'Dead end' gene clue to testicular cancer

Scientists have discovered a gene that could be responsible for causing testicular cancer, it was announced today.

A US team has found that when a gene, dubbed "dead end", is either missing or damaged it causes cancer in mice.

The same gene is present in humans and it is hoped a screening test could be developed in future to identify men at high risk of the disease.

Testicular cancer primarily affects men aged between 20 and 44 years. Although cases have doubled in the last 40 years it is still relatively rare with about 2,000 cases diagnosed in Britain each year.

The research published in the online journal Nature may offer an explanation for some cases of testicular cancer in the same way genes have been found to be responsible for about 20 per cent of breast cancers.

Angabin Matin, an assistant professor in the Department of Molecular Genetics at the University of Texas, said: "One can envision that this gene or others in its pathway could possibly be used for screening or therapeutic purposes in young males predisposed to develop testicular cancer."

The team also found a link between infertility and testicular cancer, observing that when fish did not have the dead end gene they were unable to reproduce.

Create a FREE account to continue reading

eros

Registration is a free and easy way to support our journalism.

Join our community where you can: comment on stories; sign up to newsletters; enter competitions and access content on our app.

Your email address

Must be at least 6 characters, include an upper and lower case character and a number

You must be at least 18 years old to create an account

* Required fields

Already have an account? SIGN IN

By clicking Create Account you confirm that your data has been entered correctly and you have read and agree to our Terms of use , Cookie policy and Privacy policy .

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Thank you for registering

Please refresh the page or navigate to another page on the site to be automatically logged in

MORE ABOUT