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Sydney 2005:
Tumor Immune Interactions in Myeloma
By Madhay Dhodapkar, MD
Dr. Dhodapkar opened the session providing an overview of research conducted by his research group over the last year. Topics they are exploring include: patient variability of the immune system, manipulations of the immune system, non-immune effects of immune cells, and cell targets of novel therapies. Phase 1 trial data exploring whether natural killer T (NKT) cells could be reliably and specifically manipulated in patients shows that it is possible to expand the number of NKT cells in patients. These cells mediate activation of T cell immunity by a third party dendritic cell (DC) in vivo. The question of how to maintain the expansion of NKT cells in patients by vaccines is being explored. Notably, NKT cells in patients with MM do not work as well as NKT cells from healthy individuals. Dr. Dhodapkar also looked at the potential targets of drugs on T/NKT cells. Revlimid boosts antigen dependent activation and expansion of specific NKT cells. Tumor DC interactions inhibit dexamethasone induced suppression of myeloma. Myeloma cells were thought to be more sensitive to bortezomib (velcade) however DC were shown to be equally sensitive to velcade as myeloma cells. Dr. Dhodapkar suggested that effective suppression of myeloma requires that myeloma cells and DC be targeted by velcade. Some conclusions from this research were that there is a loss of immune effector function in both innate and adaptive lymphocytes with tumor progression and that interactions between cells in the microenvironment may be involved in drug resistance or may be targets for proteasome-targeted drugs. Future research may address tumor specificity or prevention.

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