New drug discovered to treat bowel cancer

Washington D.C. : Briton researchers have recently discovered a new drug target for bowel cancer that is specific to tumour cells and less toxic than conventional therapies to treat the disease.

 Most bowel cancers are caused by a mutation in a gene called APC that in its healthy form acts to prevent cancer formation. Mutated APC genes cause excess activity of a cell signalling pathway called 'Wnt', which has been associated with bowel cancer for over 20 years.

They found a way to exclusively target 'Wnt' signalling in tumour cells that reduces growth of tumours derived from colon cancer cells without the toxic effects on healthy cells.

First author Laura Novellasdemunt from the Francis Crick Institute---a research institute in London---said that for long there has been a need to find more effective and less toxic drugs to treat bowel cancer.

"We have found a novel drug target that could provide the basis for a better therapy in patients in the future," Novellasdemunt added.

Wnt signalling is vital for many organs, so drugs



designed to block Wnt signalling in cancer cause very toxic side effects in other parts of the body.

They used the gene-editing tool CRISPR to cut the APC gene at various positions, and found a crucial part of the gene that causes dangerous levels of Wnt signalling and cancer formation.

Using a number of molecular techniques, they identified a protein involved in over activation of the Wnt pathway in cancer.

Preventing the activity of this protein by genetic deletion or blocking it with drugs caused a reduction in Wnt signalling in cancer cells and slowed down tumour growth in mice.

Importantly, the drug was found to act exclusively on the tumour cells, and have no effect on Wnt signalling in healthy cells.

The next step will be to see if deleting the gene that makes the protein in mice will prevent them from developing bowel cancer.

This will provide further evidence that the protein is a viable anti-cancer drug target.

The findings are published in Cell Reports.