According to a recent groundbreaking research article:
"Meningioma accounts for 37% of primary brain tumors. This year in the United States an estimated 32 000 people will be diagnosed with meningioma. These tumors can cause mild to severe morbidity and even WHO grade I can have a more aggressive clinical course. Therapeutic options are still limited to surgical resection and radiotherapy since more effort is needed to decipher the communal molecular mechanisms that define meningiomas despite their genetic background. Aiming to discover novel therapeutic targets, we identified STAT1 as aberrantly overexpressed and constitutively activated in most of the meningiomas examined. Its activation is dependent on the constitutive phosphorylation of EGFR and leads to increased proliferation of tumor cells. We show that specific EGFR inhibition can reduce tumor cell proliferation and we show evidence why previous trials failed.
The STAT1 gene was found to be ‘overexpressed’ meaning that the tumour grew in response to “instructions” from the STAT1 protein following the addition of a phosphate molecule. Further research showed it to be the epidermal growth factor receptors (EGFR) that were ‘driving’ these STAT 1 genes. In their research the team used drugs known to affect the biological pathways that block the EGFR, stopping it from working.
Brain tumors remain a leading cause of death for young people, and the most common cancer for young people. Therefore, this is vital work as Meningiomas are the most commonly diagnosed primary brain tumours and although patients can live for many years with these tumours no effective chemotherapy or drug options are available. Surgery often leads to more disadvantages for the patient, with life threatening complications. Targeting meningiomas with drugs is an ideal treatment option, that we all hope to become as soon as possible available.
The article concludes:
"We provide clear evidence of STAT1 overexpression in meningioma of different genotype and its correlation with increased cellular proliferation. We demonstrate that STAT1 is aberrantly phosphorylated on both phosphosites, not because of the JAK–STAT pathway activation but because of the constitutive phosphorylation of EGFR, which elicits activation of the MAPK–ERK and PI3K–AKT pathways and an increase in the overall levels of cyclin D1 and STAT1. Although the whole mechanism should be additionally studied to give a thorough understanding of the activating cascade and all the partners involved in it, our studies set the basis for re-evaluating EGFR inhibition in meningioma as a possible therapeutic option."