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Answers About the Coronavirus and Personalized CLL Care

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Published on March 11, 2020

Key Takeaways

  • Coronavirus is transferred through surfaces and person-to-person contact. It is advised to wash hands and surfaces and limit touching your face, particularly your eyes, nose and mouth. Avoid high-risk areas and unnecessary travel.
  • Pay attention to skin changes and don’t dismiss them. CLL patients are at higher risk for skin cancer, so use sunscreen, hats and sun-protecting clothes.
  • The overwhelming majority of CLL cases are spontaneous. and there is minimal hereditary risk of developing CLL. There are some patterns in families, but there are currently no commercially available tests.

This Ask the Expert program features Dr. Jeff Sharman, from the Willamette Valley Cancer Institute and Research Center, answering questions from CLL patients and care partners on treatment, testing, side effect management strategies and more. 

Dr. Sharman leads by addressing concerns regarding the global coronavirus (COVID-19) outbreak and explains how cancer patients are particularly impacted by the virus. Dr. Sharman also gives specific safety precautions for people living with CLL, who are often immunocompromised.

Watch to hear an expert perspective on questions like: "What can I do to manage my risk for skin cancer? How do I decide which treatment is right for me? Why have I attained MRD negativity but still have significantly compromised immunoglobulins? Is there a hereditary risk with CLL?"

This program is sponsored by AbbVie, Inc., Genentech, Inc. and Adaptive Biotechnologies. These organizations have no editorial control. It is produced by Patient Power. Patient Power is solely responsible for program content. 

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Transcript | Answers About the Coronavirus and Personalized 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.

Andrew Schorr:

Welcome to this Patient Power Live Ask the Expert program. I'm Andrew Schorr. Thank you so much for joining us. I'm down near San Diego, and once again, we have with us a noted expert in CLL, Dr. Jeff Sharman. He joins us from the Willamette Valley Cancer Institute and Research Center. Dr. Sharman, welcome back to Patient Power.

Dr. Sharman:

Thank you so much. Glad to be here.

Andrew Schorr:

Thank you for being with us. Also, folks, we are going to buzz through as many questions as we can. So many of you have sent them. Remember, discuss your personal situation with your own doctor. Dr. Sharman cannot practice CLL medicine for you personally over the Internet. We're going to give more general answers. Jeff, I'm going to start with the obvious question right now, and that is those of us living with CLL know our immune system is nicked, and to varying degrees we worry about all kinds of infections. Now we are in this age of coronavirus, so what are you telling people for us who see ourselves as at higher risk?

Dr. Sharman:

Thank you, Andrew. I know a lot of people have a lot of concerns about this. It's certainly the talk of the news stations and so forth. Unfortunately, from the scientific perspective, I think one of the challenges is the lack of information. Three weeks ago, we were talking about a virus in a part of China we'd probably never heard of and a cruise ship that seemed to be infected, and now we're seeing it in our communities, and science just doesn't move that fast for us to really have a ton of the type of answers. One of the things we struggle with is what's the numerator, what's the denominator? How many cases aren't coming to medical attention, because you hear about is the mortality rate 1 percent or is it 3 percent? Of course, if you don't know what number you're dividing by, it's hard to come to that answer.

Some good news in the last 24 hours, a lot of the West Coast people have changed to what we call droplet protection as opposed to airborne protection. Droplet means it's on contaminated surfaces, so you're hand-washing, religious hand-washing frequently, not touching your face, these sorts of things really can make an important difference. Avoiding those areas at high risk of transmission. Again, coming back to hand-washing and surface cleaning and so forth. That's what I'm telling my CLL patients. This has been a very dynamic topic that will likely continue to change over the next weeks.

Andrew Schorr:

Okay. Some people have planned travel. My wife and I had planned a trip to Vietnam. My doctor said don't go. I have friends who planned cruises and we've been hearing all these stories from cruise ships. What do you tell your patients about travel either to higher risk areas or have been higher risk areas, or even this sort of confined area like a cruise ship?

