We have a cure definition for myeloma. Requires: 1) Off all therapy and sustained MRD negative for 5 years 2) Negative imaging studies Presented by @NikhilMunshiMD #IMS26 @Myeloma_Society Note: 1) We need to see how this definition performs. Relapse rate for patients meeting these cure criteria must ideally be less than 5%. If not, we may have to adjust the criteria. 2) I hope the cure criteria will be the impetus to stop doing trials with endless therapy. You cannot claim cure with continuous therapy. I’m glad the field is mostly aligned on this. Cure for patients and public in any disease has a deep meaning. Cure means cure. We cannot dilute it.

Three things I recommend for using Bispecific antibodies in myeloma: 1) Prophylactic tocilizumab with first dose 2) Monthly IVIG regardless of the IgG level 3) Consider reducing frequency/stopping after excellent response. This applies to all the approved bispecifics: teclistamab, elranatamab, linvoseltamab, and talquetamab. Academic centers with expertise and close monitoring capabilities may skip the prophylactic tocilizumab but in general I do not see community adoption without it. The data on routine IVIG and early use before the IgG levels drop or infections occur is good and sufficient to move forward. It’s recommended in NCCN and mSMART. Bispecifics are better at controlling myeloma than standard triplets and quads, but pose a much higher risk of serious life threatening infections without prophylaxis and careful adjustment of dosing schedule based on response and patient characteristics. #IMS26

Profound sorry that my mentor, friend, and colleague, the legend Bob Kyle passed away. His contributions to patients, medicine, myeloma, @IMFmyeloma @MayoClinic myeloma group, and the institution are monumental. A role model who will be remembered for his integrity and commitment to patients. I owe my career to him. He leaves behind a legacy of experts at Mayo Clinic as well as world over who were influenced greatly by him. See thread for links to a video an article on him that I wrote for @MayoProceedings Post your memories below.

I am worried about the exploding number of “monoclonal gammopathy of clinical significance” entities. MGNS, MGRS, MGDS, MGTS etc It’s time to become strict with diagnosis of these disorders. MGUS is now more common because everyone is using very sensitive tests. Add to this some researchers saying you don’t even need a clone or M protein to diagnosis this. I disagree. Even for the most well documented MGCS entity, PGNMID if there is no M protein, whatever you see on the renal biopsy is most likely driven by some oligoclonal process not monoclonal. So, no M protein, no MGCS/MGRS should be the default. Over diagnosis and trying to eradicate the M protein is far more dangerous than under diagnosis. So you need a level of proof or compelling evidence that it’s the M protein that’s causing the problem. If that’s difficult to establish then it’s on us to get the testing right. Otherwise except for like established syndromes like POEMS, we need this rigor. Some entities like AL amyloidosis, cryo, PGNMID etc routine available testing gives the proof we need. Some others especially neuropathy and clots, are so common and so many causes, we simply need a very high bar for diagnosis. See our paper here: onlinelibrary.wiley.com/doi/…