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UT Southwestern researchers have discovered a biochemical mechanism underlying the spread of glioblastoma to adjacent brain tissue as well as a medicine that has previously been shown to slow tumour development in animal models.

The results, which were published in Nature Cell Biology, sparked a clinical trial that may provide patients with glioblastoma, the most prevalent type of adult brain cancer that claims hundreds of thousands of lives annually throughout the world, with new hope.

"Glioblastoma's invasive property is perhaps its most formidable barrier to treatment," said Amyn Habib, M.D., Associate Professor of Neurology, member of both the Harold C. Simmons Comprehensive Cancer Center and Peter O'Donnell Jr. Brain Institute at UTSW and a staff physician at the Dallas VA Medical Center. "We have identified a pathway that can suppress this cellular invasion, which could offer a new way to increase survival."

Despite decades of study, the outlook for the majority of glioblastoma patients is still grim, with a median survival time of just 15–18 months following diagnosis. The invasiveness of this cancer makes it tough to treat since it invades good brain tissue nearby and sends tentacle-like extensions out from the central tumour that are impossible to eliminate with surgery alone and challenging to reach with chemotherapy.

Epidermal growth factor receptor (EGFR), a protein that resides on the surface of cells, has long been thought to be the primary cause of this malignancy, according to Dr. Habib. The EGFR gene is amplified in about half of glioblastoma patients, which causes glioblastoma cells to create more molecular signals that are stimulated by this protein and promote the growth of tumour cells. Therefore, Dr. Habib continued, a number of clinical trials have concentrated on reducing EGFR, but none of them have succeeded in improving the prognosis for glioblastoma.

These signals can be sent by EGFR in glioblastoma cells in two different ways: either automatically, in a situation known as constitutive signalling, or in response to ligand stimulation. According to Dr. Habib, the distinctions between these two paths have been deemed irrelevant. Patients with increased EGFR in glioblastoma have been pooled together in clinical studies as a result.

Dr. Habib and colleagues from the Habib lab and other institutions demonstrated in the new study that when cells with amplified EGFR were stimulated with ligands, this receptor appeared to operate as a tumour suppressor, limiting invasion into healthy tissue in both laboratory and animal models.

Further experiments showed that a cytoskeletal protein called BIN3 appears to be responsible for inhibiting this invasion. When the researchers dosed animals with amplified EGFR glioblastoma tumours with an FDA-approved arthritis drug called tofacitinib that increased the amount of EGFR ligands and BIN3, tumours remained smaller and were less likely to invade healthy brain tissue. Additionally, these animals survived significantly longer than animals that didn't receive this drug.

Dr Habib noted that tofacitinib could offer a new way to extend life for patients with both amplified EGFR and a relatively high level of EGFR ligands, a strategy he and his colleagues will explore in a clinical trial launching in September. For patients without high ligand numbers, he added, strategies previously explored to inhibit EGFR could potentially extend survival.

"These approaches could offer new tools in our arsenal to fight glioblastoma," Dr Habib said.

(With ANI inputs)

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