Dr. Sharman:

Yesterday there was a paper published in one of the Lancet journals looking at the Chinese experience and how coronavirus particularly impacts patients with cancer. In their 3,000 cases that they were able to report on, and I'm using rough numbers because I don't remember the exact specifics, but it's about 1 percent of their patients had cancer, and those patients represented with cancer had higher rates of negative outcomes, meaning cancer patients did less well with the virus than non-cancer patients. Those individuals with recent chemotherapy had done less well. It's important to note this is a retrospective, observational study, and there's therefore a lot of confounding variables, such as what impact does age have? Well, the cancer patients tended to be older. Smoking status. A lot of people smoke in China, and maybe smoking was related to cancer. Again, there's a little bit of a lack of data.

Another thing that happened yesterday was that MD Anderson and Memorial Sloan Kettering issued policies for their faculty that no domestic or international work-related travel would be permitted. I think there's a genuine concern within the cancer community that travel does likely expose you to some of those more risky environments. Again, three weeks ago we were talking about a virus in a part of China we hadn't heard of, and now we're seeing it in our communities. This is moving quickly, and it's hard for good medical recommendations to keep up with that velocity.

Andrew Schorr:

Okay. We had gotten some questions people asked about with some of the newer medicines, receiving MRD, either minimal residual disease or measurable residual disease negativity, so you can't find the CLL, but their other factors in looking at their immunoglobulins and related to their immune system were not as good. Could you just explain this balance, because I know that I'm at very low MRD status, maybe not negative but close, but yet my immunoglobulins are not so hot. Does that mean I'm immunocompromised?

Dr. Sharman:

Right. Immunoglobulins are antibodies. When your doctor's measuring your antibody levels, that's one aspect of the immune system that we can measure. The immune system is this complex web of a lot of different moving pieces. To try to distill it just simply down to one measurement doesn't really capture what's going on. We know that CLL itself is an immunosuppressant cancer, meaning the presence of CLL lowers the function of the immune system. It is a cancer of the immune system, so that part probably shouldn't be too surprising. There are a lot of different pieces to your answer though. Fludarabine (Fludara), which is a medication that had been used extensively for many, many years, renders T cell function, not B-cell function but T-cell function compromised potentially forever after that point. It has some lingering effects. Venetoclax (Venclexta) may have some T-cell dysfunction to it. Ibrutinib (Imbruvica) or BTK inhibitors, some more so than others. Any of those therapy-related immunologic dysfunction, we're trying to kill off a cancer of the immune system, so we shouldn't be terribly surprised that there might be bystander effects with other parts of the immune system.

Then I think that we need to think about CLL more holistically. It's not only the cancer cells, but how those cancer cells have impacted their microenvironment. The CLL cells change the lymph node environment around them, and simply getting rid of the CLL cells may not restore that lymph node or bone marrow or spleen environment. There's probably some lingering effect even in the absence of the technical CLL cells.

Andrew Schorr:

Okay. That was a good answer. Thank you so much for that. Okay, we've got a bunch here. Let's buzz through what we can. For instance, you mentioned some of the drugs. We have these BTK inhibitors and we have a BCL inhibitor. These are approved. We've got BTK if I've got it right, we've got ibrutinib and acalabrutinib, or Imbruvica and Calquence. Then we have the BCL inhibitor, which would be venetoclax, or trade name Venclexta.

Dr. Sharman:

Yes.

Andrew Schorr:

Related to managing side effects, first of all. Some people switch from one to the other. How do you decide who starts on which one? People are wondering. Then also dealing with side effects that could come up.

Dr. Sharman:

Right. Ibrutinib was the first BTK inhibitor to market. BTK stands for Bruton's tyrosine kinase. It's an enzyme that transmits signals from the B-cell receptors. B cells have a B-cell receptor and that helps you make antibodies. I like to think of it as an electrical current that flows inside the cell through BTK, and BTK inhibitors turn that off. As a result, all the downstream actions. Ibrutinib was the first one approved, and by all means has the largest body of evidence to support it. We actually were involved in Eugene, we treated the first CLL patient in the world with it here in Eugene. That was over 10 years ago. There have been countless publications on ibrutinib. It's the standard bearer in a lot of ways. This last ASH, American Society of Hematology in December in Orlando, I got to present the pivotal data for acalabrutinib, called Calquence. That became the second BTK inhibitor approved in CLL. I would even say that there's a third BTK inhibitor available. It's not approved in CLL, it's approved in mantle cell lymphoma called zanubrutinib (Brukinsa). Each of these have some advantages. With ibrutinib you have the long term data on exposure. Calquence, it feels to me like there's probably a lower rate of side effects with Calquence. Zanubrutinib, slightly different profile than ibrutinib.

