May 6, 2003 A significant breakthrough by scientists at Cardiff University and the University of Edinburgh will enable new drugs to be developed, which could prevent bowel cancer.
Researchers led by Professor Adrian Bird at Edinburgh and Professor Alan Clarke at Cardiff have discovered a gene, called MBD2, which is essential for bowel cancer cells to grow, but is dispensable in normal cells. The findings of the research, funded in part by the Wellcome Trust and published in the journal Nature Genetics, raise the possibility that drugs which inactivate MBD2 could prevent human bowel cancer without harming normal cells. Bowel cancer is the UK's second most common cause of cancer death, after lung cancer.
Cancer is caused by cells that escape the body's controls and multiply aggressively to make a tumour. Most anti-tumour therapies attack these multiplying cells, but in doing so they also kill normal cells, such as skin cells and blood that must be able to multiply in any healthy person.
The new findings show that MBD2 is needed much more by tumour cells than by healthy cells and may therefore represent a medical Achilles' heel for this type of cancer. As yet there are no anti-MBD2 drugs, but there is now a strong case for developing them as potential anti-cancer agents.
Professor Clarke, of Cardiff University's School of Biosciences, said: "Our research provides a significant breakthrough in understanding the pathways that can lead to bowel cancer. Cancer is primarily caused by irrevocable alterations to genes, called mutations. Recent work has revealed, however, that some key genes in cancer cells are altered in more subtle ways that are potentially reversible.
"The new findings reinforce this idea, as MBD2 is known to silence genes that have no mutations in them. It now seems that colorectal cancer depends on this kind of gene silencing, whereas normal tissues can remain healthy without it. The exciting possibility is therefore that colon cancer will be treatable by drugs that interfere with the gene silencing process by targeting MBD2."
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