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Session 2: What You Should Know About CLL Treatment, Genetic Testing and Research

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Published on September 25, 2018

Watch the replay of session two of our “Understanding CLL: What You Should Know About Treatment, Genetic Testing and Research” town meeting, as a panel of CLL experts, including Dr. Jonathon Cohen, Dr. Jean Koff and Dr. Kerry Rogers, continue to discuss the latest in CLL treatment and research.

This town meeting was produced in partnership with Winship Cancer Institute of Emory University and sponsored by AbbVie, Inc., Pharmacyclics, LLC and TG Therapeutics. 

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.

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Transcript | Session 2: What You Should Know About CLL Treatment, Genetic Testing and Research

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.

Jeff Folloder:

Welcome back to the CLL Patient Power Town Hall Meeting in delightful midtown Atlanta. I hope everybody got everything taken care of at the break. We were trying to digest an awful lot of information before we got to that break and we left a little bit off. So, without any further ado, we’re gonna dive right back into it. Mona, I’ve got a question for you. One of the things that we did not discuss is stem cell transplantation. Is that an option for CLL patients, and if so, why?

Mona Shums:

It definitely can be an option for CLL patients. Of course, you have to qualify. There are certain criteria just like starting chemotherapy that would make you eligible for a stem cell transplant. Of course, one of the biggest things is that is there a donor available? We wanna make sure that we attempt to make the stem cell transplant as successful as possible, and part of that process is finding an eligible acceptable donor. And then, of course, looking at other criteria: how well did you respond to chemotherapy in the first place, what other comorbidities that you might have, because all of those factors play into the role of being eligible for a stem cell transplant to begin with. 

Jeff Folloder:  

So, who does a stem cell transplant help? We went through a giant matrix grid of people who get traditional chemo, people who get the monoclonal antibodies, the inhibitors in different combinations. What type of patient are we focusing on for a stem cell transplant?

Mona Shums:

I think probably Dr. Cohen or Dr. Koff can answer that better.

Dr. Cohen:      

Yeah, absolutely. So, the role of transplant in CLL, to be honest, has been diminishing over the last several years, but it’s still something that we think about in some selected patients. Historically, patients that had particular high-risk markers—I know we haven’t talked as much about FISH as much in particular, but patients that had a 17p deletion that was identified on FISH in the past, because we knew their outcomes weren’t quite as good with chemotherapy, would often consider moving forward with the stem cell transplant fairly early on in their disease course. Now that we have some of our novel approaches, that isn’t always the case.

Again, that’s really where the personalized approach comes into play. But for me though the place where I often think about a stem cell transplant in a CLL patient is in a young patient with limited other medical problems whose CLL really is not behaving the way we would like. And what I mean by that is—as we’ve discussed today and we’ve spent a lot of time talking about watching and waiting, for many patients the typical disease course is they get diagnosed, they may not necessarily need treatment right away.

They’ll get treatment whether it’s an oral therapy or immunotherapy, or got chemo or combination, they’ll get treatment, go into remission and stay in remission for several years, and then potentially the disease comes back, and we talk about what to do next. But in some cases, for reasons we are not always able to understand, some patients don’t always have that prolonged remission. So, maybe you get treated on sort of the shorter end of that spectrum, and maybe you then get a second line treatment, and again you don’t have a great response.

And if I have somebody who is young and fit and in otherwise eligible based on some of the criteria that Mona was describing, those are the patients where I think about a donor transplant. In a reasonable portion of patients, you can potentially, whether you call it be cured or at least enjoy a prolonged remission—especially if you go into the transplant with good disease control. And so, if somebody has had multiple relapses and is otherwise a candidate, I often will at least consider that as an option, and will have that discussion with patients.

Jeff Folloder:  

So, we’ve talked about all of the different currently available approved treatment modes for CLL patients. But what is probably on everyone’s minds and lips right now is clinical trials. And so, Jean, I’m gonna ask you when should a patient consider a clinical trial?

Dr. Koff:          

I think the answer to tat would be when should a patient not consider clinical trial? So, the reason that we have all these options for treatment is because patients like yourselves who had CLL underwent these clinical trials to test these agents, see which ones were safe, see which ones maybe outperformed the currently available treatments for CLL. And over the course of years of kind of vetting the results of multiple clinical trials, that’s how all of these agents were approved. And those patients who went on those clinical trials had access to those drugs before they were approved, before they were available in non-academic practices.

And the other half of that is that clinical trials don’t always focus on patients who need treatment. We have a variety of clinical trials that follow either with observation or with upfront treatment for patients who otherwise may not be candidates, or good candidates, for treatment if we were following the standard guidelines. And that’s one of the reasons, I think, that you should always consider whether you’re about to start treatment or you’re still on the watch-and-wait approach if you’re not already following at an academic center, that you at least get a second opinion because, again, they may offer clinical trials that are not otherwise available to you.

It’s more important probably when you’re thinking about starting treatment about seeing whether there are clinical trials available, and whether those clinical trials are a good fit for you, for your lifestyle and your preferences. And then your doctor and the clinical trial team can help determine whether you’re a good fit for the clinical trial, whether you meet the type of criteria, the patient population that they’re looking for.

But I think whether you are going on the watch-and-wait approach, you’re thinking about starting a standard therapy for CLL patients, the option of a clinical trial and seeing whether you may be a candidate, or if there’s a clinical trial that fits you, that that should always be part of the discussion.

Jeff Folloder:  

Point of order, doctor. Clinical trial—I’m just a guinea pig, right?

Dr. Koff:          

Well, there is that fear and we get a lot of those types of questions when…

Jeff Folloder:  

…is it valid?

Dr. Koff:          

I think you are volunteering and offering yourself as someone in whom a treatment that is not already approved is being tested. And what I can say is that for any clinical trial that you would be on, there has been a lot of pre-clinical testing, meaning testing of potential treatments in cells to make sure that there’s a chance that this treatment works, in animal models to make sure that the treatment does work in a living patient, even if that patient is a mouse. And to see whether that there are potential side effects that are not compatible with a good quality of life or are not safe.

And so, there is a component of you are on the front lines of getting this treatment before other people may, and part of that is we’re seeing whether, in fact, this treatment works and is safe to give. But we don’t ever give treatments that have not already gone through thorough vetting. And depending on where you are in that drug’s pathway to getting approved, it may be that that drug has already been given in multiple patients with CLL or with other diseases, and that there have already been multiple tests to make sure it’s safe. But I think there is a component of the unknown, and that’s part of doing a clinical trial.

Jeff Folloder:  

The founder of Patient Power, Andrew Schorr, is fond of saying that participating in a clinical trial is an opportunity to get your hands on tomorrow’s medicine today. I participated in a clinical trial as well, and at no point during that trial did I feel like I was a guinea pig. When my doctor told me, “I believe this clinical trial has the best opportunity to get you the best remission with the least amount of side effects possible.” I couldn’t sign the cards fast enough.

