Researchers at Sylvester Comprehensive Cancer Center at the University of Miami Miller School of Medicine are part of an international team of scientists who identified mechanisms by which some multiple myelomas become resistant to initially effective T-cell therapies.
Targeted T cells can be rendered useless if the antigen they're tracking mutates, essentially disappearing from the radar screen. Here, the researchers report mutations that thwart immunotherapies engineered to seek out two targets in multiple myeloma, allowing previously treated cancers to adapt, escape treatment and relapse.
"Recognizing these mutations and gaining a clearer understanding of the resistance mechanisms to these potent immunotherapies is pivotal," said Francesco Maura, M.D., whose lab at Sylvester conducts myeloma computational and translational research. "This knowledge plays a crucial role in devising tailored strategies and making informed choices regarding the selection of products and targets for individual patients." Maura is a senior author of the research published in"Antigenic drift" is well established as a mechanism that tumors employ to develop resistance to immunotherapy.
Over time, however, and as the cancer cells change, effectiveness often wanes. Few studies have been done to identify the reasons for this diminishing—and this is believed to be the first genomic study of"intrinsic" mechanisms of cancer cells that permit antigen escape in patients who relapsed after undergoing these immunotherapeutic approaches.
"We identified distinct and novel genomic events responsible for resistance to anti-BCMA and anti-GPRC5D immunotherapies," said C. Ola Landgren, M.D., Ph.D.
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