A recent article in the New York Times draws attention to how cancers survive and evade the immune system and highlights a new book, "The Compatibility Gene: How Our Bodies Fight Disease."  The key point for myeloma research is that inactivation of T-lymphocyte cells and natural killer cells--which should be killing myeloma cells--occurs through a mechanism called the PD-1/PD-L1 system.

 

The way it works is that the myeloma cells and many other types of tumor cells have many PD-L1 receptors on their surfaces. These receptors work as a protective shield because the PD-L1 triggers the surrounding immune cells to stop working - allowing, for example, myeloma cells to grow. Research in other cancers is much further along, and novel anti-PD antibodies have been developed which block this process and allow the immune cells to attack those cancers.  There has been great success with this in patients with melanoma, some of whom have had dramatic remissions.

 

What about myeloma? The research is not as far along, but one anti-PD1 antibody (CT-011) has been used in early testing and shows benefit.

 

This is exciting because it provides an entirely new approach to attack myeloma.  Dr. David Avigan and the research team at Beth Israel Deaconess Medical Center in Boston are exploring the use of the CT-011 anti-PD antibody therapy as part of a vaccine approach to myeloma therapy. Early results are promising.

 

So, a better understanding of what can be wrong with the immune system in myeloma patients is leading to ideas about how best to fix the problem! Stay tuned. I am sure further progress will be reported and next steps developed to improve responses and outcomes for myeloma.