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An expert panel hosted by
Sequencing immune-based therapies in B-cell malignancies
with Ulric Jäger, Sagar Lonial, and Krina Patel
Saturday, June 15 | 18:00-19:30 CEST
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T-cell-engaging therapies function to form an immune synapse between immune effectors and multiple myeloma (MM) cells. The transient durability of clinical response associated with T-cell engagers, and the mechanisms underlying these, are not fully understood. However, antigen escape is one of the key mechanisms that has been linked to resistance to T-cell engagers.1
Here, we summarize a presentation by Paola Neri,1 presented at the 5th Immune Effector Cell Therapies in Multiple Myeloma Workshop on the mechanisms of antigen escape after T-cell-redirecting therapies.
Figure 1. Antigen escape as a mechanism of resistance to CAR T-cell therapy*
CAR, chimeric antigen receptor; MM, multiple myeloma.
Created with BioRender.com.
*Adapted from Golden, et al.3
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