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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