How do I look at it? I want to know if somebody's on a proton pump inhibitor. That may disproportionately affect Calquence. If somebody's got cardiac disease, known atrial fibrillation or hypertension, that may be more problematic with ibrutinib. Mouth sores, I say mouth sores only because I know some of the questions that are coming up. I see that a little bit more with ibrutinib than Calquence. Sometimes you actually may switch back and forth within a single patient, depending upon if they have specific side effects you're trying to monitor for.

Andrew Schorr:

All right. Now let's get to the other class, the BCL inhibitor, venetoclax. Where does that come in, and combined with monoclonal antibodies like rituximab (Rituxan) or obinutuzumab (Gazyva)?

Dr. Sharman:

Right. Venetoclax was being developed approximately in parallel with ibrutinib. I mean it wasn't that far behind. It's frontal development got sidetracked by what we call tumor lysis syndrome. Tumor lysis syndrome became a problem that we had to manage and really slowed down the development of venetoclax. From a patient's perspective, it's one of the newer approved drugs. In point of fact, it was really being developed almost alongside. Venetoclax is a very different class of medication, it works differently, patients have a different experience on it. We, over the last 18 months, 24 months or so, we've obtained FDA approval to use venetoclax either in combination with rituximab in the relapsed/refractory setting, or in combination with obinutuzumab for previously untreated patients. Whether it works better with rituximab or obinutuzumab is really more an artifact of how it was developed rather than real strong scientific rationale for one over the other. Choosing between the two kinds has more to do with patient strategies and maybe some of their molecular profiles and so forth. It's become a little bit of a challenging discussion when you now have a wealth of opportunities for patients, how they want to go ahead and pick a therapy. It's not a totally straightforward discussion.

Andrew Schorr:

Right. Just one question about that, because people wonder. People have heard that with this latter approach, venetoclax with a monoclonal antibody, you may get to an MRD status, and at some point you and your doctor can decide to stop therapy, just like we were with FCR. If you can, do we know how long it can stop? Is it forever, short time, and can you go back should you need it?

Dr. Sharman:

Right. MRD is a scientifically interesting point. We want it to help inform some of our decision-making, but at least in terms of how these medications are approved, for patients who are previously untreated, it's approved to be given for one year in combination with obinutuzumab, irrespective of their MRD status. In the relapsed/refractory setting, it's approved for two years in combination with rituximab for six months. You're right on with your question, which is, can we use minimal residual disease as an information point to decide how long to treat? The field wants to know that too. I don't want to get out ahead of the science right now on this, which is trying to understand whether or not MRD can help influence treatment duration decisions. We're not there yet.

I think what I would say is that the deeper the response, the more likely it is to last longer, which seems relatively obvious. You get rid of more CLL cells. Those patients with higher MRD levels are more likely to have an earlier relapse. What it appears, at least from the limited data we have so far, is if you're MRD positive after two years, it looks like the CLL at that point is probably already on the way up rather than arguing for sustained exposure, it looks like at that point that the CLL may already be coming back in at very small levels. More to come on that, and even more so as we move into some of the combination studies that I'm sure you want to talk about. As of now, MRD doesn't tell us when to stop and when to keep going.

Andrew Schorr:

Okay. If you and your doctor agree to stop, or you want to stop, can you go back should you need it?

Dr. Sharman:

The data on that isn't really available either. I hate to be a broken record on that, but here's what we do know. There have only been a small handful of cases reported, really primarily in abstract form, about can venetoclax work a second time around? You may notice that we're talking primarily about venetoclax when we're talking about minimal residual disease. MRD for the most part, is not a discussion point when we're talking about BTK inhibitors, ibrutinib and zanubrutinib. The drugs work very differently and obtaining MRD really isn't even the goal with the BTK inhibitors. It's more an issue as it pertains to venetoclax. If you get MRD negative, can you retreat with venetoclax? I guess I would say in my clinical judgment, the longer a response lasts to venetoclax, the more willing I am to try it again if a patient experiences relapse. Look, if someone gets five, six years out of a course of venetoclax, and they have limited problems with it, by all means, retreatment may be a very reasonable approach. As of yet, we don't have good metrics for how well it works the second time around.

