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Biography

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.

Research Tags

ARCHIVAL MATERIAL BETA-CATENIN Cancer Molecular Diagnostics Cancer/Carcinogenesis CATENIN COMPLEX Diagnostic bioimaging DIAGNOSTIC LABORATORIES DIGESTIVE TRACTS DISSECTION E-CADHERIN EPITHELIAL-CELLS FROZEN SECTION GASTRIC CARCINOMAS GENE H4 D10S170 HASHIMOTO THYROIDITIS HEAD AND NECK CANCER Imaging Techniques Lipid metabolism Lung Cancer NECK DISSECTION Obesity ORAL CAVITY PAPILLARY THYROID CARCINOMA Pathology PATTERNS Prostate cancer RATIONALE RET PROTOONCOGENE RET/PTC-1 SQUAMOUS-CELL-CARCINOMA STAGING STAGING PROCEDURE TAQMAN RT-PCR TYROSINE PHOSPHORYLATION

Research Projects

Project Title

Identifying non-coding RNA repertoires of aggressive Prostate cancer

From

01/01/12

30/12/14

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

Project Type

Personal Fellowship

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

From

01/01/2014

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

Project Type

Trial

Project Title

Discovery and Clinical Implementation of Novel Predictive Biomarkers for Enzalutamide therapy

From

01/01/2014

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

Representations

Details	Date
Chairman Molecular Pathology, Faculty of Pathology, RCPI	01/02/2011

Memberships

Membership of Professional Institutions, Associations, Societies

Details	Date From	Date To
Fellow of the Royal College of Pathologists	2005	Current

Publications and other Research Outputs

Baird AM, Finn SP, Gray SG, Sheils O., Epigenetic Modifier UHRF1 May Be a Potential Target in Malignant Pleural Mesothelioma., Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 16, (1), 2021, p14-16 , Journal Article, PUBLISHED DOI

Bracken-Clarke D, Kapoor D, Baird AM, Buchanan PJ, Gately K, Cuffe S, Finn SP., Vaping and lung cancer - A review of current data and recommendations., Lung cancer (Amsterdam, Netherlands), 153, 2021, p11-20 , Journal Article, PUBLISHED DOI

Pernar CH, Parmigiani G, Giovannucci EL, Rimm EB, Tyekucheva S, Loda M, Finn SP, Vander Heiden MG, Fiorentino M, Ebot EM, Mucci LA., Gene Expression Pathways in Prostate Tissue Associated with Vigorous Physical Activity in Prostate Cancer., Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 2021, Journal Article, PUBLISHED DOI

Oner E, Kotmakci M, Baird AM, Gray SG, Debelec Butuner B, Bozkurt E, Kantarci AG, Finn SP., Development of EphA2 siRNA-loaded lipid nanoparticles and combination with a small-molecule histone demethylase inhibitor in prostate cancer cells and tumor spheroids., Journal of nanobiotechnology, 19, (71), 2021, p1-20 , Journal Article, PUBLISHED TARA - Full Text DOI URL

Hashim D, Gonzalez-Feliciano AG, Ahearn TU, Pettersson A, Barber L, Pernar CH, Ebot EM, Isikbay M, Finn SP, Giovannucci EL, Lis RT, Loda M, Parmigiani G, Lotan T, Kantoff PW, Mucci LA, Graff RE., Family history of prostate cancer and the incidence of ERG- and phosphatase and tensin homolog-defined prostate cancer., International journal of cancer, 146, (10), 2020, p2694-2702 , Journal Article, PUBLISHED DOI

Thunnissen E, Kerr KM, Dafni U, Bubendorf L, Finn SP, Soltermann A, Biernat W, Cheney R, Verbeken E, Warth A, Marchetti A, Speel EM, Pokharel S, Quinn AM, Monkhorst K, Navarro A, Madsen LB, Tsourti Z, Geiger T, Kammler R, Peters S, Stahel RA; European Thoracic Oncology Platform Lungscape Consortium., Programmed death-ligand 1 expression influenced by tissue sample size. Scoring based on tissue microarrays' and cross-validation with resections, in patients with, stage I-III, non-small cell lung carcinoma of the European Thoracic Oncology Platform Lungscape cohort., Modern Pathology, 33, (5), 2020, p792 - 801, Journal Article, PUBLISHED

Allott EH, Ebot EM, Stopsack KH, Gonzalez-Feliciano AG, Markt SC, Wilson KM, Ahearn TU, Gerke TA, Downer MK, Rider JR, Freedland SJ, Lotan TL, Kantoff PW, Platz EA, Loda M, Stampfer MJ, Giovannucci E, Sweeney CJ, Finn SP, Mucci LA., Statin Use Is Associated with Lower Risk of PTEN-Null and Lethal Prostate Cancer., Clinical cancer research : an official journal of the American Association for Cancer Research, 26, (5), 2020, p1086-1093 , Journal Article, PUBLISHED DOI

Malone T, Schäfer L, Simon N, Heavey S, Cuffe S, Finn S, Moore G, Gately K., Current perspectives on targeting PIM kinases to overcome mechanisms of drug resistance and immune evasion in cancer., Pharmacology and Therapeutics, 207, 2020, Journal Article, PUBLISHED DOI

Silva R, Moran B, Russell NM, Fahey C, Vlajnic T, Manecksha RP, Finn SP, Brennan DJ, Gallagher WM, Perry AS., Evaluating liquid biopsies for methylomic profiling of prostate cancer., Epigenetics, 15, (6-7), 2020, p715-727 , Journal Article, PUBLISHED DOI

Stopsack KH, Gerke T, Zareba P, Pettersson A, Chowdhury D, Ebot EM, Flavin R, Finn S, Kantoff PW, Stampfer MJ, Loda M, Fiorentino M, Mucci LA., Tumor protein expression of the DNA repair gene BRCA1 and lethal prostate cancer., Carcinogenesis, 41, (7), 2020, p904-908 , Journal Article, PUBLISHED DOI

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Trinity College Dublin, The University of Dublin

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Dr. Stephen Finn

Dr. Stephen Finn

Associate Professor Consultant (Histopathology)

Stephen.Finn@tcd.ie

www.topcapteam.org

Biography

Research Tags

Research Projects

Representations

Memberships

Membership of Professional Institutions, Associations, Societies

Publications and other Research Outputs

Publications