MD Anderson study shows FGL2 protein may be an effective target for glioblastoma
Researchers at The University of Texas MD Anderson Cancer Center have discovered an immune regulator that appears to dictate glioblastoma (GBM) progression by shutting down immune surveillance, indicating a potential new area of therapeutic investigation.
Findings from the preclinical study led by Shulin Li, Ph.D., professor of Pediatrics, and Amy Heimberger, M.D., professor of Neurosurgery, were published.
“Classical wisdom is that brain tumor progression is linked to oncogene activation and tumor suppressor gene inactivation; however genetic and epigenetic mutations are not the only cause of GBM progression,” said Li. “Some immune regulators can do the same thing and are key regulators of cancer, especially in certain tissues and environmental contexts.”
GBM, unlike melanoma and lung cancers, does not attract robust T cell immune responses, and, so far, immunotherapies have had little success against it. GBM is considered “immunologically cold” or unreactive likely due to tumor elaborated immune suppressive factors.
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