Andrew Schorr:

Okay. You alluded to something that I know people are curious about, and some of our patients are in trials just like this. Can you combine these modalities for a bigger bang just like we did years ago with FCR to try to hit the cancer cell in different ways?

Dr. Sharman:

Yeah, I think you've highlighted what the next two to seven years of CLL research is going to look like. For a variety of reasons, it's difficult to do clinical trials with drugs from different companies, particularly when they're not FDA-approved. Now that these drugs are approved, it becomes considerably easier to start mixing and matching. What we saw in these first generation of studies was, can BTK beat chemotherapy? Can venetoclax beat chemotherapy? The answer is yes. Those are being filled out in all their detail. Then really the next question is singlet therapy, doublet therapy or even triplet therapy appropriate? When I say things like doublet, triplet, singlet tends to be a BTK inhibitor, doublet, we don't know really know much a CD20 antibody adds to a BTK inhibitor.

Andrew Schorr:

That's Rituxan or obinutuzumab, one of those. Yeah.

Dr. Sharman:

Yeah. Thank you. The initial study said Rituxan doesn't add much. Now we have something that obinutuzumab can help in certain contexts. What about doublet with a BTK and a Bcl-2 inhibitor? That's been popularized. A couple of studies have looked at that all oral, very compelling, provocative data. People ask what does CD20, obinutuzumab, rituximab, add to venetoclax? Those sort of doublets. Then the triplet approach would be a CD20, venetoclax, and a BTK inhibitor. Literally all those studies are just now taking shape. I think we'll be seeing results from that. The first combination that I expect approval for would be based upon what we call the GLOW study. It's yet another study comparing obinutuzumab-chlorambucil (Gazyva-Leukeran) to an experimental arm. The experimental arm in this is abbreviated as venetoclax. It's hard for me to imagine that abbreviated venetoclax doesn't beat chlorambucil-based therapy. I don't know when that study's going to read out, but I kind of expect that that will be in the next 12 to 24 months we should see results from that.

Andrew Schorr:

Okay. I'm going to go back to basics for a minute. We've got this question from Debra. None of us love bone marrow biopsies, Dr. Sharman. Yeah. In this age of a lot of more sophisticated blood testing, when is a bone marrow biopsy required?

Dr. Sharman:

Fair. It's oftentimes required as a response assessment in a clinical trial. Sometimes I think you might say if I wasn't in the clinical trial, would I require it? You're right, in a lot of cases we can get by without a bone marrow biopsy. Bone marrow biopsies are useful for determining minimal residual disease. It can be different between the blood and the bone marrow. Bone marrow biopsies can be useful if somebody's experiencing low blood count. Maybe they're anemic, maybe they have low platelets, and you want to understand is this the CLL causing this, is this prior therapy, is this complications of prior therapy? It can be useful as a diagnostic. I had a patient not too terribly long ago who had a pretty sizeable paraprotein. Paraprotein is something you can detect in the blood. It can be associated with CLL, but not all that often. We did a marrow on him and sure enough, he had Waldenstrom's in the marrow too, so he had both fleas and ticks, two different diseases. I think if there's a diagnostic question as to why something's the way it is, a bone marrow biopsy can still be useful.

Andrew Schorr:

Okay. I am told that CLL patients are at higher risk for skin cancers, the scariest one being melanoma. I'm going pretty regularly, if I see something concerning, to my dermatologist. I was there last week and actually had a little biopsy and they want to—it's not melanoma, but it's something else. Robbie wanted to know about our risk of melanoma. How much is the risk for that and what kind of surveillance should we have?

