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COMy 2020 | Profiling deep minimal residual disease in multiple myeloma

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Bruno Paiva

Bruno Paiva, PhD, University of Navarra, Pamplona, Spain, discusses the take-home messages from research investigating deep measurable residual disease (MRD) profiling in multiple myeloma. The use of new technology, such as next-generation flow (NGF), allows for finding undetectable MRD response and isolating MRD clones to utilize in genomic testing to understand the mechanisms of ultra drug resistance. This will enable further research to understand the different modes of treatment resistance which can be targeted by new treatments. This interview took place during the Controversies in Multiple Myeloma (COMy) 2020 Virtual World Congress.

Transcript (edited for clarity)

Well, we are very pleased that this study is finally out there in the prestigious Blood Journal. I think that the study can be summarized around three important take-home messages.

Number one, the fact that nowadays using next-generation techniques such as flow, which was adopted in this study, are so powerful in defining an undetectable MRD response, that this was able to aggregate the poor outcome of patients with high-risk cytogenetics, including those with 17p deletion...

Well, we are very pleased that this study is finally out there in the prestigious Blood Journal. I think that the study can be summarized around three important take-home messages.

Number one, the fact that nowadays using next-generation techniques such as flow, which was adopted in this study, are so powerful in defining an undetectable MRD response, that this was able to aggregate the poor outcome of patients with high-risk cytogenetics, including those with 17p deletion.

The second take-home message is that nowadays, again, using state-of-the-art technology, it is possible not only to detect MRD, but also to isolate MRD clones and perform genomic characterization, to understand the mechanisms of ultra drug resistance. In other words, to understand why so few MRD cells were able to persist their treatment. And this is allowing us to understand and to identify different modes of treatment resistance, for example, in patients with standard and high-risk cytogenetics.

Interestingly, those with standard-risk FISH abnormalities display higher clonal selection during treatment. This was not the case for patients with high-risk cytogenetic abnormalities. By contrast, these patients developed more genetic alterations already at the MRD stage.

Number three, I think this study illustrates, or can be considered as a proof of concept, to really understand the biology of MRD clones, to not only understand treatment resistance at the MRD level, but potentially to identify new therapeutic avenues that could eradicate the MRD clone, keeping in mind that if we continue to eradicate MRD clones, for sure, we’ll be closer to finding a cure for myeloma.

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