Gene plays 'Jekyll and Hyde' in br...(functions such as providing nutrients to...),Health

Bonni, a neurologist and neuroscientist by training, decided to investigate the genetic etiology of glioblastoma by studying whether certain regulatory genes that control the generation of astrocytes during normal development also play a role in these tumors. The logic here is simple: since disease is often the breakdown of a normal biological process, the more we understand how cells get it right, the more we understand what can go wrong. And since STAT3 is a key gene that turns neural stem cells into astrocytes during normal development, what is its role in glioblastoma"

Bonni and two lead authors, Nria de la Iglesia and Genevieve Konopka, in collaboration with investigators in the laboratory of Ronald DePinho at the Dana-Farber Cancer Institute, began by genetically manipulating mouse astrocytes, then placing them into a second group of mice whose immune systems had been compromised. The findings surprised them.

Taking advantage of previously published data, the researchers looked closely at how two genes, EGFR and PTENwhose mutated forms are associated with glioblastomaaffect the function of STAT3 in astrocytes. Bonnis group found when EGFR is mutated, STAT3 is an oncogene; with a PTEN mutation, STAT3 is a tumor suppressor.

EGFR, in its normal state, is a transmembrane receptor, usually performing its functions at the cell surface, says Bonni. However, when its mutated, we find it in the cells nucleus interacting with STAT3and turning it into an oncogene. STAT3 itself is not mutated or damaged. Its the process of regulating STAT3 that gets damaged.

With PTEN, its a completely different story. PTEN is itself a tumor suppressor gene. When PTEN becomes disabled in astrocytes, these potential tumors still have STAT3 standing in their way
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