Dr. Sharman:

I would say that probably the substantial majority of my CLL patients also end up with a dermatologist. CLL, we've already mentioned how it is an immunosuppressant cancer. I think that probably skin cancers are one of these things that come up periodically and your immune system just deals with them. But then introduce CLL into the system and maybe they're less capable of just dealing with it. Obviously if you have a bigger history of sun exposure, you're more likely to experience issues or fair-skinned and so forth. I think if you want to have a take home point for this, you should pay attention to skin changes and don't dismiss them, even if your own doctor kind of glances at something and doesn't necessarily have a concern. If there's a concerning skin change that's persistent, it's worthwhile having a dermatologist look at it. Melanoma versus basal cell versus squamous or Merkel cell, they're all higher risk in CLL and not infrequent. The older you are, the more sun exposure you are, it's probably worthwhile paying attention.

Andrew Schorr:

Okay, kids. Use sunscreen. I know Esther and I are going on a trip to Utah, that's our plan, driving. No cruise ship, no planes. We're getting the SPF shirts and stuff like that. Here's a question that Peg sent in. She said many elderly CLL patients have swallowing problems. Would it be okay to empty ibrutinib capsules into applesauce?

Dr. Sharman:

I saw that question and I actually had to ask around. I wasn't sure about that. The manufacturers don't have any information addressing that issue specifically. However, a couple of things, they do talk about giving it through G tubes, which some patients, if they have a bad swallowing issue and they have a feeding tube, you can put it through a feeding tube. I guess my presumption is that you can do it. I'm always bothered by this fact that we tell our cancer patients don't handle your drugs, use gloves, do all these preventive things, careful with the toilet, but go ahead and swallow it. I'm like how's that not the same thing? They do articulate some concerns about handling it, but I think if they are allowing people to do it through a feeding tube. Ibrutinib used to come only in capsules, and then they did a reformulation. The capsules were kind of big. Then they came out with a tablet form, and the tablet's not nearly as big, and it's one tablet for whichever dose you get. That might be something to explore with a doc too. Maybe three capsules might be challenging for a CLL patient, but one tablet might be easier.

Andrew Schorr:

Okay. All right. We talked about stopping therapy, and I think that's an individual discussion with your doctor. I know people want to know about that. As people have these tests and you're introduced to this world of CLL, you hear what version of CLL you may have, and that could include, this term comes up, the 17p deletion. It's generally known that 17p has been more aggressive. With these medicines we rattled off earlier, how do they cover off 17p?

Dr. Sharman:

All the new drugs work better than chemotherapy in the 17p calculation. Nonetheless, 17p probably does less well with the newer drugs than patients lacking 17p. I would even go so far as to say that unless you're in a Third World country or a place where you don't have access to novel drugs, I would say that chemo-immunotherapy is contraindicated in the setting of 17p. Unfortunately it's still happening out there, but if I could tell your listeners that if your doc wants to give you BR or FCR and you've got a 17p, that's a red flag, and get yourself a second opinion. Ibrutinib still works great in 17p, better than any chemotherapy ever did. It just doesn't work as well in 17p as it might in patients lacking 17p. The one drug that seems to be agnostic of 17p is idelalisib (Zydelig), which is a PI3 kinase inhibitor. However that's, for the most part, something that is utilized only after BTK and after Bcl-2 for most patients. It would be unusual to use that earlier on. That's the only one that seems to be agnostic.

So 17p, just a little bit more. What we're measuring with a test called FISH, it's called fluorescent in situ hybridization, it looks at certain chromosome abnormalities that are common to patients with CLL. There are a handful of recurrent abnormalities, so 17p, which stands for a loss of the 17th chromosome, p is petite, so the short arm of chromosome 17p. There's 11q, that's also not so good with chemotherapy, but does pretty well with the targeted agents. Normal, an extra copy of chromosome 12, what we call trisomy-12, and then lack of chromosome 13q, the long arm of 13q is the most common. Oftentimes those are used as markers to tell us how well therapy is likely to work, with 17p having the most adverse outcomes of the group.

Andrew Schorr:

People don't have to freak out today just if they're told that they have 17p.

Dr. Sharman:

I think you only need to freak out with 17p if your doctor tells you they want to give you bendamustine-rituximab (Bendeka-Rituxan).

