Tag Archive for: Velcade

Relapsed and Refractory Myeloma Defined

Relapsed and Refractory Myeloma Defined from Patient Empowerment Network on Vimeo.

Myeloma expert Dr. Krina Patel reviews the difference between relapsed and refractory myeloma and how these distinctions may impact care and treatment.

Dr. Krina Patel is an Associate Professor in the Department of Lymphoma/Myeloma at The University of Texas MD Anderson Cancer Center in Houston, Texas. Dr. Patel is involved in research and cares for patients with multiple myeloma. Learn more about Dr. Patel, here.

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Transcript:

Katherine:  

Dr. Patel, could you define what relapsed myeloma is?

Dr. Patel:     

Yes, so as of today, for the majority of our patients we can’t cure myeloma to the point where we treat it, and it’s gone forever, right? I’m hoping one day we get there. And we’re getting better, but we’re not there yet. However, myeloma’s very, very treatable. So, what relapsed means is that, once you’ve had initial therapy after you’ve been diagnosed, our goal is to get that myeloma to as low as possible level so that it hibernates as long as possible. But eventually, that myeloma’s going to start waking back up. So, when it does, that’s called a relapse. That now, the proteins are coming up, the myeloma cells are growing and we need to do something to knock it back down again. So, that’s relapsed disease.

Katherine:

How is that different from refractory myeloma?

Dr. Patel:

That’s a great question. We talk about relapsed refractory all the time for myeloma. So, refractory actually means that your myeloma started waking up while on a certain medication. So, if you were on no medicines and then your myeloma came up, that’s considered relapsed. That’s not refractory. However, biggest example I can give you is when patients are on maintenance therapy after stem cell transplant, for instance. When they’re all on maintenance and their myeloma starts coming up while on maintenance, then they are considered refractory to that drug; so, if it’s lenalidomide (Revlimid), if it’s bortezomib (Velcade), whichever one it is.

So, any time the myeloma’s coming up while on active treatment, you become refractory. So, we talk about triple refractory or penta-refractory, and what that really means is how many drugs is your myeloma refractory to.

So, if you’re refractory to a proteasome inhibitor plus an immunomodulatory drug plus a CD38 antibody, right – I can give you examples of all of those, but basically different categories –then you’re considered triple refractory. And the more refractory it is, the harder it is to treat and the more novel therapies we need.

Katherine:

So, if a patient is taking three or four different drugs, how can you pin it down to know which drug or all of them are causing the refractory myeloma?

Dr. Patel:

So, it would be all of them. Let’s say, salvage therapy. You’re on three different medications or four different medications, usually three. We would say, if the myeloma’s coming up while you’re on all of them, you’re technically refractory to now all those medications.

Katherine:

All of those. Okay, all right.

The Latest in Myeloma Research: Updates From ASH 2021

The Latest in Myeloma Research: Updates from ASH 2021 from Patient Empowerment Network on Vimeo.

Myeloma specialist, Dr. Omar Nadeem, shares promising research advances in myeloma from the 2021 American Society of Hematology (ASH) annual meeting. Dr. Nadeem discusses the future of personalized medicine for myeloma, as well as positive results from a clinical study on quadruplet therapy.

Dr. Omar Nadeem is the Clinical Director of Myeloma Cellular Therapies Program and Director of Myeloma and Plasma Cell Pathways at the Dana-Farber Cancer Institute. Learn more about Dr. Nadeem, here.

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An Expert’s Hopeful Outlook on Myeloma Research and Treatment 


Transcript:

Katherine:

Personalized medicine for myeloma is slowly becoming more of a reality for patients. Can you provide an update in testing in myeloma? Are there specific markers that you’re looking for when considering patient care?

Dr. Nadeem:

So in multiple myeloma, right now the only targeted therapy that’s in development is looking at venetoclax (Venclexta), and that’s in patients that have the t(11;14) translocation.

So, this has been studied for a while, both as single agent and in combinations and the big BELLINI study, which is looking at it in combination with bortezomib (Velcade) and dexamethasone (Decadron), really has had a lot of buzz over the last few years because there was a toxicity signal with the venetoclax arm.

But now with, again, updated results, etcetera, you’re starting to look to see which are the patients that benefited and which are the patients that didn’t.

And it’s becoming very, very clear that patients that have the t(11;14) translocation tend to benefit tremendously with the combination of venetoclax and bortezomib and dexamethasone. It’s really the patients that don’t have t(11;14) or high BCL2 expression, which is something that they’re also studying, those are the patients that didn’t benefit.

