Children with Neurofibromatosis type 1 (NF1) are prone to the development of brain tumors, specifically low-grade gliomas of the optic nerve, called optic pathway gliomas (OPGs). These tumors contain a mixture of cancer and non-cancer cells, each important for tumor formation and growth. However, all of our current therapies focus on cancer cells with variable success.
In an effort to develop new treatments that target the non-cancerous immune cells in NF1-OPG, researchers in the Gutmann Laboratory at Washington University used mice genetically engineered to develop optic gliomas. Postdoctoral fellows, Drs. Jit Chatterjee and Amanda Costa, teamed up to determine when immune cells, specifically microglia and T cells, first appear in these tumors and when they produce small signaling molecules that support optic glioma progression.
By blocking these signaling molecules, called chemokines or cytokines, during the times when they are first expressed, Chatterjee and Costa showed that mice did not develop optic gliomas. Moreover, these effects were long-lasting, with mice not showing any evidence of tumor formation months after initial treatment.
These exciting findings suggest that NF1-OPG formation and progression can be prevented by interrupting immune system cell function, opening the door for more refined approaches to treating brain tumors arising in children with NF1.
This study was published in Neuro-Oncology Advances.