It’s no secret that I become impatient and frustrated from time to time over the slow progress being made by researchers to understand how myeloma cells develop drug resistance. Here are notes I took at ASH in an oral session late on the last day of the meetings:
Slow progress is being made across the board. But where is the bombshell? The magic bullet?
Doesn’t mean these therapies might not help–or it isn’t interesting following all of this. But I’m tired of hearing about an 8-10 month median PFS and similarly dismal OS numbers once patients become refractory to Rev and Velcade. Let’s stop messing around and kick this thing’s butt!
OK. I feel better! This is interesting. A Phase I study of lorvotuzumab mertansine (LM) (IMGN901) in combination with Revlimid and dex for high risk patients.
Apparently, CD56+ is expressed on the surface of 78% of myeloma cells, but not healthy plasma cells. Researchers here say they can now identify patients with CD56+. The new drug is designed to bind to myeloma cell, allowing Revlimid to work better and myeloma cells to be destroyed more easily.
Heavily pretreated patients had an OS of 56% at the end of the study. A clinical response was observed in 4 out of 5 Revlimid refractory patients. Numbers are “bumped-up” a bit, because there were some patients that hadn’t used Revlimid.
I want to take a step back and define what it means to be refractory to a novel therapy. I wrote about how difficult it is to define refractory when using living, breathing patients yesterday. My myeloma specialist, Dr. Melissa Alsina, addressed that with me just before Christmas. I will share how she–and other myeloma experts–define “refractory” Tomorrow. Their thoughts may surprise you.
Feel good and keep smiling! Pat