Glioblastoma is among the most aggressive and devastating of cancers. While rare compared with other cancers, it's the most common type of brain cancer. Even with intensive therapy, relatively few patients survive longer than two years after diagnosis, and fewer than 10% of patients survive beyond five years. Despite extensive studies focused on genomic features of glioblastoma, relatively little progress has been made in improving treatment for patients with this deadly disease.

To improve therapies for this deadly cancer, understanding the tumor cells themselves is important but not enough," said senior author Li Ding, Ph.D., a professor of medicine and of genetics and director of computational biology in the Division of Oncology at Washington University. "We also must understand the tumor cells' interactions with the surrounding environment, including immune cells and the connective tissues and blood vessels. In our study, we performed high-resolution and high-depth analyses on 99 glioblastoma tumors. Harnessing new technologies, including proteomics, metabolomics and single cell sequencing, this study is an extremely deep dive into glioblastoma tumor biology, revealing new possibilities for therapy."

The study identified new activated proteins—particularly PTPN11 and PLCG1—that serve as signaling hubs driving tumor growth in some patients; revealed gene expression patterns involved in a process called epithelial-to-mesenchymal transition that is common in tumor formation; identified four different categories by which to classify glioblastoma, based on the number and types of immune cells present in the tumors; and determined how an understudied protein modification, acetylation, may explain some functional differences between glioblastoma subtypes. These patterns provide additional information for researchers to understand how the glioblastoma subtypes they identified may vary in biological function," Liu said. "This multifaceted analysis provides an unprecedented level of detail, which is starting to connect the missing dots in glioblastoma.

Regards

John
Editorial Assistant
Immunogenetics Open Access