p53 and NF 1 loss plays distinct but complementary roles in glioma initiation and progression.

Malignant glioma is one of the deadliest types of cancer. Understanding how the cell of origin progressively evolves toward malignancy in greater detail could provide mechanistic insights and lead to novel concepts for tumor prevention and therapy. Previously we have identified oligodendrocyte precursor cell (OPC) as the cell of origin for glioma following the concurrent deletion of p53 and NF1 using a mouse genetic mosaic system that can reveal mutant cells prior to malignancy.

Transformation of quiescent adult oligodendrocyte precursor cells into malignant glioma through a multistep reactivation process.

How malignant gliomas arise in a mature brain remains a mystery, hindering the development of preventive and therapeutic interventions. We previously showed that oligodendrocyte precursor cells (OPCs) can be transformed into glioma when mutations are introduced perinatally. However, adult OPCs rarely proliferate compared with their perinatal counterparts.

Inflammation and Gliomagenesis: Bi-Directional Communication at Early and Late Stages of Tumor Progression.

Inflammation has been closely linked to various forms of cancer. Less is known about the role of inflammation in glioma, especially at the initiation stage. In this review, we first describe the unique features of the immune system in the brain.