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Making CLL Treatment Decisions With Your Doctor

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Published on July 13, 2020

Having Good Patient-Doctor Communication Is Important to Make the Right CLL Treatment Decisions

In this podcast from our central New Jersey "Dinner with the Docs" series, Carol Preston talks to Dr. Andrew Evens, director of the Lymphoma Program at Rutgers Cancer Institute and Dr. Kathleen Toomey, medical oncologist at RWJ Barnabas in Somerset about the decision-making process for CLL treatment and the importance of patient-doctor communication. This podcast highlights the discussions doctors and patients in central New Jersey shared during our first evening of "Dinner with the Docs."

This program is sponsored by Janssen Oncology and Pharmacyclics LLC. 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 | Making CLL Treatment Decisions With Your Doctor

Carol Preston:
Hello everyone. I'm Carol Preston with Patient Power, and I've been living with CLL for 14 years. Because of the novel coronavirus, we physically could not get together to dine with our docs and our participating patients in Central New Jersey. However, going virtual lent an intimacy to the conversation that wouldn't have happened face-to-face. Recently, I spoke with Dr. Andrew Evens, Director of the Lymphoma Program at Rutgers Cancer Institute and Dr. Kathleen Toomey, Medical Oncologist at RWJ Barnabas in Somerset. We discussed the decision-making process to treat CLL and patient-doctor relationships in the time of COVID-19. Here is part of that conversation.

So, Dr. Evens, can we start with you?

Dr. Evens:
There has been an explosion of scientific knowledge in the last 20 years of understanding it's not one disease, there's a lot of heterogeneity. And it really has exploded as we've learned about not just what's on the surface of a cell, but literally just like they do DNA testing at a crime scene, we on a daily basis do very special DNA testing of the CLL cells. It's in a special laboratory. You can't see it with the naked eye. But really based on the genetics, we're able to subclassify CLL into certain types and it really helps direct us when to treat and also what to treat with. So that's at the high, macro and micro level.

Carol Preston:
And Dr. Toomey, any way that you would expound upon that in terms of what you're seeing?

Dr. Toomey:
So I think we're seeing it in all of cancer, right? That we used to say, CLL, lung cancer, breast cancer, no. They're little slices of the pie. And even if you have a slice that's a couple of percent, there may be a very specific treatment for that group of patients.

Carol Preston:
So Dr. Toomey, I want ask you the following. When I get my blood check and I see the CBC and I say, “Oh my God, look what happened. My whites did this, and my reds did this,” is it okay to freak out?

 Dr. Toomey:
So, I think you bring up an important point. The point is that, and talking to my patient today, his white count is 26,000. It's been 26,000 forever. It has not changed any at all. His red count is fine. His platelets are fine. He's fine. He's fine. But it's hard for us because we see it and we go, "Oh, it's fine." But for the patient each and every time, it's like we call it, scan-xiety. It's the same thing. It's CBC-iety because it's of this importance to every patient and maybe a lot less importance to us. So we have to understand, I think, our patient's anxiety about getting blood done and about getting the results. That's why I called my patient, because I know that he's going to be worried about it until he hears from me.

And so until he can hear from me and I can say, you're fine and you're going to be fine and then until the next time, and the next time it happens again. So we just have to keep being human beings and keep reassuring our patients that this is a chronic disease and we're going to have to deal with it.

Carol Preston:
But let's take a look at our crystal ball, if we can, about the future. We can talk about CAR T-cell and it would be good to define what that is, STEM cell and treatments that go beyond popping a pill every day. So is that where CLL is headed?

Dr. Evens:
I think so. I mean, what we've talked about, ibrutinib (Imbruvica) and venetoclax (Venclexta) they're oral pills that target... and we talked about DNA. It's very complex DNA, all cancer, and we have found a few needles in that DNA haystack of needles that ibrutinib can attack or venetoclax can attack. And there are other needles, you could say, or DNA we're looking at. What you mentioned, Carol, is absolutely right. CAR T, I think that probably falls under the rubric of immunotherapy. And so we said we don't know why anyone gets cancer for the most part. With that said, a kind of big reason why is sometimes the immune system stops working and there's different parts to the immune system, but a really important part are called T-cells. T as in Tom. They fight infection, they also fight cancer.

And again, we don't know why certain patients, the T-cell stop working. But just some really seminal work about 15 years ago, originally at the NCI in a lab of Steve Rosenberg showed that if I can take... and maybe those T-cells aren't working in that lymphoma or CLL or multiple myeloma patient, but can I take them out of the body through a catheter outpatient and for over a several week period, basically make them work stronger, kind of supercharge them, make them work better.

And even kind of almost like a Lego, put something on it so when I give it back, it knows where to go. And that's a real simplistic explanation of CAR T and then it's like a onetime infusion back in the body. And so it is FDA approved right now, not for CLL, but for a more aggressive lymphoma, diffuse large B-cell. But I think this year we'll see more approvals in multiple myeloma for CAR T-cell therapy. And what I can also say, it's being studied in everything. And it's just one kind of immunotherapy. There's other cells called natural killer (NK) cells. Again, you can take out of the body, put back in. And so it literally is taking your own immune system out, make it work better, stronger, and giving it back to a patient. So it's not quite there yet for CLL, but I think we're making a lot of progress.

Carol Preston:
This is kind of a tough question from one of our viewers. And that is what happens if you put a patient on treatment and you don't see improvement? Well, either of you start.

Dr. Evens:
Thankfully it's not common. That's literally usually 5%, at most 10% of the time. So it's not zero. We can say it's the minority. And you have to try to understand when that happens, you always want to say, wait a minute. Am I 100% sure what's going on? I did all the CLL tests. Is it exactly that? Could there be a second thing going on? Or sometimes even within that short time, it can change. It can, what's called mutate or transform to something a little more aggressive. And so really what it takes is time for reflection, thinking, is there something else going on? Usually there is actually something else going on. Every now and then it's just no, but CLL and it's just not working. So thankfully you just... that's why we always think, whatever I'm starting with, great. We're always thinking, what's plan B? What's plan C? And so you kind of have to quickly course correct.

Dr. Toomey:
So I would say that the more common thing is not that something doesn't work, it’s that a patient can't tolerate it. I mean, more likely than not working is that they could take only so much, they'd have to stop after a period of time. And then once again, it’s stop and wait and watch.

Dr. Evens:
But that's a great point. Even though I love clinical trials and clinical trials are how we make everything better, when you look, Carol, at some of the initial ibrutinib clinical trials, it was only like 10% stopped for toxicity. But clinical trials, sometimes, self-select for really healthy patients and you have to have perfect kidneys, perfect liver, perfect everything. That's not always the real world. And so when you take that clinical trial medication in the real world of diabetes, a bad liver, kidneys. So a group of us had studied this and published it. In the real world it was probably more 40 to 50%. One of the most common reasons... now, this is a few years ago, we've gotten better, but one of the most common reasons to stop ibrutinib or another medication called PI 3-Kinase Inhibitors was exactly right, as Dr. Toomey said, it was toxicity.

And I think she said a great, initially, is that's the whole art. We're taught this medication for this molecular, but the bedside, the pros, the cons, the asking questions, it just is so important to have those conversations with your oncologist and to never feel bad or shamed or if you have a side effect, you want to clearly please tell your doctor, this is what's going on. And they'll tell you, don't worry about it, that's okay or they'll say, you know what? No, you need to come in. I need to do some extra tests, et cetera.

Carol Preston:
Our thanks to doctors Evens and Toomey for their insights and to the patients from Central New Jersey who joined us online. I'm Carol Preston. Your questions can help lead you to more informed treatment decisions. 


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