• Enzyme Block Slows Pancreatic Cancer Growth 
    Maggie blanks

News & Views

Enzyme Block Slows Pancreatic Cancer Growth 

Mar 30 2014

A research team from Imperial College London has shown that blocking the function of an enzyme known as Hhat slows the growth and spread of pancreatic cancer, by preventing a protein called Hedgehog from stimulating nearby normal cells to help the cancer.

The study, funded by the UK research charity Pancreatic Cancer Research Fund, examined the role of Hedgehog, whose usual job is to send signals to cells in embryos to divide and grow into the correct body parts. But while Hedgehog usually switches off when the embryo is formed, in many cancers, including pancreatic, it becomes abnormally reactivated. 

Says lead researcher Professor Tony Magee: “Signalling pathways are complex. They’re like a flow diagram, with a multitude of arrows travelling along and splitting off at many points along the way, each initiating a new chain reaction of activity.  Whilst you could potentially stop the Hedgehog signal at many points along its journey, we wanted to see if we could simply prevent the process from starting in the first place. This meant stopping Hhat from attaching a fatty molecule to Hedgehog, which is needed for the signalling.”

Professor Magee, with his collaborator Dr Ed Tate, is planning to screen a huge library of molecules for possible drug candidates that can be developed to replicate this Hhat process in humans.

Maggie Blanks, CEO of the Pancreatic Cancer Research Fund, said: “Professor Magee’s findings add further weight to a growing body of evidence which points to Hedgehog signalling as an important driver of pancreatic cancer. To prevent this signalling pathway at its starting point is both a simple and ingenious approach that could herald the development of a new treatment. As developing new treatments and early detection methods are the core focus of the Pancreatic Cancer Research Fund, we await further announcements with great anticipation.”

*The findings are published in PLOS ONE.


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