1. ¹Centre for Molecular Oncology, Institute of Cancer and CR-UK Clinical Centre, Barts and The London, School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, UK
2. ²Universidad Francisco de Vitoria, Departamento de Biotecnología, Madrid, Spain
3. ³Instituto de Investigaciones Biomédicas 'Alberto Sols', Madrid, Spain
4. ⁴Institut National de la Sante et de la Recherche Medicale (INSERM), CIC-04 Biotherapies Hepatiques, CHU Hotel Dieu, Nantes, France

Correspondence: Professor NR Lemoine, Molecular Oncology Unit, Institute of Cancer and CR-UK Clinical Centre, Barts and The London, School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. E-mail: nick.lemoine@cancer.org.uk

Received 21 September 2007; Revised 9 January 2008; Accepted 12 January 2008; Published online 18 April 2008.

Abstract

Expression of the sodium iodide symporter (hNIS) has been detected in breast cancer tissue, but frequently, not at the levels necessary to mediate ¹³¹I accumulation. Transducing the hNIS gene into breast cancer cells with adenovirus could be a tractable strategy to render breast cancer susceptible to radioiodide therapy. We constructed the replication-incompetent virus, AdSERE, in which an estrogen-responsive promoter directs the expression of hNIS. In vitro, we demonstrate that AdSERE mediates hNIS expression and iodide uptake in ER+ breast cancer cells. In vivo, we show that AdSERE-infected ER+ tumors can be imaged due to tracer accumulation; in addition, AdSERE in combination with therapeutic doses of ¹³¹I suppresses tumor growth.