This proposal of the Christiana oncologist came as something of a surprise to me. None of these is, strictly speaking, a particularly novel agent. Velcade (bortezomib) is a member of the first generation of such agents that included for example Revlimid. It has been used successfully for a decade, very often as a part some sort of combination such as this. [10/30/13: Kyprolis/carfilzomib, the next-generation successor to Velcade/bortezomib, will be substituted for it.]
Cytoxan (cyclophosphamide) is really old-school; clinical trials involving it were first conducted in the late 1950's. It's the traditional type of agent that many people continue to associate with the term "chemotherapy"; it makes the patient's hair fall out, induces nausea, and so on. I was sufficiently concerned about the potential toxicity for a post-transplant patient such as myself that I brought the issue to the attention of the Johns Hopkins oncologist. He did not exactly endorse the idea, but it also raised no red flags for him. [But he did raise a red flag over Velcade; read on.]
Technically, CyBorD is a protocol approved for newly-diagnosed myeloma patients, rather than as salvage therapy for relapsed patients. But because I have never before been exposed to Velcade, I might be expected to respond to it as if I was a treatment virgin. Its operation is fundamentally different from that of Revlimid, which simply destroys myeloma cells outright. Velcade is more subtle, disrupting the internal processes of cell growth and division, thus preventing myeloma cells from behaving effectively as, well, myeloma cells. The principal danger of Velcade for me is the potential for increased peripheral neuropathy. Weekly subcutaneous injections, rather than twice-weekly IV (the original method of Velcade administration) is supposed to minimize this, but it will have to be carefully monitored.
[Not as of 10/30/13. Instead, the next-generation successor to Velcade/bortezomib, Kyprolis/carfilzomib, will be substituted for it. Peripheral neuropathy is evidently much less of a risk with this agent, which is the primary reason for the switch. It took quite awhile for the medical insurance company to swallow this change, because technically I am not supposed to get carfilzomib until I have failed bortezomib. The Christiana oncologist had to fight an extended battle to get the required authorization to move forward with it; hence the delayed nature of this post. This peripheral neuropathy risk was something that the Hopkins oncologist warned against when I discussed CyBorD with him; I believe he may have influenced the Christiana oncologist's decision to seek this modification.]
This is a complicated protocol, about which I have much more to learn. I will be taking pills (the dex),
I will also be continuing with bisphosphonate therapy, but I am being switched from Aredia to Zometa. I will be learning about this as well.
Meanwhile, I am very happy with the current pain management regimen, which combines dexamethasone with slow-release Oxycontin. I struggle with waking up a couple of times each night, and some of my work days recently have begun at 4 AM, but my appetite is great, and my energy levels are very high.