Andrew Schorr:

Okay. Good. All right. We've talked about that before. Let's go on to the big guns, either traditionally, like stem cell transplant, and also maybe experimentally CAR T chimeric antigen receptor T-cell therapy, okay? Trying to do immunotherapy, I guess you'd say. First of all, does stem cell transplant still have a place for CLL, and for who?

Dr. Sharman:

Just to be clear, there's two types of stem cell transplant. There's what we call autologous stem cell transplant where you give it to yourself, and allogeneic, where you get it from somebody else. With autologous, really the whole purpose of autologous transplant is to just give yourself a big dose of chemotherapy and then give yourself some stem cells to repopulate. Allogeneic is really trying to use the immune system to fight off the cancer. Allogeneic had a limited role, because it gets harder with age, and most patients with CLL have higher ages. Above age 70, allogeneic gets to be quite challenging, and the median age for first-line therapy of CLL in the United States is 74. There is a role for it in younger patients who have exhausted their traditional therapies but still have disease that can be got under control, but it's really quite a small group nowadays.

I think the momentum is really moving more towards the chimeric antigen receptor therapy. If we just broadly call it cellular therapy, there's a lot of different approaches out there, whether it's T cell or MK cell. There are two that are approved by the FDA, one from Novartis and one from Gilead or Kite, to treat diseases that are a cousin of CLL, so acute lymphoblastic leukemia and diffuse large B-cell lymphoma, diseases that traditionally are much more aggressive than CLL, disease that, in the relapsed setting, oftentimes have survival measured in weeks to a few months, which, as most of your CLL patients would know, that's very aggressive. They work in that disease, and maybe even can provide some curative therapy for patients who were otherwise destined to pass away from their disease.

The technology also works in CLL. It has been slower to develop there because of ibrutinib, and because of venetoclax and because of effective therapies, the FDA has defined what we call an unmet medical need. What's the need for this drug? It's difficult to execute studies in this population when you have these other really provocative therapies available. I think it is worthwhile, particularly if patients have been exposed to a BTK inhibitor, been exposed to venetoclax, if they find themselves needing a new therapy, I think it would be very worthwhile to seek out an opinion from a cellular therapy institution. They're currently only in research for CLL. They are not FDA-approved. I think we will see an approval for patients who have experienced treatment failure of BTK and venetoclax. I think that's a little ways away but could be forthcoming.

Andrew Schorr:

Right. We have a friend like that who went through that in Seattle, and he's recovering and doing well. Those drugs that you mentioned, novel drugs were no longer working for him. Let's flip it around. Many of us have been on watch and wait or watch and worry for an extended time. Some people, and I have a friend like this in Seattle, actually, who was also likely diagnosed in 1996. He has never had treatment. Where are we? What's our understanding of people where CLL just remains dormant, if you will, but it's there?

Dr. Sharman:

Yeah. Absolutely. We call it watch and worry, watch and wait, all these things. The reality of how that got developed was largely about the fact that there are these patients out there, patients who could be diagnosed with the disease and may not ever require therapy. That might be a fifth of patients diagnosed with CLL. It's not a trivial number. They may not be as well-represented in your group of patients, because a lot of them have come in once a year for the lab count check and go on their way. They're not necessarily seeking out the information. By all means, there are patients. Furthermore, there are patients who will have incredibly durable responses to chemotherapy, and typically it's the patients with mutated B-cell receptor and 13q on their FISH, patients who may have been treated 10 years ago and are still not showing any signs of relapse. Some have questioned whether or not some of our prior FCR regimen has not given as much, even in a selected subpopulation, be a curative therapy. I still talk about FCR in my younger patients, 40, 50, who have a favorable molecular profile, because we can see these remissions that last a decade or longer.

Andrew Schorr:

Okay. I have two questions I'm thinking of. You said mutated, unmutated. A lot of us don't understand why, if the doctor comes back and the report is we are mutated, that that's kind of better than unmutated. I don't get that.

