Yesterday I started the third cycle of my Vel/Rev/dex consolidation therapy and we met with Dr. Richardson. My blood test numbers improved nicely from the last two weeks due to my 1-week holiday from the Velcade and Revlimid. My WBC went up from 2.6 last week to 4.2, and my platelets rose from 83 to 166. Both are now back in the normal range. The only nagging area that doesn't improve over time has been my anemia (Hgb and HCT are consistently low). I've been a little tired lately, which could be partly due to the anemia, but Muriel said that this is normal and that most patients suffer some fatigue while on the consolidation therapy. Other than that, I'm doing fine. I won't get the blood and urine phosphoresis and immunofixation results until next week, but those results have been improving steadily since my ASCT.
Muriel Gannon and Paul Richardson both said that I am doing great! We also ran into Kathy Colson, who was the head nurse on the MLN9708 clinical trial. She said that these trials are still going great with 98% overall response rate, which is extremely good. She also said that I am still the "poster child" (so to speak) for how well this drug is working. Nice!
While meeting with Dr. Richardson, I had a chance to ask about some of recent research I have been posting on lately. My first question was on the recent Actemra (tocilizumab) paper showing the improved M-Spike in the patient being treated for Rheumatoid Arthritis who also had Smoldering Myeloma (SM). He was very interested in this paper, so I gave him a copy. He felt it might be significant, since it is well known (but not by me) that IL-6 is a particularly important enabling factor in precurser forms of MM (MGUS and SM), more so than in active MM.
I also asked him why MM research on Actemra seems to have dried up so quickly. I gave him an excerpt from another paper co-authored by his boss, Dr. Ken Anderson, in 2011 extolling the virtues of tocilizumab as an anti-IL-6 agent (see Section 3.2):
Antibody-Based Therapies in Multiple Myeloma
His answer was very informative but a bit oblique. He said that trials for the anti IL-6 monoclonal antibody, elotuzumab, are showing excellent results (OK, that's good). Another antibody, daratumumab, has been effective against MM by binding to CD38 on the MM cell (that's good too, but it's not IL-6). A third anti-IL-6 antibody, siltuzumab, has not been shown to be effective (too bad, but doesn't that strengthen the case for studying Actemra?). All this was very interesting, but he didn't quite answer my question. I didn't pursue it further, but I might bring it up again next time.
I also asked him about the other paper I blogged about recently regarding finding the RNA component, ACA11, which is found to explain the poor prognosis for high-risk t(4;14) patients. Richardson has a high opinion of the author, Michael Tomasson, from Washington University in St. Louis, and said he is a good researcher. That's encouraging, but when I asked him whether this would be a fruitful area for research, his response was pretty much what I expected. He said that since Velcade and Revlimid both overcome the high-risk prognosis of t(4;14), he doesn't see it as a high priority now.
"But, but.", I was tempted to ask, "If I become refractory to these agents, what would I do then?" I guess this is a question for another time. Hopefully, I will never need to ask it.
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