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Exploiting fly genetics to prevent clinically-significant prostate cancer

Code: BC-DTP_2026_55

Title: Exploiting fly genetics to prevent clinically-significant prostate cancer

Primary Supervisor: Paulo Ribeiro

Email: p.baptista-ribeiro@qmul.ac.uk

Institute: Barts Cancer Institute

Secondary Supervisor: Prabhakar Rajan

Email: p.rajan@qmul.ac.uk

Institute: Barts Cancer Institute

Lay Summary:

Prostate cancer is the commonest cancer in men, affecting >50,000 men/year, disproportionately affecting Black men and individuals with a family history, with survival correlated with socio-economic status. We have identified diagnostic and early detection inequities amongst Black ethnic group and lower socio-economic status patients in North East London, which may have social and genetic determinants.

Previous research has identified changes within genes in early prostate cancer before it causes symptoms. It is unknown if these genes are switched on in the prostate with ageing and whether finding them earlier can help us screen for and/or prevent prostate cancer. Screening remains controversial because we lack reliable tests to distinguish aggressive (will grow and spread) from non-aggressive tumours (will not affect life expectancy), as treatments have serious, long-lasting side-effects.

Our project uses the fruit fly Drosophila as a model to better understand the genetics of early prostate cancer. Flies have an equivalent organ to the human prostate and, because they grow very quickly, allow very rapid genetic studies that would take years in humans. We will test the function of several important human prostate cancer genes in the fly prostate. We will validate our results in human prostate cancer cells and patient samples (of different ethnicities/socio-economic backgrounds), to ensure the genes identified are relevant to humans.

Our findings will help develop new early diagnosis tests for aggressive prostate cancer and treatments to prevent its development. Future work will involve patients from diverse socio-economic and ethnic groups to help co-design research studies and clinical trials.

Aims:

We will pursue the following aims:

1: Functional characterisation of PTEN-loss-deregulated genes

2: In vivo assessment of the role of AS in early PCa events

3: Validation of prospective prevention-associated genes in PCa samples

References:

[1]: Armenia et al. The long tail of oncogenic drivers in prostate cancer. Nat Genet, 2018; 50:645-51.

[2]: Martin-Caraballo. Regulation of molecular biomarkers associated with the progression of prostate cancer. Int J Mol Sci, 2024; 25:4171.

[3]: Del Giudice et al. FOXA1 regulates alternative splicing in prostate cancer. Cell Rep, 2022; 40:111404.

[4]: Lauria et al. Identification of altered biological processes in heterogeneous RNA-sequencing data by discretization of expression profiles. Nucleic Acids Res, 2020; 48:1730-47.

[5]: Cham et al. Targeting the PI3K-AKT-mTOR Pathway in Castration Resistant Prostate Cancer: A Review Article. Clin Genitourin Cancer, 2021;19:563.e1-563.e7.

[6]: Rawat and Heemers. Alternative splicing in prostate cancer progression and therapeutic resistance. Oncogene, 2024; 43:1655-68.

[7]: Urbanski et al. MYC regulates a pan-cancer network of co-expressed oncogenic splicing factors. Cell Rep, 2022; 41:111704.

[8]: Hsu et al. The spliceosome is a therapeutic vulnerability in MYC-driven cancer. Nature, 2015; 525:384-8.

[9]: Villegas. One hundred years of Drosophila cancer research: no longer in solitude. Dis Model Mech, 2019; 12:dmm039032.

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