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Better prediction of brain cancer outcome

26 June 2012



Assoc Prof Lim (seated, second from right) with his team of researchers

Glioma cells Parkin-expressing glioma cells

Soft agar cancer assay (right) showing the dramatically reduced tendency of parkin-expressing glioma cells to form colonies
Singapore scientists at NUS, National Neuroscience Institute (NNI) and Singapore Institute for Clinical Sciences (SICS) have found the reason behind the fast progression of some brain cancers that can kill patients within a year.

Until now, little is known why glioblastoma multiforme (GBM), the most aggressive form of glioma brain tumour, can develop so rapidly. The multi-institutional study, led by Assoc Prof Lim Kah Leong at the NUS Yong Loo Lin School of Medicine's Department of Physiology, determined that parkin, a tumour suppressor, plays a role in reducing the tumour's growth. The level of parkin expression in glioma cells can affect the progression of the disease and survival - patients with more parkin in their cancer cells survive longer with lower grades of tumour.

This discovery could mean more targeted treatment and better prediction of outcomes, noted Assoc Prof Lim. "Instead of generalising malignant brain cancer patients, we can now differentiate their tumours based on their molecular characteristics. This is impactful as the molecular differences in gliomas cannot be accounted for by histology alone, which currently determines the treatment regimens. In essence, our finding will help improve the diagnosis, prognosis and potentially treatment of brain cancer patients," he explained.

Other investigators of the work published recently in leading journal Cancer Research included Dr Carol Tang, Research Scientist at NNI, and Assoc Prof Ang Beng Ti, Consultant at NNI's Department of Neurosurgery and a senior principal investigator at SICS.

Brain cancer affects about 3.5 per 100,000 individuals globally; this means about 700 people worldwide are diagnosed with a malignant brain tumour every day. The prognosis for the majority of these tumours remains grim, especially for patients with GBM. Even with the best drug-of-choice, patient outcome is only about a year of survival following diagnosis.

"We are trying to screen for compounds that can mimic parkin-mediated tumour suppressing effects," Assoc Prof Lim revealed. Of particular interest is the effect of drugs that regulate the cancer-related pathway which parkin acts on.

Notably, scientists have recently shown that parkin gene mutations occur frequently in a wide variety of tumours. Depending on the cell type involved, parkin may act as a cell protector (in nerve cells) or tumour suppressor (in dividing body cells).


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