Faster way to track genetic mutations that cause cancer found

Washington: Scientists claim to have successfully devised a faster and cheaper method to uncover genetic changes that cause cancer, which can help develop personalised medicine for treatment of the deadly disease. By studying fruit flies, researchers at ASTAR’s Institute of Molecular and Cell Biology (IMCB) will now be able to rapidly distinguish the range of genetic changes that are causally linked to cancer like, “driver” mutations, versus those with limited impact on cancer progression. [caption id=“attachment_398770” align=“alignleft” width=“380”]  Agencies[/caption] This research paves the way for doctors to design more targeted treatment against the different cancer types, based on the specific cancer-linked mutations present in the patient. The study is published in the journal Genes & Development. “Many genetic changes arise in cancer cells and changes continue to accumulate during the progression of disease to metastatic cancer. The current challenge is to understand which of the many genetic changes are important drivers of disease progression” said Dr Stephen Cohen, Principal Investigator at IMCB and team leader of the report. Though very different in many ways, fruit flies and humans share similarities in a remarkable two-thirds of their genomes. Many of the genes found in humans are also present in the flies. Similarly, various signalling pathways involved in tumour formation are also well conserved from fruit flies to humans. Studies have shown that about 75 percent of known human disease genes have a recognisable match in the genome of fruit flies. Leveraging on their genetic similarities, Dr Hector Herranz, a post-doctorate from the Dr Cohen’s team developed an innovative strategy to genetically screen the whole fly genome for “cooperating” cancer genes. These are the genes that appear to be harmless and have little or no impact on cancer. But in fact, they cooperate with other cancer genes, so that the combination causes aggressive cancer. The team was specifically looking for genes that could cooperate with EGFR “driver” mutation, a genetic change commonly associated with breast and lung cancers in humans. SOCS5, is one of the several new “cooperating” cancer genes to be identified through this innovative approach. Most of these new-found genes have yet to be identified as cancer genes in human or mouse models. PTI