Dr. Rogers:

There are just two things I wanted to add because that was such a nice description of clinical trials. One is that there are clinical trials that compare two different FDA-approved regimens sometimes, or an FDA-approved standard of care regimen to one that’s new and similar. And the only reason we would even do that is because we think the one that we’re studying is at least as good as the standard of care, and we wouldn’t be doing the study if we didn’t suspect that it might be potentially better. So, there are some standard drugs and then there’s some times where there are trials where it’s the first time that drug has ever been given to a person before.

So, it’s always important to ask the physician and clinical trial team what exactly the questions are in the study, what the experience is with these drugs because it might be excellent studies in mice but not a lot of studies in people, or it might be something that’s approved in a different cancer and thousands of people have been treated. I think that deciding to participate in a clinical trial, as was just pointed out, is sometimes the best treatment available for individuals.

But like any other treatment decision is always a weighing of both positive factors; like this might be the best treatment outcome, or sometimes the medication’s provided, which matters for people versus drawbacks, which can be more travel time because there might be more visits to ensure that you’re safe and that the treatment’s working. Also, clinical trials frequently require that people get more bone marrow biopsies because we need to know what’s happening with the study. So, yeah, all of you that were up over—like anyone hitting seven potentially has been in a clinical trial.

So, there are some potential drawbacks too. So, all those factors have to go into deciding if this is the right thing for you. So, if your doctor says this is the best treatment, this is something that appeals to you, that’s great. But there are some people whose goals, which are not to drive back and forth to the cancer center all the time, might not be consistent with being in a trial. And then hopefully there’d be some good standard of care options. 

Also, I’d just like to add on a personal note that I have some pet guinea pigs I don’t use for research, so I think it’s really funny when people ask me, “Am I gonna be your guinea pig?” And I’m like, “No, actually I have some. I have two of them. So, that role is already taken.” And that they have a very nice lifestyle.

Jeff Folloder:    

Very well done. And since we’re talking about clinical trials, it’s the new stuff that’s probably top of mind. Let’s talk about some of those things that are in clinical trials. Mona, I’m gonna start at the end. The one that has been getting an awful lot of press, both in the media, on the news, this thing called chimeric antigen receptors or CAR T-cell therapy. Some people are having grand slam home runs, and some people are not in great shape. What is CAR T-cell therapy? How does it work? And how might it help us?

Mona Shums:  

So, it is very exciting. It’s kind of up and coming, very exciting. Basically, what they’re doing—it’s kind of like a targeted transplant. We talk about targeted chemotherapy and so forth. It’s personalized transplant. So, you actually take your own cells, remove your own blood cells and they add a type of virus to those cells. And what they’re hoping or what they’re doing or what they’re finding is that when they give you back those specific cells, your own cells back, those cells specifically target the cancer cells.

And with that, meaning with certain chemotherapies, when we give you the chemotherapy, we’re not only attacking the rapidly-growing cancer cells, we’re also attacking your healthy cells, which is why when you’re receiving chemotherapy there’s always—we see the drop in your white blood cell count and in your hemoglobin and your platelets. And with that comes side effects: infections and risk of bleeding and weakness and so forth. So, with CAR T, if we can specifically target those cancer cells and we have minimal other healthy cells that are affected, that we’re reducing some of those side effects. 

Jeff Folloder:  

Kerry, you guys are the rock stars with this cutting-edge medicine. As far as CAR T cells go, is there currently a way to predict who’s gonna benefit from it and who it’s not so much?

Dr. Rogers:     

That’s a good question. So, I actually found out at the break that I’m the only one on the stage that doesn’t take care of people for stem cell transplants. I refer people for that. So, probably looking at predictors of outcome might be answered by someone else. But I can say who I think would benefit most from this treatment. So, CAR T-cell therapy is very exciting. But you can only get it as a participant in a clinical trial right now for CLL. It’s approved in some other cancers. So, that kind of gets back to why one might wanna participate in a research trial or a place where some people—their best treatment might be with these CAR T-cell therapies in a research trial.

So, I generally refer people to consider a trial with CAR T-cell therapy if I think that none of my standard therapies or currently available clinical trials that aren’t CAR T cells are going to give them the best outcome. So, if I don’t have something else I can offer people that I think will be as effective or work as well for them, and I think they’re well enough and willing enough to engage in the process of a CAR T-cell treatment, which is not a short or small undertaking, then that’s who I would send for it. And I think someone else might be able to answer who—predictors of who benefits the most.

Dr. Koff:          

Yeah, so that’s the million dollar question. In all patients who are getting any type of CAR T therapy now. So, CAR Ts have really just—they’ve just been approved for certain malignancies in the last couple years, and just to reframe what Mona was talking about, what this therapy does is it harnesses the power of your own immune system to target and attack the CLL cells themselves. And so, the idea is that when you draw blood and you process the T cells, which are part of your immune system, and you basically engineer them to attack a marker on the cancer cell.

Jeff Folloder:  

I knew there was a way to get Arnold Schwarzenegger back into this conversation. You’re creating little terminators aren’t you?

Dr. Koff:          

Absolutely, that’s a great way to think of them, as mercenaries. And so, those are going to attack only the cells expressing that particular marker. And because they’re part of your immune system, what the hope is is that even after we infuse the T cells, and they attack any CLL cells that may be in your body, that because they’re not just drug that are gonna get flushed out through your kidneys or other ways, that some of those T cells will live for a long time, maybe for the rest of your life, and continue patrolling and seeing whether there are any other CLL cells that need to be taken out.

So, right now where we are in this research is, like I said, the CAR Ts have been approved for a couple other malignancies, and even in those malignancies we are still trying to find out what the markers are of the patients who are most likely to benefit. And we still don’t know even in those patients with malignancies for which it’s approved. In CLL we’re still not even at the point yet that we’ve completed the clinical trials showing efficacy of the CAR Ts that are engineered to take out CLL. So, we’re still looking at that information.

And even now that CAR Ts are approved in some of these other malignancies, there is still a lot of research being dedicated to trying to find those markers of patient immunity or the cancer cells themselves that mark a patient who is most likely to respond to CAR Ts and have a long durable response. So, we’re still, I think, pretty far away from that in the other malignancies but also in CLL we’re even a little bit further behind right now.

Jeff Folloder:  

This is just fascinating stuff because in my mind I see little itty bitty terminators patrolling my bloodstream and knocking out the CLL cells. It’s very, very exciting. But, as you mentioned, we don’t know just yet who’s going to be the most receptive to this type of treatment. And there are downsides; there have been some not so good results from the CAR T-cell trials as well. And it’s something that I know everyone on this stage is keeping tabs on, and it’s something that we need to keep tabs on because this is the leading edge of research. We’ve got a bunch of stuff going on here now. I saw lenalidomide and I’m thinking to myself, “Isn’t that an old drug?” 

Dr. Cohen:      

So, lenalidomide (Revlimid)—it’s a very interesting story just because it’s found its way into the management of a number of different diseases that we see. And I would argue that most people still don’t really understand honestly how it works. But we know that it does impact the immune system in a number of ways. And so, lenalidomide either by itself or in combination with other therapies has been investigated in a number of settings in CLL and does appear to be promising.

