Amy B. Heimberger, MD, discusses the potential of FGL2 as a multi-modality regulator of tumor-mediated immune suppression in patients with glioblastoma.
Amy B. Heimberger, MD, professor, Department of Neurosurgery, The University of Texas MD Anderson Cancer Center, discusses the potential of FGL2 as a multi-modality regulator of tumor-mediated immune suppression in patients with glioblastoma. Heimberger presented on this topic at the 2015 Annual Meeting of the Society for Neuro-Oncology.
There is a lot of excitement surrounding immunotherapies and immune checkpoint inhibitors in glioblastoma, Heimberger says. It’s also understood that the mechanisms that the tumor uses for immunosuppression are very heterogenous. Because of this, Heimberger and her colleagues are researching pathways or mechanisms that deal with more than one mechanism of immune suppression.
FGL2 is a secreted protein that exploits multiple mechanisms of immune suppression to “stay behind” the detection of the immune system, Heimberger says. As FGL2 works on more than just immune checkpoints, Heimberger thinks that it could have a more profound impact for patients and could ultimately help more patients.