Last Saturday, Gretchen and I had the pleasure of attending the Dana Farber Patient Symposium in Boston. It's an amazing sharing event, where the doctors and nurses connect with the patients and caregivers to communicate what's going on in the MM community. As usual, Drs. Ken Anderson and Paul Richardson highlighted the event, where they focused on the latest research and results from the recent ASH Meeting. It was also an opportunity to meet other MM patients and share our stories. I give DFCI a lot of credit for spending the time to meet with us patients to connect, communicate, share, and answer questions as they did. It shows that they are not just concerned with conquering this disease, but are responding sympathetically to the issues and concerns of their patients. Very classy.
I also connected to an online video teleconference session on Monday, sponsored by the Multiple Myeloma Research Foundation (MMRF), summarizing the major news from the ASH Meeting. From both of these events, I got a pretty good idea of the current status and progress in the battle against MM.
I previously reported on the encouraging clinical trial results with Kyprolis (carfilzomib), pomalidomide, and MLN9708 presented at the meeting, which open up a lot of new opportunities for MM patients. For newly-diagnosed patients, there may not be too many improvements to the existing up-front therapies, because they already work so well. However, MLN9708 could eventually replace Velcade as an oral pill to replace infusion therapy with fewer neuropathy issues, which would be a big plus. The big news is that the options for those with relapsed/refractory Multiple Myeloma (RRMM) are improving greatly. As for Kyprolis and pomalidomide, the DFCI team thinks they are probably best left in reserve for relapsed patients, at least for now.
There is a tremendous amount of laboratory research going on to find the best way to target the MM plasma cells. One of the most intriguing presentations at the Patient Symposium was of research on immunization therapy, coupling the patients own immune cells with their myeloma cells and then re-injecting into the patient. Some trials are underway, particularly for post-transplant patients. I wish I understood the presentation better, but this person was way up in the clouds, and despite my MIT education, most of what she said eluded me completely. However, the concept is that if you can get your own body to reject the myeloma, it never forgets, which is one of the pathways to an actual cure. This is the kind of research that might eventually conquer this disease, but we have to wait and see.
It was encouraging to note the substantial progress on a number of other potential MM therapies. Myeloma cells have several surface markers that are potential targets for tracking them down and destroying them, without seriously harming the healthy cells. This is a different approach from normal chemotherapy, which targets the bad guys, but also causes a lot of collateral damage to the good guys, a lot like carpet bombing an enemy stronghold.
Without going into a lot of detail, there are a promising research and clinical trial results, including monoclonal antibodies, such as elotuzomab (targets CS1) and daratumumab (targets CD38); HDAC inhibitors, such as panobinostat and vorinostat; CDK inhibitor dinaciclib; KSP inhibitor ARRY-520; and aurora kinase inhibitor MLN8237, to mention a few. The Chinese also reported good results with a new therapy, Circularly Permuted TRAIL (CPT). It's exciting to note the progress as the researchers are homing in on specific and individual therapies to attack MM. Everyone is optimistic that there will be a lot of progress in the next few years.
It was interesting to note that there is progress in early treatment of patients with Smoldering Multiple Myeloma (SMM). Until recently, the protocol was to do watchful waiting until it developed into full-blown MM. That perspective is changing, and progress is being made in catching the disease earlier and keeping it from progressing. Several clinical trials are underway to validate this approach.
I didn't notice a lot of attention at the ASH on high-risk disease, so I asked Dr. Richardson on Saturday what progress was being made to improve prospects for people with cytogenetic abnormalities, such as t(4;14) or del(17p). His response was that both Kyprolis and pomalidomide, along with the new monoclonal antibodies, should be very effective with high-risk patients, which is good news for me!
Of course I could ramble on about more specifics, but I think this gives the general overview of where things stand in the fight against MM today. While they aren't there yet, it's an encouraging story, and with all of the energy and talent focused on this battle, I'm very encouraged that they will break down the barriers one by one until they find a way to control or even cure MM. I'm optimistic that I will still be here to benefit from their efforts.