What we’ve seen though that’s a little bit different than some of the other types of cancer where we use it is that patients with CLL that receive lenalidomide can actually have a flare of their tumor that can cause a lot of symptoms and side effects. And so, typically if we’re going to use it, we start it at a low dose and those patients have to be monitored very closely. So, it’s not for everybody, but it certainly is a promising therapy in CLL and a number of other malignancies. If it’s okay, I wanted to go back just for one brief minute to the CAR discussion. 

Jeff Folloder:  

Sure.

Dr. Cohen:          

And you brought it up just when you were talking about lenalidomide, but one of the things I think is also important for people to recognize is that although we are fortunately not seeing some of the more common chemotherapy-associated side effects, that any time that you do administer a therapy that stimulates the immune system, by so doing you can cause sort of the immune system to flare and it can be associated with pretty significant and life-threatening side effects. And so, that’s why that therapy is not for everybody. We have a CAR T program at Emory; they have one at OSU as well.

And part of what we do is evaluate patients to determine whether or not they’re candidates for that therapy. And my hope is that 15 years from now we’ll be looking back at discussions like this and we’ll have figured out number one how to identify who are the best candidates, and number two how to avoid those toxicities while not compromising the effect of the therapy. But we’re still very early in that regard. So, if you were thinking about this as a therapy, it’s definitely worth bringing up with your physician and potentially exploring in an academic center.

But just know that it’s not necessarily for everybody, and your physician may or may not feel that you’re the ideal candidate given what’s going on in your own situation.

Jeff Folloder:  

We’re gonna talk about some of the other promising CLL research avenues going on, but I wanna reinforce a common thread that we’ve been talking about since the beginning. We’re encouraging each and every one of you to tell your doctors, tell your mid-level providers, tell your nurse; tell everyone what’s going on in your life. Open up the path of communication, to ask questions, to become an informed patient. Become your own patient advocate.

There is something that I like to say at these town hall meetings. I believe it not just in my heart and my head, but it’s been borne out by clinical research. Patients who take an active role in their own care have better outcomes, period. So, if you’re asking these questions, if you’re showing up for your doctor’s appointment, you say, “Doc, tell me about CAR T-cell trials and are they right for me? Tell me about lenalidomide. Tell me about these new monoclonal antibodies. Tell me about these combination therapies.” You’re gonna have a better outcome. You’re more engaged. You’re more likely to become a compliant patient and stick with your regimen.

You’re more likely to give the feedback to your healthcare team that they need to make sure you’re getting the right thing. So, from my personal perspective, if you guys go home with one thing, and only one thing, it’s become an active participant in your own care, please. So, we’ve got monoclonal antibodies, anti-ROR1 and anti-CD19. We’re expanding the universe in these monoclonal antibodies.

What you don’t see up here is something that intrigues me because it’s what my doctor brought up. He said that I’m not gonna need treatment right away. He said it’s probably gonna be six months, a year, a year-and-a-half, two years down the line. And most likely what we’re gonna do for you is we’re gonna give you a DNA vaccine and we’re gonna have you eat a few pills called venetoclax. And I’m like, “Okay, that sounds great.” And then I went, “DNA vaccine?” Who wants to tackle what the heck a DNA vaccine is?

Dr. Koff:          

I can talk a little bit about the theory behind that. So, the great thing about the research community is that every institution that conducts clinical research, they may have different options in different clinical trials because no one institution can offer all of the same treatment therapies. And at large academic centers we may have a lot of clinical studies but we don’t have all of them.

And so, this would be an example of a very new kind of technology and the idea is that if you can essentially vaccinate a patient with, again harness the power of the immune system, and by vaccinate I mean that you would expose the patient through probably a shot to DNA that may link your CLL but may be similar to your CLL cells’ DNA. And the idea is that your immune system sees this DNA when you vaccinate and sees it as, “Wait, this is a foreign agent. I need to get rid of this.” And so, the idea is that it sees that target in the vaccine and then applies that same process to your CLL cells when it then recognizes that same DNA in the CLL cells.

So, it’s very similar—the idea behind it is very similar to the flu vaccine. You inject a patient with a little bit of flu or a little bit of a piece or protein or DNA from the flu, your immune system says, “Oh, that’s foreign; I need to attack it.” And then if and when you’re exposed to the flu, it attacks those same flu particles. Same idea here except the target that you’re offering to your immune system is linked to your CLL cells and so that your immune system then attacks those cells that have that same DNA pattern.

Jeff Folloder:  

Science fiction becoming science fact, hopefully slowly. And just to put a fine point on this type of research, one of the reasons why I’m now actually okay with being in watch and wait is every day that I’m in watch and wait is another day they have to work on this cool new stuff. So, every day I can wait something better is more likely to show up down the line. And I’m seeing heads bopping up and down here. Go ahead.

Dr. Rogers:     

I’ve been waiting to point this out, but we’ve talked about ibrutinib (Imbruvica) as an FDA-approved medication, but I know Dr. Cohen and myself—I don’t know which institutions he had been at. But the first time that I ever took care of someone taking that was when it was only in clinical trials and it was known by a drug name that was PCI and a bunch of letters. Venetoclax (Venclexta) used to be known as GDC-199. So, the reason we have these therapies now that we’re offering as very effective, extremely good treatments is because people took them when they were given to people for the first time or before they had regular drug names.

And on the converse I’ve seen a lot of people benefit from those treatments that couldn’t have gotten them outside of participating in a clinical trial. So, I just wanna make that point because they’re two very big drugs in CLL that have been developed in the last few years.

Jeff Folloder:  

If we could get the next slide up because you just mentioned the inhibitors. There are all kinds of new inhibitors coming on board now. What is going on with the new inhibitors?

Dr. Koff:          

I can take that. So, based on the successes that we’ve had with the BTK inhibitor and ibrutinib is the first generation of that, there’s a lot of excitement about improving that base frame of the BTK inhibition in different drugs that are a little bit different from Ibrutinib but still target BTK, but may do so more effectively in certain diseases and may do so without as many side effects and may be potentially easier to take for patients. And so, basically building on the success of ibrutinib as a BTK inhibitor, and so acalabrutinib (Calquence) is one of those inhibitors. We actually have a clinical trial on a third-generation BTK inhibitor at Emory, so people are continually trying to improve something that works.

In terms of looking at other pathways in CLL other than BTK, so we talked about those survival pathways and the anti-death pathways, what’s listed on this slide are other agents that are trying to target those specific pathways to make the CLL cells more likely to die. The Lin inhibitors in CLL have not been as effective as we would have liked. They did phase two trials meaning that they were looking for efficacy, looking how effective those were back in the early 2010s.

And the results were such that we didn’t have enough of a response signal that they wanted to move forward significantly to test it in more patients. The PI3 kinase inhibitors—So, idelalisib (Zydelig) is the first generation of that line of drugs and it is approved for CLL. Again, these are drugs that are targeting that same pathway that we’ve had success with in the first-generation drug. And trying to target that pathway more effectively and with less side effects, so that patients have better, deeper responses for longer, and that they also have less side effects. The other thing that I would say with all of these drugs is that we start looking at them in the single agent form.

