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Dr Francesco Crea

Profile summary

  • Central Academic Staff
  • Senior Lecturer in Cancer Genetics
  • Faculty of Science, Technology, Engineering & Mathematics
  • School of Life, Health & Chemical Sciences
  • francesco.crea

Professional biography


2006 MD (cum laude), University of Pisa

2010, PhD (cum laude), Sant'Anna School of Advanced Studies


2008-2009 Guest Scientist, Cancer Stem Cell Section, National Cancer Institute at Fredercik, USA

2012-2015 Post Doctoral Fellow, BC Cancer Agency (Canada). 


2015 American Society of Clinical Oncology Merit Award

2015 Multi Institutional Prostate Cancer Meeting \Poster Award

2014 Prostate Cancer Foundation BC post-doctoral Award

2013 Michael Smith Foundation Trainee Award

Editorial Board Memberships:

Epigenomics; The World Journal of Gastroenterology. 

Research interests

Non-coding RNAs (NC-RNAs). NC-RNAs represent a vast and largely unexplored area of the human transcriptome (Crea et al. Cancer and Met Rev 2014). We have studied the role of micro-RNAs and long non-coding RNAs (lncRNAs) in prostate cancer progression. In particular, we have discovered and patented PCAT18, a prostate cancer-specific lncRNA that drives metastatic progression (Crea et al. Oncotarget 2014). We are currently developing therapeutic strategies to target PCAT18. 

Cancer Epigenetics. We have explored the role of epigenetic effectors as novel biomarkers and therapeutic targets in human neoplasms. 

1) We have demonstrated that an EZH2 (Polycomb) inhibitor effectively kills prostate cancer stem cells in vitro and in vivo. Based on this and similar results, EZH2-targeting drugs are being investigated in clinical trials. (Crea et al. Mol Cancer 2011; Crea et al, Crit Rev Hemat Oncol. 2012 )

2) We have identified and functionally characterized an  EZH2 genetic variant that accurately predicts prognosis in colorectal cancer patients (Crea et al. Ann Oncol 2012; Fornaro et al. Ann Oncol 2012; Fornaro et al BMC Cancer 2015). 

The epigenetic/non-coding interactome. Based on our results and on other studies, we have proposed a new paradigm of cancer progression. We show evidence supporting the idea that an epigenetic/non-coding interactome drives key features of cancer progression, including drug resistance and metastatic spreading (Crea et al. Trends Mol Med 2015).

Full list of Publications:

Internal Collaborators: Prof. Nacho Romero (non-coding RNAs and metastatic tropism; lncRNAs in ageing); Dr. Martin Bootman (calcium-dependent prostate cancer progression). 

Teaching interests

OU modules

I exploit my research experience in cancer biology, epigenetics and non-coding RNAs to enrich the OU students' learning journey and to make sure that we teach the latest and most important developments in these fields. We are also working on new assets that develop the students' analytic skills and their understanding of human diseases. 

SK299 (Human Biology)

S294 (Cell Biology)

S211 (Paramedic Practice).

S317 (from Genes to Species)  

Post-graduate students' and PDRA supervision: Rebecca Mather (PRDA); Perla Pucci (PhD student, primary supervisor); Sameer Ayaz (PhD student, primary supervisor);  Maryam Latarani (MPhil student, primary supervisor); David Roig-Carles (primary supervisor);  Stephen Chandler (PhD student, co-supervisor since 10/16; previously on Work Experience Placement); Eduardo Frias (PhD student, co-supervisor);  Ester Pascual-Baixauli (Visiting Student); Roberto Silvestri (Visiting Student); Najara Juan Larrea (Erasmus+ MSc). 

Impact and engagement

In collaboration with the BC Cancer Agency, we are currently developing new therapeutic and diagnostic tools for prostate cancer. These new technologies are based on the discovery and characterization of previously unknown long non-coding RNAs. 

External collaborations

Prof. Hardev Pandha, University of Surrey

Prof. Johan DeBono ICR London 

Dr Helen Fillmore Portsmouth University 

Prof Yuzhuo Wang, BC Cancer Agency (Canada)

Prof Alfredo Falcone, University of Pisa (Italy)

Dr. Luca Quagliata, University of Basel (Switzerland)

Dr Paolo Frumento (Sweden)

Research Activity

Externally funded projects

Epigenetic enrichment of circulating tumour DNA to enable deep profiling for cancer early detection (EpiEnrich)

RoleStart dateEnd dateFunding source
Lead01/Jan/201931/Dec/2019CRUK Cancer Research UK;EPSRC EPSRC Engineering and Physical Sciences Research Council;STFC Science & Technology Facilities Council
Circulating tumour DNA (ctDNA) contains valuable information for the early detection and stratification of prostate cancer. Current methodologies are unable to capture ctDNA with sufficient efficacy. This project aims to employ cancer-specific histone post-transnational modifications to enrich ctDNA from the plasma of cancer patients. We will initially use pre-clinical models to optimize the technique. If we are successful, we intend to apply for follow-up funds to test our application in the clinics. The OU (F Crea, Joint Lead applicant) is part of a multi-disciplinary team: PI (Charlie Massie, Cambridge). Other academics involved as CoI/joint applicants: Nick Leslie (Heriot-Watt), Pedro Estrela (Bath), Tingting Zhu (Oxford), Paul Milner (Leeds).

Long non-coding RNAs implicated in neuroendocrine prostate cancer initiation and progression: novel therapeutic targets for an incurable disease.

RoleStart dateEnd dateFunding source
Lead01/Dec/201630/Apr/2020CRUK Cancer Research UK
Neuroendocrine prostate cancer (NEPC) is the most aggressive prostate cancer type. This disease is resistant to all available therapies, highly metastatic and rapidly fatal. We believe that the elucidation of NEPC-driving pathways could pave the way for the development of effective therapies. Long non-coding RNAs (lncRNAs) are a vast and mostly uncharted region of the human transcriptome. Despite their emerging role in cancer biology, no study has assessed the relevance of lncRNAs in NEPC development. Our collaborator Dr. Wang (BC Cancer Agency) has developed a unique collection of patient-derived prostate cancer models. This collection includes the first-in-field model of transdifferentiation from prostatic adenocarcinoma to NEPC. Aims. We propose to study the role of lncRNAs in NEPC development. The objectives of this study are to determine: 1) whether transcriptomic profiles of lncRNAs in PCa pre-clinical models can elucidate the mechanisms of NEPC development. 2) if selected lncRNAs are promising therapeutic targets for NEPC. Accordingly, our specific aims will be: AIM 1: Identification, functional and clinical characterization of NEPC-driving lncRNAs. AIM 2: Development of innovative therapeutic strategies to prevent NEPC development. At the end of this project, we hope to shed new light on an incurable disease, and to identify viable therapeutic targets, which will be investigated in future translational and clinical studies.

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