Sydney, Aug 13 (IANS) A new discovery about where and how the most malignant type of brain tumour originates could spur better therapies and improve understanding of how tumours are initiated. A team of scientists, led by Brandon Wainwright from the Institute for Molecular Bioscience at the University of Queensland, Australia and Robert Wechsler-Reya from Duke University in the US, studied medulloblastomas, which mostly afflicts children.

“Almost half the people who develop these tumours die from them, and those who survive often suffer severe side effects from the treatment,” Wainwright said. “Improved treatments are urgently required, but in order to develop these, we need a deeper understanding of the molecular and cellular origins of medulloblastomas.”

The team found that medulloblastomas can originate from two types of cell: multipotent neural stem cells (NSCs) and granule neuron precursors (GNPs).

NSCs are stem cells that can become most types of cell within the nervous system, while GNPs are similar to stem cells but only give rise to one type of cells, known as granule neurons.

“There was good evidence that either cell type could be the origin of medulloblastomas, but no one considered that both sets of evidence could be correct, and that these tumours could actually begin in two different cell types,” Wainwright said.

“Identifying the normal cell that gives rise to a tumour is important because it allows direct comparisons between tumour cells and their normal counterparts so that key differences and vulnerabilities in the tumour can be identified,” he said.

“Also, recent studies suggest that cells resembling the original cell may persist in mature tumours and can be critical in ensuring its survival. If so, these cells would be an excellent target for treatment.”

The team made their discovery by examining a gene called Patched, which is involved in the regulation of both neural stem cells and GNPs. When the gene is inactivated, medulloblastomas develop.

However, when inactivation occurs, it happens in all cells, so there was no way of knowing in which cell the tumour had begun. The team took advantage of an allele, or version, of Patched that allows inactivation of the gene in either GNPs or neural stem cells, and found that the tumours developed no matter in which cell Patched was inactivated.

The study could also have wider implications for treating other types of cancer, as the team also found that cancer doesn’t always originate in the same way.

The study was published in the scientific journal Cancer Cell.