So, we just give these clinical trials one agent to see how that agent works and what safety effects are associated with it. And if we see that a drug is working well and patients are able to tolerate it, one of the next steps that we use, and one of the pathways that we’re using for some of these drugs in clinical trials at Emory, is combining these drugs with other either approved drugs or sometimes with other drugs that are being tested in clinical trials to see if combination therapy actually improves your ability to control the CLL.

Jeff Folloder:  

Outstanding. There’s lots of really new impressive exciting stuff coming down the line. The rather large elephant in the room is the cost of this stuff. This is expensive stuff and not everybody’s insurance has the same type of coverages that some of the—I guess we call them Cadillac policies do. There are a couple of terms that I have heard bandied about, and I want to know what their role is in CLL treatments. So, Dr. Cohen I’m gonna ask you are there any generic medicines that can be used in CLL treatment? And what are biosimilar drugs? What does the term biosimilar mean and can patients maybe get a little economic relief from biosimilars?

Dr. Cohen:      

So, most of the currently available oral therapies that are FDA approved are still at the point where there is not a generic available for those treatments. I think that—we talked a little bit about it earlier; cost is definitely something that comes into play in my mind when selecting a treatment for a particular patient. Again, there can be all the science in the world to justify doing a particular therapy, but if it’s one that the patient may not be able to take on a daily basis because of the expense, then it’s unlikely to help them or at least to help them in the way that we would like. And so, this is definitely a big challenge.

And ironically the patients I find that may have the hardest time getting medication are the ones that actually do have insurance and prescription drug coverage because if you don’t have prescription drug coverage, many of the companies have ways to help with obtaining that medication. And also, I would say that even those patients that do have prescription drug coverage, they are copay assistance programs.

But patients that sometimes do have the means to pay their copay, even though it’s still a big pot of money, are often the ones that are in the toughest spot because maybe you’re in a financial position where you can afford a few hundred dollars a month, and so you may not qualify for the patient assistance. But if you’re going to be on a drug for five years—It’s one thing to do that for a couple months, but to do it for five years, that can really start to eat away at your retirement savings or what have you. So, it’s a challenge.

I would say, and I know that sometimes the pharmaceutical companies have the reputation of only going after money and only trying to earn money, and we could have a whole discussion about the industry. But I would say that at least on a personal level, I work with many folks at the companies that manufacture some of these oral therapies that really do try very hard to come up with ways to ensure that anybody that is appropriate for a particular therapy is able to get it. And so, many of them have funds set aside to assist patients. Now, again, that doesn’t necessarily help every single patient and, again, we could have a whole discussion about that, but… 

Jeff Folloder:  

…in a different Patient Power.

Dr. Cohen:      

Yeah, exactly. But I guess I would say that there are ways to help patients in the medication, and it’s important that you speak with your physician about what your out-of-pocket cost is and see whether or not there may be something that they can do in collaboration with the company. Just real briefly, I know you had asked about biosimilar. So, this is an area of interest. And so, what a biosimilar is is basically a drug that is almost identical to an FDA-approved drug and is felt to have identical activity.

And, in fact, in order to be approved it’s actually tested against the other sort of standard therapy to make sure that it has identical activity. And many of these tend to be a little bit more affordable, and so it’s an area of interest in trying to lower cost for patients. Right now probably the ones that are the most used are for some of the growth factors, like filgrastim (Neupogen) or Neupogen that you may have used if you received chemotherapy, and then rituximab (Rituxan) has some biosimilars targeting CD20 that are in development.

Jeff Folloder:  

Outstanding. We are coming up on the point of the event known as the Q&A, the question-and-answer session. So, I hope each of you has taken some time to scribble down some notes. We’re going to have folks in the audience with microphones. When you have a question, raise your hand; wait until the microphone comes to you. Speak loudly and clearly. Those of you who are online, again, that’s [email protected]

If you’ve got a question but don’t wanna get on the microphone, just hand it to one of our fabulous assistants and they will ask the question for you. Before we get to the first question in the room, I’ve got one that’s been queued up. This one comes from one of the Facebook CLL Support Group communities. Can I diet and exercise my way to health? Will it stave off CLL?

Dr. Cohen:      

So, it looks like you’re looking at me, so…

Jeff Folloder:  

…I’m looking at you first.

Dr. Cohen:      

I’ll take that one. So, this is an incredibly common question that I’m asked. And it most commonly comes up in a patient that has newly diagnosed CLL, that’s not on therapy and wanting to know what can they do to try to prevent the disease from progressing. And what I would say is that eating a healthy diet and being active are incredibly important things that you can do, but I would not rely on that to be the reason your disease progresses or doesn’t progress.

And what I like to remind people is that if your disease progresses to the point where you need treatment in nine months or nine years, if it happens to hit you a little bit earlier on the course, it’s not because you didn’t exercise, and it’s not because of something you did or it’s not because of something you ate. Okay, it’s just that some people have disease that progresses a little bit faster than others. The reason though that I think that having a healthy diet and exercise are important is number one I think it helps with fatigue symptoms. I think it helps you stay healthy in general.  

We talked before that patients are going to be—with CLL, even if they’re not on treatment, they’d be susceptible to more infections. And so, the more active you are the healthier you are, the better you are, the more likely you are to be able to stave off infection. And it also, in my mind, puts you in a position where when you do need treatment that you have sort of the whole plethora of therapies available to you because you’re more likely to be fit. So, that’s where I think it’s helpful.

But what I hate for patients to do is start forcing down particular foods that they hate or making themselves so crazy about a particular diet or exercise, and then if the disease still progresses, then they feel like they’ve done something wrong. And that is not the case.

Jeff Folloder:  

Just as a point of order, the patient power crew last night tried to convince me that Brussels sprouts were worthwhile. Not gonna happen. Not gonna happen.

Dr. Cohen:      

They probably just weren’t cooked right. Because if they’re cooked right…

Jeff Folloder:  

…there is no right way to cook Brussels sprouts. Not even bacon saves Brussels sprouts.

Dr. Koff:          

And just a side—sorry, just a side bar of that is patients, when they come in they often—they’re taking several different types of medications, whether it’s for their CLL or not. But there are a large lieu of supplements that are out there as well. Some are FDA-approved and some are not.

And so, we always encourage people that if you are taking them to include that when you go to your physician, your practitioner, to let them know what exactly you’re taking, even if you think it’s just a vitamin or a supplement. It could at some point interfere or interact with chemotherapy that could be given or future can be given. And some of them can also affect—some of them if you take them for too long or if there are unknown side effects, they can affect your heart, your kidneys, your liver. So, it’s important to tell your clinician what exactly you’re taking.

Jeff Folloder:  

Let’s stay along the lines of what people are doing with their bodies. Kerry, here’s a question that we got from the audience. Says there’s a lot of buzz around fasting and eating a ketogenic diet and the positive impact on cancer. What are your thoughts on fasting and keto for CLL?

