Project No. 06

Hormone Therapy: Old Dog, New Tricks

New approaches to hormone therapy to keep it working for longer

S c r o l l   R i g h t

What could this achieve?

Hormone therapy is a mainstay of prostate cancer treatment but for many patients, it will eventually stop working. This project will explore new approaches to hormone therapy to keep it working for longer.

How?

Professor McEwan and his team will investigate novel drug combinations that target the androgen receptor, a protein which sends messages to cancer cells to tell them to grow and spread, in a different way to current hormone therapy.

The Future- whats next?

The team have identified a new drug target on the androgen receptor and a series of potential drugs. They are now looking to test whether these drugs have the potential to become new treatments.

What could this achieve?

Hormone therapy is a mainstay of prostate cancer treatment but for many patients, it will eventually stop working. This project will explore new approaches to hormone therapy to keep it working for longer.

How?

Professor McEwan and his team will investigate novel drug combinations that target the androgen receptor, a protein which sends messages to cancer cells to tell them to grow and spread, in a different way to current hormone therapy.

The Future- whats next?

The team have identified a new drug target on the androgen receptor and a series of potential drugs. They are now looking to test whether these drugs have the potential to become new treatments.

Project Start

November 2019

Research Facility

University of Aberdeen

Budget

£130,000/year

End

November 2022

The Project

Because prostate cancers rely on male hormones, many men are treated for prostate cancer with hormone therapy, ADT, which blocks the action of male hormones (androgens). The problem is that in some men, after some time, cancer will learn to grow and spread despite ADT.

This drug discovery project aims to stop androgens from fuelling cancer even after resistance to existing drugs develops. Androgens promote cancer by attaching to proteins called androgen receptors (AR). After the AR is “switched on” by androgens, it sends messages to the cancer cell which cause it to grow and divide. The AR is made of two different parts: the part outside the cell, where androgens attach to, and the part inside the cell, which sends the messages which trigger the cancer. ADT stops androgens from working by sticking to the outside of the AR, so there’s no room for the androgens to attach.

But in some men, the AR itself changes, so that the outside bit is missing. There’s nowhere for ADT to stick to, and the receptor is always switched on. The researchers will target drugs to a different, but equally important part of the AR: the part which is inside the cancer cell. They will use two different types of experimental drugs to do this: small drugs to stop the AR sending pro-cancer signalling, and new protein drugs called SoloMERs, which will lock the AR into place so that the small drugs have a better chance of working. Using this strategy, the team hope they can “switch-off” both normal and drug-resistant ARs.

Check back soon to find out more about Professor Iain J. McEwan’s research project!

 

 

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