Hormone Therapy: Old Dog, New Tricks

Professor Iain J McEwan, Dr Irene Hunter and Dr Craig Jamieson


Dates: November 2019- November 2023

Location: University of Aberdeen

Amount: £396,710

In 2023, Professor Iain J McEwan, Dr Irene Hunter and Dr Craig Jamieson successfully completed their PCR project. The team have identified potential drug combinations that could make hormone therapy work better and for longer. Developing kinder treatments that continue to work beyond current resistance means that patients will live longer and with fewer side effects. The next step for the researchers is to continue to validate their drug combinations so that in the future they could be tested in clinical trials.

Early detection of prostate cancer saves lives

Hormone therapy is one of the main forms of prostate cancer treatment, but it will stop working for nearly all patients.

stop palm hand

Hormone therapy works by stopping the androgen receptor (AR) from telling cancer cells to grow. Sometimes, different versions of the AR are made, called AR variants (ARVs) and hormone therapy doesn’t work on these.

Image of drugs that may help to treat prostate cancer bone metastasis

This project aimed to find drug combinations that target a different part of the androgen receptor, so that they still work on ARVs. This would mean they still work after resistance to current hormone therapy treatments.

test tubes infographic

The team have identified potential drug combinations that could be used to target ARVs and make hormone therapy work better and for longer. They will now be testing these combinations, and the hope is that the most effective can be taken forward into clinical trials.

Hormone Therapy: Stopping resistance in its tracks

Dr Luke Gaughan, Dr Laura Walker, Dr Dominic Jones and Ryan Nelson


Dates: January 2020- November 2023

Location: Newcastle University Centre for Cancer

Amount: £406,369

November 2023 marked the successful completion of Dr Luke Gaughan, Dr Laura Walker, Dr Dominic Jones and Ryan Nelson’s PCR project. The team have identified key proteins involved in ARV production and the growth and spread of prostate cancer. The researchers have also begun to conduct further tests to establish whether these proteins have the potential to be drug targets. Once the team have established their potential targets, drugs could be developed that block these proteins, stopping the production of ARVs and preventing resistance to hormone therapy.

Early detection of prostate cancer saves lives

Hormone therapy is one of the main forms of prostate cancer treatment, but it will stop working for nearly all patients.

Hormone therapy works by stopping the androgen receptor (AR) from telling cancer cells to grow. Sometimes, different versions of the AR are made, called AR variants (ARVs) and hormone therapy doesn’t work on these.

This project explored how AR variants (ARVs) are made and how to stop this process to keep hormone therapy working for longer.

The team have identified key proteins essential for making ARVs and have begun testing to see if we could target these proteins with drugs to keep hormone therapy working for longer.

Clipping prostate cancer’s wings

Dr Jennifer Munkley, Dr Ning Wang and Dr Kirsty Hodgson


Dates: August 2021- November 2023 

Location: Newcastle University and the University of Sheffield  

Amount: £273,534  

In 2023, Dr Jennifer Munkley, Dr Ning Wang and Dr Kirsty Hodgson successfully completed their PCR project. They discovered that special sugars, glycans, which surround prostate cancer cells just as feathers surround birds, make tumours grow very fast and makes them more likely to spread to bone. They have shown that using drugs to block these glycans could clip prostate cancer’s wings. 

image of prostate cancer spread that can lead to bone metastasis

Prostate cancer often spreads to bone. This can be very painful and there is currently no cure.

Image of Glycan sugar surrounding cell

Glycans are special sugars which coat all cells in the body but are different to sugars found in food. 

Image of two different types of glycans that make prostate cancers

The team proved that two glycans are important for prostate cancer cells to both grow and spread to the bone, and they have generated proof-of-principle data to show these glycans can be targeted therapeutically. Excitingly, new drugs that block/inhibit glycans have recently been developed and have shown promise for treating other cancers.

They are now testing if cutting-edge glycan-targeting drugs, developed within the last two years, could block prostate cancer spreading to bone.

AI: Will my cancer return?

Dr Anna Wilkins and Dr Erik Sahai


Dates: June 2021 – January 2023

Location: Francis Crick Institute, London

Amount: £100,000

In 2023, Dr Anna Wilkins and Dr Erik Sahai successfully completed their PCR project. They proved that their technology can identify patterns which mean someone’s cancer may be more likely to return. This marks a huge step forward for more personalised treatment. The researchers will now take their technology forward to make it work even better and test it using tissue from men with advanced disease.

