Very briefly, I think that myeloma is yet to solve the question of the cell of origin, which has been tried to be answered for the past 20 years. Well, using multiomics, we showed that you could trace up to B-cell precursors, and obviously including more mature B-cells, the BCR clonal sequence that you can find in the myeloma cell. So, in other words, by looking at the specific myeloma immunoglobulin gene rearrangement, this can be detected in more immature stages...
Very briefly, I think that myeloma is yet to solve the question of the cell of origin, which has been tried to be answered for the past 20 years. Well, using multiomics, we showed that you could trace up to B-cell precursors, and obviously including more mature B-cells, the BCR clonal sequence that you can find in the myeloma cell. So, in other words, by looking at the specific myeloma immunoglobulin gene rearrangement, this can be detected in more immature stages. However, in this study we also show that the recurrent driver mutations and copy number alterations are only present in the plasma cell and are absent in these more immature cells that may carry the clonal B-cell receptor and may also carry mutations that are random and probably happened with age and led to a clonal lymphopoiesis from which the myeloma cell emerges. Now, from the clinical point of view, the consequence of this is that when we want to monitor response, we need to focus on the plasma cell compartment and not that much on more immature cells that may carry some of these alterations.
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