Grand Island

The American Society of Hematology (ASH) Annual Meeting is by far the most exciting meeting of the year for those of us with myeloma. Clinical trials are updated, new drugs are discussed, and promising treatment combinations are presented.

Excitement of support group leaders (SGLs) at the 56th American Society of Hematology (ASH) Annual Meeting and tremendous progress against myeloma come together in oral presentations, posters, and abstracts in which minimal residual disease (MRD) is discussed.

Myeloma is an incredibly complex genomic disease. Gene alterations can cause cell metabolic pathways to become activated or silenced. If pathway activation causes an oncogene (tumor promoter) to become more highly expressed, aggressive cancers are quite likely to develop. On the other hand, inactivation of a tumor suppressor gene can cause cancers to grow unimpeded by the body’s normal immuno-protective mechanism. Immunotherapy research aims to promote tumor suppressor genes and impede naturally occurring oncogenes.

It is interesting that my favorite moment at the 56th American Society of Hematology (ASH) Annual Meeting corresponds quite directly with my least favorite moment. Myeloma therapy has undergone an unprecedented change the last decade and new therapies have extended our median survival to much longer than it was ten years ago.