So, really fine tuning that to that particular population and using a combination like that is, I think, an example of where things are headed in myeloma. However, outside of that right now with where things stand, we don’t have targeted therapy to that extent beyond that.

Katherine:

Dr. Nadeem, with the ASH meeting closing out 2021, what are you excited about in myeloma research right now?

Dr. Nadeem:

We’re seeing very impressive results with using quadruplet therapies for newly diagnosed multiple myeloma patents. So, they get a combination of a CD38 monoclonal antibody like daratumamab (Darzalex), and then combining it with our typical agents. So immunomodulatory, drugs, proteasome inhibitors, and steroids. So, an update at this meeting with the phase-2 GRIFFIN trial, which was presented by my colleague Dr. Jacob Laubach, basically giving an update after 24 months of maintenance therapy.

This trial looked at a combination of dara plus RVD, which is lenalidomide, bortezomib, and dexamethasone, with transplant and maintenance, for patients with newly diagnosed myeloma. And what we’ve seen with each update of this study, that the response rates with the quadruplets are significantly better with the triplet. And more notably, we’re seeing very high rates of minimal residual disease negativity in favor of the quadruplet, which usually translates into a greater prognosis for patients.

So, median PFS is still not reached for this particular study, but you can start to see now that the curves are starting to separate and hopefully with longer follow up, we’ll see even a clearer result showing that patients that receive a quadruplet therapy at the newly diagnosed phase of their myeloma therapy benefit tremendously. So, this was a really important update at ASH this year.

How Will I Know If My Myeloma Treatment Is Working?

How Will I Know If My Myeloma Treatment Is Working? from Patient Empowerment Network on Vimeo.

How do multiple myeloma experts determine if treatment is working? Expert Dr. Rafael Fonseca explains factors that are examined when assessing treatment effectiveness and why it’s important for patients to speak up about side effects. 

Dr. Rafael Fonseca is the interim director of Mayo Clinic Cancer Center and serves as the director for Innovation and Transformational Relationships at Mayo Clinic in Arizona. Learn more about Dr. Fonseca here.

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Transcript:

Katherine:

Once on therapy, how is the disease monitored, and how do you know if the treatment is working?

Dr. Fonseca:

Well, fortunately, we use the same markers. Once a person is in therapy, we will be monitoring. We monitor at least on a monthly basis of those myeloma protein markers. Once a person reaches a great level of response, sometimes we complement that with an analysis of the bone marrow. Of course, it’s more invasive, so we don’t like to do a lot of them, but we do them as needed. As we go forward and monitor patients, we will be looking for signs that those proteins remain in a low level as stable as an indicator that the disease is under control.

Now, if I saw someone and then I start seeing that there’s an increased concentration of those proteins or we see something else clinical, we might need to do a little bit of a regrouping and test again in great detail to determine if the person is experiencing regrowth and the disease is so-called relapsed.

Katherine:

Why is it so important for patients to speak up when it comes to symptoms or treatment side effects?

Dr. Fonseca:

Well, that’s a great question. If you don’t speak about them, we don’t know about them. It seems very obvious, but then we cannot make the proper adjustments. I’ll give you a couple of examples. I already talked about dexamethasone, but a common drug we use is something called bortezomib. Bortezomib is a proteasome inhibitor.

That’s a mouthful, but it’s one of the key type of drugs we use. It’s given as an injection under the skin. Not to be confused, by the way, with daratumumab. Faspro is the name of that medication, so not to be confused with that is bortezomib, which we have been using for many years.

Bortezomib has a potential toxicity that is called peripheral neuropathy. If patients have peripheral neuropathy, that can go from very mild where you have some numbness and tingling, to the more extreme cases that it’s associated with pain, discomfort, even weakness and disability.

Well, if we don’t know that’s happening, then we can’t react to it and we can’t adjust doses or switch to something different altogether. You can imagine now we have more options, but in the old days, I always tell patients, “You might be tempted not to say anything about this because you might be thinking, boy, this is working. I don’t want to interfere with my treatment. I can live with the peripheral neuropathy.” But if it gets worse, despite the fact that the treatment is working, the person might have a very significant impingement on their quality of life.

More so now that we have so many alternatives, it’s important not to get us into a path that we might reach a point of an irreversible chronic complication from treatment.