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IMS 2026 | Identifying tumor-reactive T-cell clones to guide personalized immunotherapy in multiple myeloma
David Avigan, MD, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, discusses potential clinical applications of identifying tumor-reactive T-cell clones in multiple myeloma at the single-cell level. He highlights the potential to identify highly immunogenic shared neoepitopes to guide personalized vaccines and engineered T-cell approaches, as well as strategies to sustain immune responses following CAR-T or bispecific therapy and reduce the risk of relapse. This interview took place at the 23rd International Myeloma Society (IMS) Annual Meeting in Glasgow, UK.
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Transcript
I think there are a couple of possibilities here. Our particular vaccine is a somewhat dirty vaccine in that we take a whole tumor cell from the patient and we use that as a source of antigen and that way we don’t really need to know the most immunogenic peptides. But it may be more efficient if one had a next generation vaccine that really focused on shared neoepitopes that had the highest capacity to induce potent T cell responses that were effective in lysing myeloma cells...
I think there are a couple of possibilities here. Our particular vaccine is a somewhat dirty vaccine in that we take a whole tumor cell from the patient and we use that as a source of antigen and that way we don’t really need to know the most immunogenic peptides. But it may be more efficient if one had a next generation vaccine that really focused on shared neoepitopes that had the highest capacity to induce potent T cell responses that were effective in lysing myeloma cells. So this could be an in vivo biologic guide to say these are the best targets to go after. And one could do that either through expanding T-cells and using an adaptive T-cell strategy or by a primary vaccine strategy. The other thing that we’ve been thinking is pairing these kind of approaches with some of the other cell-based immunotherapies, such as BiTEs or CARs, because those tend to cause a very dramatic response. They often diminish over time. And it’s those patients that get the secondary T cell activation that seem to stay in remission. And we could potentially find the antigens that drive that and then supplement those T cells to prevent recurrence later on.
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