Dr. Rogers:     

Yeah, so people always ask me, “Oh, I have cancer now. Does that mean that I can’t have any sugar?” And the answer to that is no. So, in CLL specifically I know of no scientific data that fasting or having a ketogenic diet is going to fix chronic lymphocytic leukemia. I know of no scientific evidence that that is helpful in any way for CLL specifically. And, yes, people should still eat sugar. It’s really painful to eat no sugar whatsoever. The other thing I wanted to say is when they say, “Oh, can you exercise and diet your way to health?” Yes, but other markers of health not fixing or reducing the CLL or treating the CLL.

So, there are plenty of ways that diet and exercise can improve your health but don’t improve just the cancer or just the CLL. So, that’s kinda the way I like people to think about it. So, there might be other reasons that someone wants to go on a ketogenic diet or go on a low-sugar diet. But I know of no proof in CLL that it’s an anti-cancer treatment.

Jeff Folloder:  

Jean, I have an interesting question that came in from online, and it’s something that we haven’t touched on today, but it is top of mind for a lot of people. Would you please tell us about Richter’s transformation, what it is, and what you can do about it, how to find out the latest treatment programs for it. What is Richter’s?

Dr. Koff:          

Sure. So, we’ve talked a lot about CLL which is a specific type of lymphoid malignancy that in a lot of patients tends to grow slowly and may be around for a long time without causing problems. And CLL is very similar in that type of clinical behavior and also in what types of treatments it responds to to a group of lymphomas that we call the indolent lymphomas, and indolent meaning that kind of tends to be slow-growing; there may be a watch-and-wait approach. The other big bifurcation in between groups of lymphomas; you have the indolent lymphomas, and then you have a group that’s known as the aggressive lymphomas.

And as you might imagine, those aggressive lymphomas, their natural history is usually that they grow quickly. They can cause problems very quickly. And you do not watch and wait with aggressive lymphomas. They need to be treated in a timely manner or they can often become life-threatening. And what Richter’s transformation describes is an event that happens in about 10 percent of all CLL cases over time, which is that for reasons that we don’t completely understand, those more indolent-behaving CLL cells transform into a more aggressive lymphoma that often resembles a type of lymphoma called diffuse large B-cell lymphoma. 

And at that point treating somebody whose underground or Richter’s transformation with kind of the non-aggressive chemotherapy agents that we often use in CLL will not be expected to control this new more aggressive component of lymphoma. Now, when I see a patient with CLL, at the back of my mind I always want to be thinking I’ve made sure that I don’t think this patient has a Richter’s transformation. And because it’s an aggressive lymphoma, it often has a very different kind of clinical presentation than your average CLL patient.  

So, the reasons that I might suspect that a patient has a Richter’s transformation might include that I’ve been following them for a long time, and all of the sudden they become very sick very quickly. So, they have fevers, chills, night sweats, those B symptoms that come on all of a sudden. Or I know that they have lymph nodes throughout their body that are scattered and maybe a bit larger than normal, but overall have not been growing very quickly. And then all of a sudden, one lymph node starts growing very, very quickly.

That might signal to me that that population of B cells that’s in that lymph node alone have undergone that transformation to that more aggressive lymphoma. Now that can happen in the absence of Richter’s transformation. Sometimes CLL patients just have an aggressive kind of uptick in their disease. And at that point we would think about changing or starting treatment. But I always rule out whether there’s an aggressive lymphoma there. And our typical treatment for Richter’s transformation—there’s no standard of care.

But in a fit patient with Richter’s transformation, I think most physicians across the United States who specialize in CLL would recommend an intensive chemotherapy regimen and consideration of a stem cell transplant for patients who have documented Richter’s.

Jeff Folloder:  

That’s a lot to digest. Do we have some questions here in the audience? Okay, let’s get a microphone up here. Here comes the first one.

Female Speaker:              

Thank you. Hi. I’m a 30-year—30 years I’ve been battling this CLL. And I’m at a crossroads right now a little bit because recently my doctor told me that clinically I’m doing great, Imbruvica for two-and-a-half years. And she mentioned to change my chemotherapy. And I’m a little nervous about that, haven’t hooked up with her after she said that a few weeks ago. And I was wondering if you have had intravenous chemotherapy in the past, which I have, I’ve had it all, splenectomy and all. And I’m wondering can I go back to chemotherapy intravenous or is it a myth saying I can’t do that?

Jeff Folloder:  

Great question.

Dr. Rogers:     

I can take that.

Jeff Folloder:  

Go for it.

Dr. Rogers:     

So, for people who are taking ibrutinib which is also known as Imbruvica, which we talked a lot about today, after taking that there’s kind of two ways that people stop taking it. So, it’s something you take indefinitely, and I like to say you take it until one of a few things happens. Either you take it until it stops working anymore, meaning the CLL comes back, they lymph nodes, the white count, those things while you’re still taking it, or it becomes intolerable or side effects develop. So, some people develop things like atrial fibrillation. Some people need to be on blood thinners which don’t combine well.

Some people have rashes or GI side effects that means that they have to stop it. And then there’s a small group of people where something changes with their health or their life where it doesn’t make sense to continue with it just because they have other problems that it’s no longer the best treatment. People that have been taking ibrutinib and where it has stopped working, where the CLL comes back while you’re taking it, the most effective therapy that we’ve found to date is venetoclax, the most effective approved therapy. And that’s kind of one particular category that I think of as Ibrutinib resistance, meaning it’s no longer controlling the CLL.

And that definitely needs to be handled by a CLL specialist because stopping the Ibrutinib suddenly can be dangerous. So, if it ever stops controlling your CLL, that’s an important reason to seek a very expert opinion. However, people that stopped taking it because they have side effects or it didn’t make sense in their life anymore, there’s actually very good evidence or reasonably good evidence that chemotherapies can work after it. That not just venetoclax but other targeted agents like idelalisib can work.

So, I like to think of it as if the Imbruvica stopped controlling the CLL well, that’s a very specific situation and really the best standard of care is venetoclax. Obviously, doing a clinical trial would be a good option. If the Ibrutinib or Imbruvica is still working but someone stopped taking it for other reasons, then you’ve still got kind of like the whole variety of treatments that you could still take that will probably still work. As it’s a newer drug, we don’t have as much experience with the after ibrutinib treatments just because we’ve only had it for so many years.

So, it would be a good time to sit down with the person that said that to you to say, “Why should I stop taking this? What is it that changed or that is interesting?” And also, I’ve had some people that just said like, “Hey, it’s been three years; I’m done with this.” And some of them have done well for years after stopping and it was just that they’re like, “I’m sick of taking this pill, my CLL’s great. I’m just gonna not do it even though the standard way is to give it.” Did you have a follow-up for that one?

Female Speaker:         

Yes, please. So, what I’m worried about is because I’m doing so well and I’m feeling great, she basically told me that it’s obviously in my marrow. So, it’s like a Band-Aid. Is it a Band-Aid? I’m feeling great; my glands are down. I feel good; but what about the marrow if it’s not doing anything in there? 

Dr. Rogers:     

Well, CLL actually it’s always in the bone marrow and the ibrutinib generally doesn’t eliminate all the leukemia to below the point of detection, like that MRD status we were talking about. So, most people who are living well and doing great on ibrutinib still have some leukemia cells and that’s okay. When I’ve seen it not work very well in the bone marrow sometimes, actually I’ve diagnosed a couple people with a second problem in the bone marrow, not just CLL.

