Friday, May 14, 2010

New findings could advance fight against BC

Recent findings by scientists could help advance the fight against breast cancer (BC). A team at the University of Kentucky (UoK) Markey Cancer Center has identified a key molecular mechanism in BC that enables tumour cells to metastasise, while a separate study has uncovered five new regions of the genome that increase a woman's risk of developing the disease by between 6 and 16 per cent.

The work conducted by the UoK could lead to new lines of research aimed at developing treatments for metastatic BC (MBC). The research, published in the 13th April online issue of The EMBO Journal (10.1038/emboj.2010.63), focused on the process by which tumour cells stop clinging to other cells and become motile. The increased motility of tumour cells at the initial step of metastasis is similar to epithelial-mesenchymal transition (EMT). In all EMT processes, cells lose the expression of E-cadherin, which functions as a "molecular glue" that attaches cells to one another. The team explained that when E-cadherin is broken down, tumour cells start to migrate and spread throughout the body.

A protein called Snail acts as a master switch in the cell's nucleus to suppress E-cadherin expression and induce EMT in the cell. Agents that can disrupt the interaction of Snail are thought to have great therapeutic potential for treating MBC. Leading on from these findings, the scientists at the UoK are keen to develop drugs that can treat metastatic cancer.

Separately, a study funded by Cancer Research UK (CRUK) and the Wellcome Trust has found five new regions of the genome that increase a woman's risk of developing BC by between 6 and 16 per cent. As more of these low-risk sites are found, scientists believe that it may be possible to create tests for a combination of them that together significantly increase risk, which could ultimately help doctors to make decisions about prevention, diagnosis and treatment for women who are more likely to get BC.

The scientists scanned the entire genetic code of over 4,000 women with BC and a family history of the disease for genetic variations that appeared more often compared to healthy women. They then tested the most promising regions in over 12,000 women with BC and 12,000 women without the disease in an international collaboration. Although the results now take the total number of gene regions linked to the risk of BC to 18, scientists are still unsure which genes are causing this increased risk. Lead author, Professor Doug Easton, director of CRUK's Genetic Epidemiology Unit at the University of Cambridge, commented: "While each of these sites have a small impact on breast cancer risk, by finding more of these genes, we may be able to develop a test that can predict more reliably a woman's risk of developing breast cancer."

Alice Rossiter - Editor, Cancer Drug News

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