Glioma, the most prevalent form of adult brain cancer, has a five-year progression-free survival of <5% and is exceedingly difficult to manage. In the lab we explore the interface between gliogenesis and glioma tumorigenesis. Previously we and others implicated glial cell fate determining factors –such as NFIA– in glioma formation suggesting that transcriptional regulators of developmental gliogenesis are reutilized during glioma tumorigenesis. This type of developmental interface with malignancy is very poorly defined in glioma. Drawing parallels between development and disease provides a means to identify new mechanistic avenues to explore that may lead to new treatments
During her post-doc Dr. Glasgow determined that NFIA is critical for glioma tumorigenesis and that NFIA has a function in the developmental trajectory of gliomas, where it influences glioma subtypes. In separate studies she found that the Nfia locus forms the developmental glial-specific architecture in malignant glioma and that this chromatin conformation is necessary for NFIA expression in glioma. However, the mechanisms for this activity are unknown. Currently we are exploring this question as will as the role of chromatin architectural proteins on glioma formation.