So, it sounds like a good chance to sit down with your doctor and find out what the specific concern is because it sounds like whoever it was probably tried to explain it but it’s so hard to absorb all that. So, it’s really a very kind of wide number of reasons people might stop taking it. So, I would definitely have a sit down about that one. Hopefully, some of that was helpful to talk with him or her about it. 

Jeff Folloder:  

I know we have a bunch of questions here in the audience, so who’s next. We’ve got hands going up everywhere. Got a microphone coming. And again, before you start talking, try to keep these questions general so that everybody can get something from this. We’re not really in a position to diagnose or treat very specific instances and questions of that nature. So, go for it.

Male Speaker: 

Okay. I’m currently being treated for renal cell carcinoma. And my hematologist said, because I’m being treated for the renal cell, I can’t be treated for the CLL. Is there something coming up where I could be treated for both at the same time?

Dr. Koff:          

So, often we have patients who may have two cancers at the same time. And what happens with that is that you want to make sure that you’re treating the cancer that’s most likely going to cause problems. And one of the luxuries that we have with CLL is that often it doesn’t need to be treated. A lot of you have been on or are on watch-and-wait. And, again, if the CLL is not causing problems right now, a lot of times we can defer treating the CLL until you either meet indications for treatment, which would be my first consideration.

But also there may be something else going on like another malignancy or maybe a surgery or something like that that takes precedence because that health issue is more important at this time, and CLL often gives us the luxury of waiting to treat until that other more pressing urgent health issue is addressed. And I have lots of patients with CLL who I co-manage with my solid-tumor colleagues where I evaluate the patient. I see whether their CLL needs to be treated right now. And if there’s no pressing indication, then I tell my colleague, “You definitely need to take care of this solid tumor first, and then after that’s taken care of, we’ll re-evaluate and see if the CLL needs to be treated.”

Jeff Folloder:  

Makes sense. We had some questions back here.

Female Speaker:         

Hi. I just wanted to know if any of you all can speak to the heritability of CLL and potential implications for future prevention. Both of my parents have CLL and one of my grandparents, so I was just kind of curious if it’s…

Jeff Folloder:  

…it’s a great question. Is CLL hereditary? 

Dr. Cohen:      

So, I guess it’s my turn.

Jeff Folloder:  

It’s your turn.

Dr. Cohen:      

That’s a challenging question that comes up frequently in my clinic. So, what I typically will tell somebody is that, in general, this is not something that is inherited across generations. So, if I see a new patient, and not always but frequently they may be middle-aged or older, and maybe they have grown kids, or maybe their kids are getting ready to have children. There’s not necessarily any screening that we recommend for those children other than making sure that they’re following up with their physician regularly like they normally would. We also don’t have any…

Male Speaker: 

We hear everything you’re saying so...

Jeff Folloder:  

Here’s one right here.

Female Speaker:         

Here you go. 

Jeff Folloder:  

And let’s get the audience mike over here; there’s a bunch of questions.

Dr. Cohen:      

So, I was—to finish up. So, we also don’t have a specific gene that the same way we do for breast cancer or for some other cancers where we know that if you have this, we can specifically test and predict your risk of developing breast cancer, for example, down the road. Now, having said that, we occasionally do have families like yours where there are multiple members of the family that have CLL or that have lymphoid malignancies and there is a lot of—that’s an area of active research. I actually just had a patient just the other day with that type of a what’s going on in that particular family and why—is there really a genetic predisposition? And our answer is no.

And so, I don’t counsel people for any specific screening. But in specific situations where there are multiple family members, we do sometimes refer those patients to genetic counseling. And that’s an area where we’re hoping to learn a little bit more.

Jeff Folloder:    

Okay. Hang on. We’re gonna try to get to everyone, I promise.

Female Speaker:

Good morning.

Jeff Folloder:  

Good morning.

Female Speaker:         

I am here in support of my mother who will be receiving Rituxan soon. And in terms of negative reactions to it, specifically shaking or anything like that, do you have suggestions on how she could possibly, or anyone else could possibly reduce their chances of having any type of negative reaction?

Jeff Folloder:  

I can give you a little bit of feedback from the patient perspective, although I didn’t have Rituxan in my clinical trial; I had a next generation of a similar drug, a CD20 monoclonal antibody. And I was told before my first administration flat out I was going to have reactions to it because it’s something that my body did not have any experience with. It was a new something being put in my body. And as preparation for that, with the IV drips and all that, there were steroids and diphenhydramine (Benadryl) and all kinds of fun stuff. And when I had those reactions, I had my wife right there next to me.

So, even when I didn’t recognize there was a reaction going on, like red spots all over my body, wow I have spots, yeah, that’s a reaction. Now I have circles; now I’ve puffed up. As long as you can clearly communicate to the staff, the medical staff something’s going on here, and they will be checking on you. As soon as a reaction happens, they are right there to do something about it. The goal is to not make you long-term miserable. The goal is to recognize that you’re having a reaction, take care of the reaction, and then start the infusion again. Now, the first infusion took a long time, because I had a lot of reactions.  

But the second infusion did not take a long time, nor the third, nor the fourth, nor the fifth. As soon as my body recognized it, we were good. So, I would tell you from a patient perspective there’s probably gonna be some reactions. But make sure you’re clearly communicating and the reactions will be taken care of. How did I do? 

Dr. Koff:               

Unfortunately, there’s not really anything that you can do. It’s kind of like an allergic reaction; it’s not really something that you can do to prevent it. But, like you said, it’s really just you’re being monitored very closely when that’s being infused. And so, people are trained to recognize different types of reaction.

Male Speaker: 

…reaction puts you in a corkscrew. I had it twice; they just cut it off. So, you just cut it off; you don’t…

Dr. Koff:               

…correct, they’re…

Male Speaker: 

…I got rashes, I couldn’t breathe. And so, my doctor said, “That’s it.”

Dr. Koff:          

Yeah, and then if you’re intolerant to a medication, then obviously that would preclude you from getting any more treatment. But, for the most part, there are reactions that can be—being premedicated with certain medications will help prevent those reactions from happening again.

Jeff Folloder:    

I know you wanna say something. Go for it. 

Dr. Cohen:          

I was just going to say I would highlight that that is not the norm for those of you that may not have received rituximab, but we do occasionally have patients that get really sick. One of the other things that I’ll take into consideration at that point before I decide to discontinue it entirely—obviously, it depends on the severity, but even somebody that may end up in the emergency department or being admitted, if I really feel that the rituximab is a critical part of their treatment—We have, for example, admitted people to the intensive care unit and administered it very slowly over a period of 12 hours as an inpatient in order to make sure that we could safely administer the drug.

And so, that may or may not be feasible every single time, but these are all things that you can discuss with your physician because in most cases, even with the most severe reactions, we’re able, not all but in most, we’re able to, if we really feel like it’s critical, get patients through the treatment.

Jeff Folloder:    

Yes, ma’am.

Deborah:        

Yes, my name is Deborah.

