Glioblastoma cell patterns found

Swedish researchers have reported progress in understanding the cellular origins of different types of glioblastoma tumours.

These brain tumours vary widely, partly depending on the different kinds of brain cells in which the tumour originated. Because this heterogeneity is limiting the discovery of effective therapies, researchers at Uppsala University, Sweden, investigated further.

Dr Lene Uhrbom and colleagues explain that a tumour’s cell of origin can be either an immature neural stem cell or a more differentiated glial cell. They carried out tests using mice, analysing how the activity of a many genes differed between tumours with different origins.

This showed that tumours originating from immature neural stem cells develop faster than those from more differentiated glial cells.

Dr Uhrbom says: "We discovered that several important characteristics of the cancer cells could be linked to the tumour’s cell of origin. Immature neural stem cells gave rise to glioblastomas that grew faster and were more malignant than those that originated from glial cells.

"Tumours from neural stem cells also contained more glioblastoma stem cells, cells that are believed to give rise to tumour recurrence after therapy."

The team also compared the gene activity of glioblastoma cells from about 60 human patients. This also showed that patients could often be divided into subgroups that showed a link between gene activity, tumour cell characteristics, and cell of origin.

"The cell of origin has a direct influence on the characteristics of human tumours," says Dr Uhrbom.

There was also a correlation between the cell type of origin and sensitivity to cancer drugs, they found.

"We hope the gene signature we identified can provide the basis for an improved classification of glioblastoma patients and for identifying new targets for therapy," Dr Uhrbom concludes.

Jiang, Y. et al. Glioblastoma cell malignancy and drug sensitivity are affected by the cell of origin. Cell Reports 25 January 2017; doi: 10.1016/j.celrep.2017.01.003 [abstract]