Researchers have found a genetic signature within long tumors that seems to predict whether an immunotherapy drug will work and who will benefit most.
This new immunotherapy drug unleashes the immune system on tumors and has had remarkable success, but only for some cancer patients.
Tumor cells can hid from the immune system by activating a receptor, on the surface of the immune cells known as T cells. Instead of attacking the tumor cells, the T cells leave the tumor cells alone.
The new drug is an antibody that inhibits the receptor and frees the T cells to wipe out the tumor cells.
In clinical trials the receptor blockers and other checkpoint inhibitors have extended the lives of patients with several cancer types for years, far longer than conventional treatments.
The U.S. Food and Drug Administration have approved several of these drugs for melanoma.
Unfortunately, checkpoint inhibitors work only for some people and researchers are scrambling to figure out why.
One hypothesis is that checkpoint inhibitors are more likely to work on tumors that have more mutations.
Some recent studies support this view. Melanoma patients with more neoantigen-coding mutations in their tumors were more likely to respond to a checkpoint inhibitors that blacks a protein called CTLA-4.
The same also hold true for lung cancer.
The study found that patients are much more likely to respond to the drug if their tumor had more of the type of mutations that result in an altered protein. For example, 72% of the patients with at least 178 mutations responded for 6 months or longer compared with 8% of those with fewer mutations.
Researchers are also exploring the possibility of giving patients a personalized vaccine made from the neoantigens in their tumor to bolster their response to a checkpoint inhibitor.
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