Jeff Folloder:  

Hi.

Deborah:        

Hi. I wanted to ask Dr. Koff a little more about her research with autoimmunes and lymphoma. Is it any particular one like diabetes, lupus, any connection?

Dr. Koff:          

Yeah, so a lot of my research centers on the fact that we’ve seen a link between certain autoimmune diseases and people who have those autoimmune diseases are at increased risk for getting certain types of lymphomas. And so, I’m trying to explore what the connection is because right now we don’t really understand why they might be at increased risk. And so, my research focuses on mainly lupus, rheumatoid arthritis, and Sjogren’s syndrome. But I think there’s a lot—this is kind of a new field where we’re really exploring the biology, the biological link, now that we know that there’s an epidemiologic link.

Jeff Folloder:  

I’d like to point out to the online audience, don’t despair if we don’t get to your questions. We do a lot of stuff online, and I wanna let you know that coming up on Thursday, September 27th, we are going to have a dedicated ask the expert session. You can visit patientpower.I-N-F-O/events to sign up. And you’re probably gonna be getting an email about it as well. I know we have a couple of more questions. This gentleman up front—can we get a microphone to him? Hold up. You’ll be next. I promise.

Male Speaker: 

I’m good? Okay.

Jeff Folloder:  

You’re live.

Male Speaker:  

Again, thank you all for being here today. This is great. I’m back to the diet thing. And so, Dr. Cohen you said genetics not so much really involved. We all ask ourselves are we just unlucky? A lot of people say that just as a stat. And yet science doesn’t say there’s luck or unluckiness. It’s science behind it. There’s an imbalance to the body. Something went wrong. And so, I always come back to what’s either going in my body or what I’m coming in contact with have to be involved. So, to the diet question, Dr. Rogers, you did say, yeah, a healthy diet would be good for you. But ultimately the takeaway here is that what I’m getting is ah, diet has nothing to do with it. Keep eating the lousy diet that you’re eating.

And there are—again, I can’t cite to the specifics right now but the studies that go between the western world and where you get indigenous people where cancer doesn’t exist, you gotta do the—But what is your takeaway to where cancer doesn’t exist in certain parts of the world?

Dr. Koff:          

I can take that one. So, I think right now our understanding of why some people get certain diseases and why others don’t is really in its infant stages. We have a lot of new technology in the last 20, 30, 50 years where we’re able to look at genetics. We’re able to look at very detailed diet plans, family history, other medical problems. But there is still a very, very complex interplay of, like you mentioned, diet, genetics, what you’re born with, and what comes out later. Why do these cells deign the mutations that they do and become malignant, go rogue and become a cancer? And right now we still don’t know. 

A lot of research outside and within clinical trials are looking at these questions of what is the complex interplay of factors you’re born with, factors in your environment that lead you to get CLL while somebody else may not. But I think right now we still don’t have a pinpointed answer, and I don’t think it’s gonna be one single factor. It’s going to be multiple, multiple things that are all feeding into the ultimate development of cancer cells from normal cells.

Dr. Rogers:        

And so, for the record, I didn’t tell everyone to eat terribly. A lot of people with CLL can expect to die of something else. And heart disease is still a very bad problem.  

Male Speaker:  

Question. So, I’m in the watch and worry one week now. So, I read about the clinical trials where they are taking stage zero CLL TP53 deletion and starting to giving them the inhibitors to see if they can kill the CLL cells early on knowing that this patient can be high-risk and are there any results? Is that true first? Are there any results from these trials? And should we be considering these if you wanna go through the side effects?

Dr. Rogers:     

I can talk about that because at Ohio State we actually have had two very recent what we call early intervention studies. So, we’ve all been very clear the standard of care is to wait until you have a reason to do treatment. And we know for sure from pretty large-scale research studies that giving those chemotherapies or IV chemotherapy treatments sooner does not help people live longer or better. So, for chemo chemotherapy or the cytotoxic drugs, giving them sooner we know for sure doesn’t help. Though what you’re bringing up is a very good point.

We’ve developed new medicines for CLL; ibrutinib which we’ve talked about, and lenalidomide which we’ve talked about among others. So, we haven’t yet looked at whether giving these new drugs is going to be helpful to give them sooner. So, there are reasons not to do it, like exposure to side effects. But there might be some scientific rationale to do it. Both of the drugs I mentioned, lenalidomide which is Revlimid and ibrutinib modulate the immune system. So, that might be helpful for some people. 

And then researchers have showed that while we see CLL cells in the blood as one type of cells, as CLL leukemia cells, it’s actually not just one type of CLL cells. People get different what we call clones or sub-populations of these that, while they look the same, when you delve into their biology they really aren’t. And we know that the more IV chemotherapies people take, the more different types of these CLL cells you get, we think that that’s not a good thing.  

So, there’s some idea that if you give a drug like lenalidomide or Ibrutinib earlier, it’ll be more effective because your CLL has not been exposed to these other treatments, and it hasn’t undergone changes, hasn’t become more clonally complex, which a big word, and so it might work better. So, that’s kind of the reason, and we would not suggest this at all for very low-risk CLL folks because if you could expect to not need treatment for five, seven, or ten years, that’s not a good time to try something sooner. Plus, I think I’ll be dead before that study’s finished enough to know the answer, right, retired, at least.

For people with high risk, like deletion 17p, those set of CLL patients can expect to need treatment sooner. So, that’s a good group where you wanna look at hey, does one of these new drugs really help people live better or longer or treat the CLL better? So, that’s kind of the group of people where this is a research question.

We have a study of lenalidomide as an early intervention. It’s actually also mainly studying responses to vaccines. So, both pneumococcal, the pneumonia shot and influenza vaccines—so it looks at does giving lenalidomide change vaccine responses? But it is giving treatment before the usual reasons to treat. So, that study is completed enrolling, meaning more people aren’t joining the study, but is still in follow-up. So, people are either still taking the lenalidomide or being followed and watch or wait after stopping it for some reason, and has not been formally reassessed for several years.

The last time we’ve looked at everyone in it, it was looking like it was going to delay the CLL requiring treatment or progressing or coming back in some way, but also that’s kind of the main question about vaccines so it’s a little hard to know and certainly not sufficient to say that this is something you should start offering people, right? So, this is a small research study; it’s not something I would recommend as a standard or outside of a research study.

And we also have one that just recently completed, well it completed enrolling, and that was with Ibrutinib. And instead of taking it indefinitely, it was a two-year treatment because you don’t wanna start early and then keep taking it for years and years and years. That doesn’t sound like something most people wanna do. That doesn’t really thrill us either. One way to potentially limit costs of some of these drugs is to give them in combination for shorter.

And I’m very interested, as I’m sure everyone else is, in figuring out who should stop taking drugs like Ibrutinib and how to discontinue it in certain people, not for everyone, but for some. So, we actually just finished a study also looking at vaccine responses, but there were people who were treated early with two years of Ibrutinib, and I don’t have results of that study because it hasn’t been going on long enough to know. So, to answer your question in people with high-risk findings, we had two studies in our institution that were enrolling both lenalidomide and ibrutinib.

