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Wednesday, June 6, 2012

More Questions for Richardson

Yesterday I got my first consolidation treatment of Velcade, Revlimid, and, of course, dexamethasone.  Based on experience, I took the dex last night, which allowed me to get a decent night's sleep.  I don't know about tonight though.  I might just be in the mood for an extended post, so grab your seat belts.

After yesterday's meeting with Dr. Richardson, there were still some questions on my mind about the recent immunofixation test results and their interpretation.  Everyone (Richardson, Claudia, Muriel) was upbeat and telling me that the post-transplant finding of a faint M Spike was no big deal, because these "aberrant" results are often noted after a stem cell transplant.  OK, maybe, but I was not completely put at ease by this explanation.  It seemed a little too pat and dismissive for me.

One thing kept bugging me.  My most recent immunofixation test revealed the presence of a double gammopathy with an IgG Lambda clone.  This is the first time while I've been at DFCI that tests have demonstrated anything other than IgA Kappa MM.  Where did this IgG clone come from?  This triggered my memory that I had seen this somewhere before.  I mentioned to Dr. Paba Prada yesterday that I recalled an early test result showing that I had two monoclonal gammopathies.  She couldn't find that in the DFCI test records, so today I went through my past tests and found what I was looking for.  When I had my first bone marrow biopsy back in May 2011 (ouch...painful memory of Dr. Rabinowitz of Lahey Clinic), the pathology result showed that I had both IgA Kappa and IgA Lambda monoclonal gammopathies!  Somehow, this result had faded into the background of my memory over the past year.

So, today I decided to try to educate myself.  The paper I mentioned in my last post about multiple MM clonal gammopathies piqued my interest, so I decided to do a little online research. I Googled various topics, such as "clinical significance of t(4;14) heterogeneous subclones in Multiple Myeloma", among many others.  I did find a reference to the fact that there is a significant chance of finding a new clonal gammopathy different from the original clone after a stem cell transplant, which gives rise to "secondary MGUS" which may not have any adverse clinical significance.  Here is a link to a discussion of this topic in the remote chance that anyone might be interested;  Secondary MGUS.  I have a feeling that this is what Dr. Richardson was trying to tell me about yesterday.  In other words, it's no big deal, and it doesn't necessarily mean the MM is coming back any time soon.  OK, that would be nice.

However, I also came across some other articles that gave me a better appreciation of the challenges I may face having the high-risk t(4;14) cytogenics.  I'm learning a little more on the topic of heterogeneous subclones, which is a fancy way of saying that my type of t(4;14) MM is subject to frequent chromosomal changes, giving rise to multiple monoclonal gammopathies, which can coexist and/or change with time.  Typically, one of the gammopathies is dominant (that would be the IgA Kappa in my case), but there could be a secondary indolent clone lurking in the background.  One possibility is that the therapy can successfully suppress the dominant clone, but the indolent clone might be resistant to the therapy.  (I'm sure all of you will be eager to devour a reference article expounding on this topic;  Genetic Abnormalities in Multiple Myeloma.)  Once the dominant clone is under control, the other clone can then become dominant and lead to disease relapse.  Nice!

This give rise to a rather important question.  Is my newly-found IgG Lambda monoclonal gammopathy simply a "secondary MGUS" of minor significance?  Or is it possible that this clone has been waiting all along for the chance to shine and flourish?  I don't know if my medical team has ever noticed or now remembers that Lahey Clinic test result.  Those results were forwarded to DFCI before I started treatment there, but they could have been overlooked or forgotten.

I certainly plan to take up this issue with Dr. Richardson.  If he is unaware of the Lahey pathology report, would that change his opinion about the importance of my latest results?  If so, what would that mean?  I have a feeling that I already know the answer to that, which is to keep doing what I am doing and hit this thing with everything, including the kitchen sink (which I fixed today, by the way, in my copious spare time.)  I still have to fix the toilet in the master bath, but I don't plan to throw that into the mix.

One good result of my research (which I have mentioned in earlier posts) is that recent trial results have confirmed that initial induction therapy with Velcade and Revlimid, followed by post-transplant consolidation therapies including Velcade and Revlimid tend to overcome the negative prognosis usually associated with the t(4;14) translocation.  Hopefully, the MLN9708 in my induction therapy will prove as beneficial as Velcade, and my current VRD consolidation and Rev maintenance should best suit my situation.  At this point, I can't think of anything that I would have done differently before or would plan to do differently now.  Time will tell.

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