Tony Finelli

MD, MSc, FRCSC

Chief of Urology, University Health Network
GU Site Lead, Princess Margaret Cancer Center
Associate Professor
University of Toronto

Phone

(416) 946-2851

Assistant(s)

Biography

Dr. Tony Finelli is a urologic oncologist and surgeon investigator at the University Health Network (UHN) in Toronto and an Associate Professor at the University of Toronto. He is the Chief of Urology, GU Site Lead at the Princess Margaret Cancer Center and the inaugural GU Oncology Lead for the province of Ontario (Cancer Care Ontario).

Dr. Finelli conducts health services research in urologic oncology with an interest in identifying gaps in care and designing knowledge translation strategies to overcome them. He is also actively involved in clinical trials. He has published more than 100 peer-reviewed manuscripts and holds peer-reviewed funding for research in prostate and kidney cancer.

Dr. Finelli’s clinical practice focuses on the management of urologic malignancies with minimally invasive and robotic techniques. He has performed live surgery for instructional purposes in more than 10 countries. Dr Finelli is recognized nationally and internationally for his contributions to minimally invasive urologic oncology.

Areas of Specialty and Research Interests

Affiliated Hospital(s)

Princess Margaret Cancer Centre (UHN), Toronto General Hospital (UHN)
 
 

Latest Publications

Modulating ATP Binding Cassette (ABC) Transporters in Papillary Renal Cell Carcinoma Type 2 Enhances its Response to Targeted Molecular Therapy.

Related Articles

Modulating ATP Binding Cassette (ABC) Transporters in Papillary Renal Cell Carcinoma Type 2 Enhances its Response to Targeted Molecular Therapy.

Mol Oncol. 2018 Jun 13;:

Authors: Saleeb RM, Farag M, Lichner Z, Brimo F, Bartlett J, Bjarnason G, Finelli A, Rontondo F, Downes MR, Yousef GM

Abstract
Papillary renal cell carcinoma (PRCC) is the most common non-clear cell RCCs and is known to comprise two histological subtypes. PRCC2 is more aggressive and is molecularly distinct from the other subtypes. Despite this PRCCs are treated together as one entity, and they show poor response to the current therapies that do not target pathways implicated in their pathogenesis. We have previously detected ABCC2 (an ABC transporter), VEGF and mTOR pathways to be enriched in PRCC2. In this study, we assess the therapeutic potential of targeting these pathways in PRCC2. Twenty RCC cell lines from the Cancer Cell Encyclopedia were compared to the Cancer Genome Atlas PRCC cohort (290), to identify representative PRCC2 cell lines. Cell lines were further validated in xenograft models. Selected cell lines were treated in vitro and in vivo (mice models) under five different conditions, untreated, anti-VEGF (Sunitinib), ABCC2 blocker (MK571), mTOR inhibitor (Everolimus) and Sunitinib + MK571. Sunitinb+ABCC2 blocker group showed a significant response to therapy compared to the other treatment groups both in vitro (p = <0.0001), and in vivo (p= 0.0132). ABCC2 blockage resulted in higher Sunitinib uptake, both in vitro (p = 0.0016) and in vivo (p = 0.0031). Everolimus group demonstrated the second best response in vivo. The double treatment group showed the highest apoptotic rate and lowest proliferation rate. There is an urgent need for individualized therapies of RCC subtypes that take into account their specific biology. Our results demonstrate that combined targeted therapy with sunitinib and ABCC2 blocker in PRCC2 has therapeutic potential. The results are likewise potentially significant for other ABCC2 high tumors. However, the results are preliminary and clinical trials are needed to confirm these effects in PRCC2 patients. This article is protected by copyright. All rights reserved.

PMID: 29896907 [PubMed - as supplied by publisher]