Beyond Monoclonal Antibodies: How a Range of Immune-Based Therapies Are Changing Multiple Myeloma

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While newly diagnosed multiple myeloma patients have good reason to be optimistic in light of recent advances in treatment, a subset of patients with high-risk and relapsed disease continue to receive little benefit from the gold standards of therapy. Even as immune-based therapy using monoclonal antibodies continues to mature and become available to larger groups of patients, researchers are pressing forward with research into a wide-range of immune-based treatments to treat the full spectrum of disease. 

In this video, Dr. Kenneth Anderson, the chair of the Myeloma 2014 workshop in Boston, shares his excitement, suggesting that, more than ever, patients have good reason to feel confident in the face of this complex and heterogeneous disease.


Made possible through an educational grant from the Patient Empowerment Network, which received support from Millennium: The Takeda Oncology Company and Celgene Corporation.


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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:

Hello and welcome to Patient Power, I’m Andrew Schorr. Recently, in Boston, there was a meeting called Myeloma 2014, where experts from around the world gathered to discuss the latest in myeloma, and they were excited! Dr. Ken Anderson, from the Dana-Farber Cancer Institute, a world expert, shared his excitement with us.

Dr. Anderson:

This Myeloma 2014 is probably the most exciting myeloma meeting we’ve ever had. The reason is that we have, together with our patients, made amazing progress. The immunomodulatory drugs and the proteasome inhibitors, used together in the context or not of transplant, have clearly changed the natural history of this disease. This meeting, though, in 2014, is really setting the stage, or the framework, for us to go to the next level, to make myeloma a chronic disease and honestly to have curative potential in many cases. Advances that were described here started with the new knowledge of the genomics of the myeloma cell, showing, in fact, how complicated it is even at the time of diagnosis, how there are multiple clones within a given patient, and how there is heterogeneity—or differences—that really contrast different subgroups of patients that really have different outcomes. Those advances have not only helped us understand the biology, but they have identified new targets for treatment.

And so we have at this meeting entirely new classes of agents: CRM-1 inhibitors that take advantage of turning on these tumor suppressor genes that, in turn, suppress the cancer; entirely new classes of agents such as the IAP antagonists that block survival signals in myeloma cells; whole new classes of agents that actually add on to our immunomodulatory drug and proteasome inhibitor base. 

I think abnormalities on the cell surface or inside a myeloma cell are fair targets.  This meeting, secondly, has talked about epigenetics. So that means, in plain English, targeting the host, the interaction of the myeloma cell with the patient, the bone marrow microenvironment and the immune system. And that is very, very exciting. So, for example, in the epigenetic therapies, we have a couple of examples; the isoform selective, or more selective histone deacetylase inhibitors or the bromodomain inhibitors, are two classes of drugs that patients should probably know about because they are likely to add to our armamentarium against myeloma.

I think, though, one of the most exciting developments in cancer in general, but in myeloma in particular—and it’s really exciting here this year—is the immune-based strategies. We have several kinds of immune-based strategies.

We have monoclonal antibodies in myeloma looking very, very promising. Not only having responses in high-risk relapsed disease but lasting now in the order of years.

A second kind of immune strategy is vaccination. So we can vaccinate now against myeloma, either the entire myeloma cell, or we can vaccinate against proteins that are on the cell’s surface—if you will, the fingerprint of the myeloma cell. And we can vaccinate just as we vaccinate for tetanus or smallpox, etcetera. We can vaccinate for myeloma.

The other immune area, the other really exciting development—and patients have probably heard about this in the solid tumors; in kidney cancer and melanoma—not myeloma—melanoma, and lung cancer—there is the ability now to take the breaks off of the immune system in the patient and allow the immune system to do what it really wants to do, which is recognize the cancer as foreign and reject it. And the medical term for this is checkpoint inhibitors. They are PD-1 and PDL-1. PDL-1 is on cancer cells, including myeloma and PD-1 is on the cells from the immune system that are trying to reject the myeloma. And when that circuit is made, PDL-1 to PD-1, it’s a break on the immune system. And so what is now being done in myeloma and other cancers is to block that, or blow the fuse on that circuit, and now we allow the immune system to do what it’s always wanted to do but has been shut down by the cancer, that is, it can now react against the myeloma.

And in the era of monoclonal antibodies and vaccines and these checkpoint inhibitors, lenalidomide (Revlimid) also plays a role. Because lenalidomide, pomalidomide (Pomalyst) and thalidomide (Thalomid) are immunomodulatory drugs, at least, in part, they work by modulating the immune system. So you can imagine a day which is coming very quickly, where as we previously combined chemotherapies, and more recently we’ve combined the novel agents—immunomodulatory drugs and proteasome inhibitors—going forward we will build on that base and we will have combinations of immune approaches.

And I think the most exciting thing is to emphasize from this meeting is that myeloma is very complicated genetically, and it starts complicated. And if it is allowed to evolve, it gets even more complex. And so what is one way to deal with very complex, always changing systems? It’s the immune system. When we get an infection, we clear the infection. In this instance, if we can allow for the immune system to recognize the myeloma and reject it, that is more efficient, honestly, than any combination of targeted agents that we might come up with.

So, hence the huge excitement in myeloma and in cancer more generally. So, in summary, it’s been an unbelievably exciting meeting. I think patients should be very, very optimistic for the future.  Important to really seek out a center of excellence for myeloma because the changes are happening so fast that you really do need to visit and be followed, at least in conjunction with someone who’s really on the cutting edge of myeloma medicine. So it’s a very optimistic time, honestly, chronic illness for myeloma in many cases, and there is a cure on the horizon. 

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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Page last updated on May 27, 2014