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Personal Information
Name Finn, Stephen
Main Department Histopathology
College Title Associate Professor Consultant
College Tel  
Fax +35318963285
Dr. Stephen Finn MB BAO BCh FDS PhD FRCPath FFPATH, is a Associate Professor, Consultant Pathologist and Principal Investigator at The University of Dublin, Trinity College and at St. James’s Hospital Dublin, a tertiary referral cancer institution. He is co-director of the Cancer Molecular Diagnostic Laboratory, the only fully accredited molecular diagnostic laboratory in Ireland. His clinical practice is limited to Urological, Gastrointestinal and Liver pathology. Dr. Finn is former Senior Scientist and Staff Pathologist to the Centre for Molecular Oncologic Pathology at the Dana Farber Cancer Institute, Boston, USA. Dr. Finn continues to have strong personal and collaborative links to the Harvard School of Public Health, the Dana Farber Cancer Institute and the University of Orebro in Sweden. Dr. Finn is a member of the Irish Prostate Cancer Research Consortium (PCRC) and the Transdisciplinary Prostate Cancer Partnership ToPCaP. Dr. Finn, a current recipient of the Prostate Cancer Foundation Young investigator Award, and is committed to forging a career as an independent researcher focused on prostate cancer and bringing his skills as a clinician, pathologist and scientist to bear on critical questions of clinical relevance to men who suffer from aggressive prostate cancer.
Details Date
Chairman Molecular Pathology, Faculty of Pathology, RCPI 01/02/2011
Membership of Professional Institutions, Associations, Societies
Details Date From Date To
Fellow of the Royal College of Pathologists 2005 Current
Research Interests
HEAD AND NECK CANCER Imaging Techniques Lipid metabolism Lung Cancer
PATTERNS Pathology Prostate Cancer Prostate cancer
Research Projects
Project title Identifying non-coding RNA repertoires of aggressive Prostate cancer
Summary Abstract: Although there has been significant progress in the basic understanding of why prostate cancer (PCa) arises and how it progresses, these advances, unfortunately, have not translated into a cure and have most often have been disappointing with little benefit to men with aggressive PCa. Clinically relevant biomarkers are lacking and simple prognostication in PCa remains elusive outside of the now decades old pathological Gleason scoring system. Our hypothesis, supported by miRNA data from our laboratories, is that non-coding RNA signatures (including known and novel miRNAs) play a key role in aggressive PCa. In addition, cancer stemness is associated with poor prognosis and aggressive PCa. Therefore, we further hypothesize that non-coding RNA expression profiles, particularly miRNA, are linked to stemness in cancer and a clinically aggressive phenotype. In this application, we aim to model stem cell rich PCa and profile biologically aggressive PCa (high Gleason grade) to identify, in hypothesis neutral experiments, non-coding RNAs associated with aggressive and progressive prostate cancer. miRNAs and their isoMirs will be defined in our holoclone stem cell models and high Gleason score tumours, from the biorepository of the Prostate Cancer Research Consortium (PCRC) in Ireland, and compared to founder cells and indolent prostate cancer respectively. Using advanced bioinformatics we will look for stemness and aggression signatures and use these in a smaller focused panel to assess in relation to outcome in richly and meticulously annotated prostate cancer databases from the Physicians Health Study and Health Professionals Follow Up Study. This study will also uniquely identify ncRNA other than miRNA (piRNA, snoRNA, transcribed ultra-conserved regions) and we expect that these will also contribute to the signatures derived. This study will for the first time provide an in depth profile of isoMirs in prostate cancer. We will also integrate existing and newly undertaken gene expression profiles to examine ncRNA in relation to gene expression patterns and pathways with the aim of deriving integrated ncRNA and mRNA profiles in clinically aggressive PCa. Validation will be performed in independent cohorts and in databases of our collaborators in the United States (Harvard School of Public Health). The latter resource allows us to assess outcome in relation to Prostate cancer specific death rather than PSA failure and is annotated for protein pathway, gene expression profiling and clinical data. Aggressive disease in the Harvard datasets is characterized by the presence of metastases or death from PCa. Finally, in a proof of concept study, we will examine the utility of the profiles discovered to monitor disease progression in circulating tumour cells from patients with aggressive metastatic prostate cancer. With the emergence of ncRNA-based therapeutics there is clear translational potential. The ultimate aim is to translate to the clinic non-coding RNA profiles that can be used to inform treatment options for patients with aggressive prostate cancer.
Funding Agency Prostate Cancer Foundation
Type of Project Personal Fellowship
Date from 01/01/12
Date to 30/12/14
Person Months

