As Dorothy so correctly exclaimed, "There's no place like home." After a good night's sleep needed to catch up from an extraordinarily busy ASH, I thought I'd provide some final thoughts.
I've always said the good news about being diagnosed today with Myeloma is that there are so many more treatments available than when I was diagnosed in 1995. And it's never been truer after seeing more options presented at this year's ASH. Of course, the "bad news" about being diagnosed with MM today is there are so many treatments without knowing which works best for you. There's lots of overall statistics with details about responses according to different MM risk groups and other factors but nothing that says "this is the best treatment for you". However, the good news is that if a treatment is going to work, patients typically will show a response in 1-3 mos (cycles). If you're non-responsive, then try another treatment...i.e. manage your disease.
While it's believed that deeper responses lead to longer progression -free survival and overall survival, that's again part of "overall averages." I had a near complete response from an old induction treatment called VAD and a complete response from a tandem auto transplant...however, the response only lasted 18 months, after which I relapsed. Stay educated and try to consult with an MM expert whenever possible.
What I saw at this year's ASH was a better understanding of why patients either relapse (treatment stops working) or are refractory (treatment never worked). Even though Velcade and Revlimid protocols show high response rates, most patients still relapse. This year's meeting had several presentations identifying resistance mechanisms and pathways associated with these drugs. That's why Vorinostat plus Velcade might work in a patient refractory to Velcade. Or why R/R MM patients respond better to Elotuzumab plus Revlimind plus Dex than R/R MM patients respond to Rev plus Dex alone. Or why adding Perifosine to Velcade plus Dex shows responses in patients refractory to Velcade. It's all about "synergy" of drugs combinations used to treat MM, where combining drugs produce better responses than the sum of responses each drug yields.
And the other thing I learned is that not all IMIDs (Thalidomide, Rev, Pomalidomide), Proteasome Inhibitors (Velcade, Carfilzomib, Marizomib), HDAC Inhibtors (Vorinostat, Panobinostat), etc are alike even though they fall within the same category of drugs. As such, one could be R/R to Velcade but Carfilzomib may work...and I presume the reverse could also be true. There are different underlying cell interactions in these drugs even though they fall in the same general category.
Finally, treatment phases of induction (first-line treatment/s), SCT transplant (or not, early or late), consolidation (or not) and maintenance (if so, how long) all continue to be areas of study for newly diagnosed patients. Clinical trials typically begin with R/R patients and then move towards newly diagnosed patients. I think it's so important to enter a clinical trial if you have the opportunity. Typically a trial (especially phases II or III) offers you the best treatment, medically you're monitored very closely, and perhaps it's actually more affordable. Most important, it's the way we advance treatment options for ourselves and future MM patients.
I hope I get a chance to blog from next year's ASH in Atlanta. In the meantime, I'm spending most of the next 2 days pulling together all of my notes for presentation to our SF Bay Area MM Support group. If you want a copy, just reply to the blog with your email information or contact me through the IMF.
Thanks for reading,