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23 new genes linked to cancer spread

16 January 2017

By Dr Loredana Guglielmi

Appeared in BioNews 884

Researchers have identified 23 genes that are linked to metastasis – the spread of cancer cells to other parts of the body.

Once cancer has spread it becomes much harder to treat, and metastasis is the cause of 90 percent of cancer deaths. It is hoped that identifying these new genes could lead to treatments that prevent the spread of cancer.

Researchers at the Wellcome Trust Sanger Institute in Cambridge bred 810 mice that were genetically modified to be missing single genes. They injected them with melanoma skin cancer cells and assessed the spread of tumour cells to the lung. Of the 23 genes they identified as important, 19 were linked to metastasis for the first time.

Mice lacking one particular gene, Spns2, showed an increase of their immune response to cancer cells colonising the lung, reducing metastasis by 75 percent.

'We found that mice lacking Spns2 have a different ratio of immune system cells than normal, which seems to prime the immune system to remove cancer,' said Dr David Adams, lead author of the study, which was published in Nature. 'Drugs that target this [gene] could help reduce or prevent the spread of tumours through the body.'

'This work supports the emerging area of immunotherapy, where the body's own immune system is harnessed to fight cancer,' said Dr Anneliese Speak, co-lead scientist on the study. Immunotherapy approaches to treating cancer have proved highly effective, leading to complete regression of cancer in some patients.

Dr Justine Alford of Cancer Research UK, which part-funded the study said: 'This study in mice gives a new insight into the genes that play a role in cancer spreading, and may highlight a potential way to treat cancer in the future.'

'Cancer that has spread is tough to treat, so research such as this is vital in the search for ways to tackle this process,' he added.

BBC News | 12 January 2017
Cancer Research UK | 11 January 2017
Nature | 12 January 2017
Science Daily (press release) | 11 January 2017


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