Australian researchers have tracked an elusive cancer-promoting gene that appears to be behind aggressive breast cancers, paving the way for crucial therapeutic drug treatment for the deadly disease, NDTV reports.
Researchers from the University of Queensland, together with Albert Einstein College of Medicine in the US, developed a statistical approach "to reveal many previously hard-to-find genes that contribute to cancer", Xinhua news agency reported.
"Even if a group of people all have the same type or even subtype of cancer, the molecular make-up of that cancer is different from person to person because the activity of genes varies between people," said Jess Mar, Associate Professor at the varsity.
In the study, published in the British Journal of Cancer, the team used a method to "zoom in" on genetic information from cancer patients and identify genes with two distinct "bumps" of data -- low activity in one group of patients but high activity in another.
Analysing breast cancer data from a major cancer genome patient database, the researchers identified five genes that were "over-active" in a subset of breast cancer patients and followed up on the most promising target, known as CBX2.
"Previous studies have shown that most healthy female tissue has low levels of CBX2 activity, while an aggressive subtype of breast cancer has been shown to have high levels of CBX2 activity," Mar said.
"This suggested a possible link between CBX2 activity and breast cancer, but the nature of that link hadn't been investigated," she said.
"So we switched off the gene in a human breast cancer cell line and this slowed down the growth of those cancer cells, suggesting that CBX2 might promote tumour growth."
If further tests confirmed that CBX2 was an "oncogene", it could be a potential therapeutic drug target for aggressive types of breast cancer, Mar said.
"Identifying 'hidden' oncogenes that are unique to smaller groups of cancer patients will open up new therapeutic avenues and move us closer to personalized medicine," she said.