I’ve never run a consecutive, four part series before. Seemed to go over well. Lots of emails and positive feedback. It was kind of Chuck to be so open and share with us that way, don’t you think? In the meantime, some news and notes I’d like to share have been piling-up. Let me get to some of that important news now.
Last night my myeloma and transplant doc, Melissa Alsina, spoke to our support group. In addition to providing the group with insightful information about auto transplant information, she also discussed her work with allo (donor) stem cell transplant patients, along with several clinical studies she’s involved in. Dr. Alsina answered a lot of nagging questions for me. I’ll be writing about that tomorrow.
Which brings me to some other unanswered therapy questions that I may have found answers to earlier this week. It seems clear at this point that myeloma isn’t a single cancer, but many different cancers–sometimes even within the same individual. The IMF’s Dr. Durie, Japanese myeloma expert, Dr. Kazuuyuki Shimizu, Dr. Alsina and many others all agree that myeloma can change and morph with time, making it a heterogeneous disease that shouldn’t be treated with a “one-size-fits-all approach.”
The problem is our docs don’t have enough information to do this effectively yet. For example, there seems to be some question whether it’s a good idea to use alkylating agents like melphalan, cytoxan or bendamusting as up-front therapies. These drugs can damage DNA and may help our bodies develop new clones.
Really? So what about up-front SCT using melphalan. Sort of an oxymoron, isn’t it? Regardless, maybe cytoxan or bendamustine aren’t the best choices for induction therapy. But since this link hasn’t been established through clinical trials in people, it remains an open question.
Or how about his one. An article in the Summer Edition of the IMF’s Myeloma Today posed this question:
If myeloma clones change over time, isn’t it possible and potentially useful to reintroduce therapies to which a patient has become refractory (resistant) earlier in the disease course?
According to Dr. Alsina and others, the answer is YES! This can happen two ways. Cells can be reconditioned during transplant to become more receptive to treatments that had stopped working prior to SCT. And/or myeloma cells changing on their own with time can become receptive to former treatments again.
That’s one argument for going back to therapies that have worked well in the past, before moving-on to something new; or after a new therapy doesn’t work as well as hoped. Combining old and new may also be worth a try.
Here’s a link to the newsletter PDF:
The helpful article, IMF Hotline Coordinators Answer Your Questions – “What is clonal evolution?” can be found on Page 8. You may also note a Black Swan update on page 5.
Feel good and keep smiling! Pat