Project title EXPECT Trial: Evasion of immune editing by circulating tumour cells is an exercise-modifiable mechanism underlying aggressive behaviour in obese men with prostate cancer
Summary 1. Abstract 1.1 Background Obesity, known to be associated with a pro-inflammatory, pro-thrombotic humoral milieu, confers a worse prognosis in prostate cancer (PrCa). Circulating tumour cells (CTCs) are identified in the blood in advanced cancer. Their quantitation provides prognostic information. “Cloaking” of CTCs by adherent platelets impedes NK-cell clearance of CTCs from the circulation, enhancing metastatic spread. NK-cell function in blood and in solid organs is quantitatively and qualitatively reduced in obesity. Platelet cloaking may be enhanced in obesity due to the pro-inflammatory, pro-thrombotic state, and may be a mechanism for worse cancer-specific outcomes in this group. Obesity and its biochemical effects may be influenced by lifestyle changes such as exercise. Physical activity reduces levels of systemic inflammatory mediators and so an aerobic exercise intervention may represent an accessible and cost-effective means of ameliorating the pro-inflammatory effects of obesity. 1.2 Objectives To determine whether 1. Platelet cloaking of PrCa CTCs is more prominent in men with obesity than without 2. Regular exercise can improve quality of life (QoL) and ameliorate platelet cloaking 3. The degree of platelet cloaking varies with levels of systemic and primary tumour inflammation and coagulability 4. Expression of an obesity-associated lethality gene signature leads to variation in platelet cloaking 1.3 Setting and Methods This international multicentre prospective study will recruit 200 men with metastatic PrCa, dividing them into exposed and non-exposed groups based on BMI ≥ 25. Participants will be recruited from centres in Dublin (Ireland), Örebro (Sweden) and London (UK), and will be randomized to intervention and comparison groups. Blood samples will be taken at recruitment (T0) and at three (T3) and six months (T6). Project 1: CTCs will be enumerated in the T0 samples. Adherent platelets will be quantified and compared between the exposed and non-exposed groups, and correlated with clinicopathological parameters. Project 2: The intervention group will undertake a regular supervised aerobic exercise programme, whereas the comparison group will not. T3 and T6 blood samples will be assessed for CTC numbers and platelet cloaking. Changes will be compared with the T0 sample and between exposed and non-exposed and intervention and comparison groups. Participants will complete a detailed questionnaire to assess quality of life and other parameters at each visit. Project 3: All blood samples will be assessed for NK-cell number and activation, markers of systemic inflammation, adipokines and serum factors related to platelet activation. The prostate needle core biopsies will be examined microscopically for atrophy and inflammation, by morphology and immunohistochemistry, with particular reference to NK-cells. All variables will be correlated with platelet cloaking. Project 4: NCBs will be assessed for expression of an obesity-associated lethality gene signature (whose genes are known to play a role in obesity or platelet aggregation and coagulation), and correlated with platelet cloaking. 1.4 Impact This study aims to elucidate a potential mechanism by which obesity confers a worse prognosis in PrCa, two increasingly prevalent diseases in the western world. We hope to show that a low-cost, accessible intervention can improve QoL and potentially ameliorate the effects of obesity through alterations in the systemic adipokine and inflammatory mediator profile.
Funding Agency World Cancer Research Fund
Type of Project Trial
Date from 01/01/2014
Date to
Person Months

Project title Discovery and Clinical Implementation of Novel Predictive Biomarkers for Enzalutamide therapy
Summary Scientific Abstract: Building on funding secured from Bayer and Astellas to perform a clinical trial (Phase II Study of Radium-223 in Combination with Enzalutamide in progressive Osseous-Predominant Metastatic CRPC) this translational project will discover new mutations in the Androgen Receptor and validate existing candidates in the Androgen Receptor Ligand binding domain (W741C and F876L) for response to Enzalutamide (ENZ) using serial, liquid biopsies, tissue biopsies and rapid autopsy tissues. Critically we will develop these assays for accurate stratification of patients and for use in routine blood samples collected from patients before and during Enzalutamide therapy using cell free circulating DNA and circulating tumour cells allied to massively parallel next generation sequencing.
Funding Agency Irish Cancer Society
Programme Movember Transformative iPROSPECT
Type of Project
Date from 01/01/2014
Date to
Person Months

Publications and Other Research Outputs
Peer Reviewed
Nguyen PL, Ma J, Chavarro JE, Freedman ML, Lis R, Fedele G, Fiore C, Qiu W, Fiorentino M, Finn S, Penney KL, Eisenstein A, Schumacher FR, Mucci LA, Stampfer MJ, Giovannucci E, Loda M, Fatty acid synthase polymorphisms, tumor expression, body mass index, prostate cancer risk, and survival., Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 28, (25), 2010, p3958-64
TARA - Full Text
Meyer MS, Penney KL, Stark JR, Schumacher FR, Sesso HD, Loda M, Fiorentino M, Finn S, Flavin RJ, Kurth T, Price AL, Giovannucci EL, Fall K, Stampfer MJ, Ma J, Mucci LA, Genetic variation in RNASEL associated with prostate cancer risk and progression., Carcinogenesis, 31, (9), 2010, p1597-603
Nucera C, Porrello A, Antonello ZA, Mekel M, Nehs MA, Giordano TJ, Gerald D, Benjamin LE, Priolo C, Puxeddu E, Finn S, Jarzab B, Hodin RA, Pontecorvi A, Nose V, Lawler J, Parangi S, B-Raf(V600E) and thrombospondin-1 promote thyroid cancer progression., Proceedings of the National Academy of Sciences of the United States of America, 107, (23), 2010, p10649-54
TARA - Full Text
Fiorentino M, Judson G, Penney K, Flavin R, Stark J, Fiore C, Fall K, Martin N, Ma J, Sinnott J, Giovannucci E, Stampfer M, Sesso HD, Kantoff PW, Finn S, Loda M, Mucci L, Immunohistochemical expression of BRCA1 and lethal prostate cancer., Cancer research, 70, (8), 2010, p3136-9
Flavin R, Smyth P, Barrett C, Russell S, Wen H, Wei J, Laios A, O'Toole S, Ring M, Denning K, Li J, Aherne S, Sammarae D, Aziz NA, Alhadi A, Finn SP, Loda M, B S, Sheils O, O'Leary JJ, miR-29b expression is associated with disease-free survival in patients with ovarian serous carcinoma., International journal of gynecological cancer : official journal of the International Gynecological Cancer Society, 19, (4), 2009, p641-7
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Last Updated:02-OCT-2014