely to tell you their good outcome. I think folks come in and they’re terrified because of the things that they have read online, so I think open dialog is really important. We do deal with it a lot, and that’s part of what as a nurse practitioner we offer. It’s a lot of psychosocial support and education and things like that.
I’m not necessarily making the treatment decisions like these guys are. I’m helping support the patients once they have decided or these guys have decided what they’re going to take and kind of then demonstrate that we are trying to help the patient through the process. It’s very difficult. There’s not really a right or wrong thing other than I often tell patients; pump your brakes and come to me with specific questions that you have.
I’m glad you brought up the scary stuff about what you read on the Internet because what we’re going to talk about now—and Dr. Faber, I’m going to toss this to you first—is the new stuff; combination therapies, stem cell transplantation, non-chemotherapy combinations and clinical trials, and this thing called CAR T-cell therapy in clinical trials. If you Google some of this stuff it’s a horror show but we’re learning a lot really, really quickly. How do you work with your patients for these additional CLL treatment options? How do you present them?
I alluded to, in one of my first answers that a lot of the care begins even before we meet you so to speak, and when you have so many therapies and so many endless combinations and then for myself as a transplanter, which we now call cellular therapy and not transplanting in many respects, really thinking about sequencing these over the time and the life of you as the patient I think begins even before we meet. As Dr. Marinella mentioned, there are some higher-risk features of the special testing that we do and there is definitely data that, with things like FCR and FCR-based and rituximab and ofatumubab-based that CLL is going to return much sooner than what we want to see.
Sometimes when it does, it’s hard to get individuals back into remission to do a cellular therapy. So, there still is a role for an allogeneic stem cell transplant in some patients. Now, the drug Ibrutinib has changed that a little bit especially for our patients that are a little bit older and an allogeneic transplant may not be the right choice. And so, that becomes—as I said there are decisions that are much, much earlier and that we should have a plan for you as you ask questions to years five, ten, and fifteen.
I think that’s really important, and working with a really good center—in your case like MD Anderson, where you were—I think is paramount in working together. Dr. Marinella alluded to that, too. So, how can we put this all together and have a few more minds and eyes is very important to distinguish that.
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