Dr. Sharman:

You're absolutely right. You would think if you have a mutation or something, that that's necessarily bad. This has to do with some fundamentals of B-cell biology, and probably the fact that CLL can arise from two different stages of B-cell development, one which is later in development, a more mature B cell. It is part of the intrinsic behavior of a B cell to undergo a mutation process, and CLL can probably happen either before that or after that. If it's the more mature cell, we'll call it the more refined, more dignified, more well-behaved, I guess you can say, whereas think of the unmutated as the earlier. They're the punk teenagers who might be more problematic.

Andrew Schorr:

Okay. I got it. One question that has come up, John sent it in, and a number of people asked about it, was related to family history. First of all, could you tell us what our understanding is now of CLL running in families, or more broadly if maybe there wasn't another case of CLL, but somebody had another blood-related cancer or a lymphoma or even a rare Waldenstrom's or multiple myeloma. Do we say, well, we all had some blood-related cancer and it runs in our family, and maybe our younger offspring should have some kind of testing or surveillance?

Dr. Sharman:

Yeah. If I could put a plug in for Dr. Jennifer Brown, I'm sure you've had her on your programs before, she's really the leader in research in this area. She has identified a number of recurrent what we call germ-line abnormalities that lead to predispositions to these different blood disorders. What I tell my patients is that the overwhelming majority of CLL cases are spontaneous and that there is only a minimal increased risk of family members having similar disorders. However, all of us who do lymphoid malignancies will encounter families that have, are disproportionately enriched for either CLL or lymphoma or myeloma or other forms of acute lymphoblastic leukemia and so forth. What Dr. Brown has found is there are some, they're not common, but some things that can be passed through egg or sperm and can cause familial lymphoproliferative disorders. We don't currently have any sort of commercially available testing to readily identify that for patients. It's primarily in the research context. Again, Dr. Brown at Dana-Farber in Boston is the main person. She's actually, I believe, still doing active research on that. If you are a family that has four or five members, particularly if they're still alive and can be tested, she's got a lot of cool tools to look into that.

Andrew Schorr:

Okay. We're going to get to that. We've gone a few minutes longer. I want to mention, first of all, we'll get Jennifer Brown on again. We've had her many times. We are doing another CLL program with somebody you know, Jeff, Ian Flinn down in Nashville, Tennessee Oncology. We're also going to tackle this whole infection risk with another doctor from Tennessee, and that's Dr. Sydney Hester, an infectious disease specialist. We're doing that, folks, on March 28th from Nashville. We'll see how many of you in that area want to be together with us. We'll clean all the surfaces. We'll do everything we can, and then you can watch it, of course, like a live TV show just like this.

Dr. Sharman, I always like to end with this last thing, and that is you are both a researcher and a CLL specialist, and you're also a leader throughout the US Oncology Network in this field. How positive, hopeful do you feel for those of us living with CLL now?

Dr. Sharman:

For my patients who are newly diagnosed, I find it to be an exquisitely uncommon circumstance that a patient will pass away from their disease. There's almost always some sort of external circumstance, whether it's dementia or social or whatever it is. It is very uncommon. That doesn't mean it doesn't need to be managed. We oftentimes have to do things along the way. Occasionally there are patients with really bad CLL, but for the substantial majority of patients this is something we will live with and not die from. I think you have that optimism having lived through the recent transformation of how we treat this disease. I think it's a remarkable time for patients with CLL. The pace of progress has just been explosive. I think there's a lot of reason to be optimistic that we can manage this disease for most patients.

Andrew Schorr:

Great news. I want to, on behalf of the CLL community that I get to talk to a lot, Dr. Sharman, I want to thank you for your devotion to not just treatment every day in the exam room or if you sometimes see people in the hospital but for research. Thank you for being a part of this and your colleagues around the world. Dr. Jeff Sharman from Willamette Valley Cancer Institute and Research Center. I said it right. Sometimes I don't. Andrew Schorr here in California. Jeff, thanks for being with us once again.

Dr. Sharman:

My pleasure. Thank you, Andrew.

Andrew Schorr:

Okay. Andrew Schorr here for Patient Power. We'll have other live Ask the Expert programs. Remember the town meeting coming up on the 28th. You can register for that. I hope this has been helpful. We'll keep the questions coming. Cll@patientpower.info and we'll keep plugging away at them, all right? Remember, knowledge can be the best medicine of all.

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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