16 August 2010
Washington, DC USA
In a finding that could lead to new and effective treatment for brain tumour, scientists have discovered a pathway between deadly cancerous cells which they believe could be blocked to inhibit their growth and malignancy.
An international team of scientists at the Ludwig Institute for Cancer Research (LICR) at the University of California claimed that they have found a new signalling pathway between glioblastoma multiforme (GBM) cells – the most aggressive form of malignant glioma, or brain tumour, cells.
Reporting their findings in the journal Genes & Development, the scientists said if the GBM cells are blocked or disrupted, it could significantly slow or reduce tumour growth and malignancy – the process of getting worse. According to scientists, more than other types of cancer, GBMs are diverse assemblages of cell subtypes featuring great genetic variation. Anti–cancer therapies that target a specific mutation or cellular pathway tend to be less effective against such tumour heterogeneity.
"These myriad genetic alterations may be one of the primary reasons why GBMs are so lethal," said Frank Furnari, a professor of medicine at LICR and co–author of the study.
Even with maximum effort, the median patient survival rate for a diagnosed GBM is nine to 12 months – a statistic that has not changed substantially in decades, he said. However, Furnari and his colleagues noted in GBMs only a minority of tumour cells possess a mutant form of epidermal growth factor receptor (EGFR) gene. These cells drive the tumour’s rapid, deadly growth.
Furnari said, "Most GBM tumor cells express wild–type or normal EGFR. Yet when expressed by itself, wild–type EGFR is a poor oncogene. The mutant cells are instructing other less malignant tumour cells to become more malignant," he said. "If we can inhibit or block this cellular communication, the tumour does not grow as quickly and may be more treatable," Furnari added.
Researchers have already identified two molecules that appear to trigger EGFR activity on non–mutant tumour cells. The findings may also provide clues in the bigger picture of how GBMs and other cancers survive and thrive.
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