I expect that we’ll know more about what happened to those people. But in order to make it a standard, I expect we’d have to do a larger study, pre-select people to either treatment early or observation watch and wait and kind of see what happens. So, it’s an active research question with non-chemotherapy agents. I’m sorry, that was very long.

Jeff Folloder:  

Excellent. I think we have time for one more question. We’ve got a microphone right there.

Female Speaker:         

Hi. I was just diagnosed with CLL this year. So, a couple things stood out to me that I wanted to ask. You were talking about a CLL specialist. That’s kind of new to me, and I’ve kind of heard it when I’ve been researching this. But how do I find one? And the other thing was you were talking about the flu vaccine, and what if you are unable to get the flu vaccine? I got that for many years because I have other health challenges. But I have other sensitivities where I am unable to get the flu shot. I am focusing right now on my immune system, and I am doing natural things to boost my immune system. I make my own elderberry syrup, just doing things that my doctor has suggested, and I’m doing well.

So, I just wanted to kind of—what other options beside the flu shot?

Jeff Folloder:  

Two great questions.

Dr. Koff:          

I can take the first question. So, I was talking with some of my patients who are here who were referred to a CLL specialist from their hematologist. And I’ve talked to other patients who asked the same thing. How do I find a CLL specialist? So, one of the first places to ask is your doctor who is treating you, “Do you know anybody who specializes in CLL who I can go to?” That would be my first step because they may already have relationships with someone like one of us, and they already know and trust. If they are not familiar with somebody who is close by to you, or they’re not sure who is CLL, the first thing I would do is look for an academic center that has a cancer center associated with it.

And so, in the southeast the two that we think about kind of in our area, depending on what part of the state you’re from and where you’re coming from, would be places like UAB, Emory, any of these large academic centers that also have a large cancer center. And if you or your doctor calls to make a referral to that center, their team can usually refer you to say, “Oh, what’s your diagnosis? CLL? Well, Drs. Koff, Cohen, and somebody else see CLL; we’ll book you with the first available appointment.”  

So, it’s not that you have to necessarily find the CLL specialist who’s closest to you yourself, but looking at those academic centers first and those are places, again, that have a big cancer center that may do clinical trials, that often have a stem cell transplant center associated with it as well. That’s gonna be a good first look to find those people.

Jeff Folloder:  

And just to add on to that, a lot of the online resources and support groups, an example would be ACOR, A-C-O-R.org. They publish every quarter an updated list of CLL specialists, not only in the United States, but all around the world. So, a little bit of research is likely to give you a lot of information. But the first place, I agree, the first place to go is your doctor for a referral. I need to see a CLL specialist.

Dr. Cohen:      

And I would just add to that, that most of the time when we see a patient that comes from one of our colleagues, unless there is a very specific treatment that they can only get at Emory, most of the time I will see the patient, we’ll have our pathologist review their tissue to make sure that we’re all in agreement with the disease and with the prognostic markers. I’ll talk with the patient at length about some potential options and recommendations. And then most of the time they’ll end up going back to their doctor. And so, especially if you’re from out of town, we try very hard to limit visits to actually our center to those that are absolutely necessary.

And so, sometimes people don’t like the idea of having to drive all the way to Atlanta. But usually I may see somebody one time and say, “This is what I think would be a good option for you. Come back if you need me.” And then they go back to their referring doctor. And so, we have a very good relationship with those physicians and they know how to contact us when something comes up. And just real briefly, your second question about flu shot, and this was something that I had meant to mention earlier. So, for the caregivers and family members in the audience, one of the best things that you can do to help your loved one, who is the patient, is to you yourself get vaccinated.

And that’s what I would recommend in your case is the people that are going to—that live with you or that spend a good amount of their time with you that are able to get the vaccine, that they try to get the vaccine because if it doesn’t come into your home, then it decreases the likelihood that you will get it yourself. Now, it’s obviously not 100 percent, but that is something that I recommend for all of my family members that come with their loved ones is that in addition to the patient getting vaccinated, if able, that they themselves get vaccinated. 

Jeff Folloder:  

Great advice. We have time for one more question over here.

Male Speaker: 

Yes, I was reading Dr. Google…

Dr. Cohen:      

Oh, Dr. Google.

Male Speaker: 

and he said that CLL patients were 600 times more likely to get skin cancer and especially melanoma. And I was wondering do we need to be seeing a dermatologist on a regular basis or anything?

Jeff Folloder:  

Yes.

Dr. Rogers:        

Yes.

Jeff Folloder:  

And I do it every year.

Dr. Rogers:     

Yes, actually, you hear the statistic on CLL patients are more likely to get skin cancer, and then I find out every time I go to clinic there’s one or two people that got a skin cancer removed. I’m like, “Boy, I really believe this is true, that this is a higher risk for skin cancer.” Fortunately, while it does increase the risk actually of getting any other type of cancer probably because of the effects on the immune system, skin cancers seem to be particularly common. And a lot of them actually aren’t the melanomas but are squamous cell carcinoma or basal cell carcinoma.

And those are the ones which you can just remove, and as long as you get it removed, you can just move on and it doesn’t cause more problems. It’s far more common to have those. And actually if you don’t get them removed, they can eventually cause problems or become disfiguring if they increase in size. So, I actually do recommend everyone I see with CLL to go see a dermatologist and get an annual skin exam. And then, of course, as they develop relationships with dermatologists after—maybe if they find a skin cancer, then usually they have a follow-up schedule. Even the younger folks I see with CLL who are maybe in their 30s or 40s, and they’re like, “I don’t need to get my skin checked.”

Jeff Folloder:  

Oh, yes, you do. 

Dr. Rogers:     

And I’ll just put an extra pitch in there too for other forms of cancer screening. So, there are not special crazy recommendations for cancer screening, but I know a lot of people that really don’t enjoy getting colonoscopies. You have to drink that stuff; it just doesn’t sound like the fun way to spend a Tuesday. So, if anyone is on the fence about getting their screening colonoscopy at 50, if you have CLL, that’s an even better reason to just have a sit down with your primary care provider, talk over your options for colon cancer screening, get it done.

And I’m happy to send people for them, but usually I tell them to hash it out with their primary care doctor because that’s a whole conversation. But it’s not just skin cancer screening, it’s all of the usual age-appropriate cancer screenings.

Dr. Koff:          

And going along with that, so not just seeing your dermatologist, but because you are at increased risk for any type of skin cancer, if you weren’t doing it already, you need to put on sunscreen any… 

Jeff Folloder:  

…wear a hat.

Dr. Koff:          

Wear a hat any time you go outside.

Jeff Folloder:  

A big thank you to our sponsors AbbVie, Pharmacyclics and TG Therapeutics. I’d like to let you guys know that this program was produced by Patient Power in collaboration with the Emory Winship Cancer Institute. A big thank you to our promotional partners, CanCare, CLL Canada, ACOR.org, and the CLL social media community. I’d like to thank each of you for taking the time out to come listen to what we had to say. You’re taking an active role in your own care. You’re going to have a better outcome. I am wishing each and every one of you the very best of health. Live well.

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.

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