Sometimes cancer returns following treatment, but doctors cannot predict which will return. If we could predict this, we could make sure that those with a high risk of cancer returning can have their treatment changed to reduce their risk and those with a low risk can avoid overtreatment and associated side effects.

time hourglass

Studies have found patterns in the prostate tissue that can predict whether a cancer is likely to return. Identifying these patterns needs to be done by a highly skilled individual, and it is time consuming and expensive.

Dr Wilkins and Dr Sahai developed computer software to do this automatically and quickly. The researchers used the software to analyse tissue samples collected from patients with prostate cancer during the CHHiP clinical trial. They proved that their software works and can identify patterns associated with prostate cancer returning.

Dr Wilkins and Dr Sahai will now be testing their software further. They will prove that it can analyse a wide range of patient tissue, for example, by testing it using tissue from men who have more advanced prostate cancer. They will also continue to make improvements and make the software work even better.

Immunotherapy for prostate cancer

Dr Christine Galustian


Dates: March 2020 – July 2022

Location: King’s College, London

Amount: £400,000

2022 marked the successful completion of Dr Christine Galustian and Dr Efthymia Papaevangelou’s project. They developed a novel immunotherapy which successfully treated both local tumours and cancer that had spread in mice. As a result of our funding and guidance, this treatment will now be tested in humans in a clinical trial.

Immunotherapy harnesses the body’s own immune system to fight cancer. Unfortunately, the biology of the prostate means that it has ben difficult to get immunotherapy to work in prostate cancer.

Drs Galustian, Papaevangelou, and Esteves experimented with a new form of immunotherapy in which they attached an immunity protein called IL-15 to a chemical “tail” which anchored it to the place where it was injected. They hoped this would make it both safer and more effective than other forms of immunotherapy.

The team discovered that when they combined their tailed IL-15 with another drug that affects the immune system, it increased survival in mice by 90% and proved that tumours which were successfully treated with this combination did not grow back. They also gathered important insights into how this therapy affects the biology of the tumour.

Based on their promising results, Dr Galustian has just received funding to develop a clinical trial, to start establishing is this therapy is as safe and effective in humans as it is in mice.

Prostate Cancer Stem Cells

Dr Aamir Ahmed


Dates: May 2018 – September 2021

Location: King’s College, London

Amount: £660,516

2021 marked the conclusion of Dr Aamir Ahmed’s project. This team’s work added to the evidence that Wnt signalling plays an important role in prostate cancer, and worked on an objective and quantitative method to identify new protein biomarkers to help predict prostate cancer prognosis.

Cancer stem cells produce cancer cells and divide continuously to drive tumour growth. They can also survive treatment and restart tumour growth when treatment has stopped.

Wnt signalling is one way your cells communicate and is important in regulating stem cells.

This team tested drugs used in other illnesses to see if they could stop Wnt signalling in prostate cancer.

In addition to his research work, Dr Ahmed has been a good friend to PCR and its supporters, having hosted many lab tours and met many of our supporters and patients.

Modelling Prostate Cancer

Professor Matthew Smalley and Dr Boris Shorning


Dates: October 2017 – January 2021

Location: Cardiff University

Amount: £335,895

2021 marked the successful conclusion of Professor Matt Smalley and Dr Boris Shorning’s project. We are incredibly proud of what they have achieved, and of how well they collaborated with other PCR researchers. The insights they gained into why cancers spread and the potential for an anti-diabetes drug in prostate cancer give the field a clear direction towards new therapies.

Professor Matt Smalley and Dr Boris Shorning developed innovative, world-first models to test the effectiveness of treatments for metastatic prostate cancer, to see if they are good enough and safe enough to move into humans.

Over the three years of this project, they collaborated extensively with other PCR researchers, and played a crucial role in testing compounds developed by other researchers to see if they prevented prostate cancer growth.

They also provided critical insights into the role of Plexin B1, a molecule which controls how cells respond to their environment. They compared two forms of Plexin B1 (normal and mutated), to see which increases metastasis.

They showed that increased levels of the mutated, but not the normal form, stimulates cancer to advance, and, looking at patient data, they discovered that patients with mutated Plexin B1 have worse outcomes compared to patients without Plexin B1 mutations.

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