1. ¹Department of Physiology and Pharmacology, Hypertension Research Unit, Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel
2. ²Hypertension and Atherosclerosis Section, Boston University School of Medicine, Boston, MA, USA

Correspondence: Professor T Rosenthal, Department of Physiology and Pharmacology, Hypertension Research Unit, Sackler School of Medicine, Tel Aviv University, Ramat Aviv, Tel Aviv 69978, Israel. E-mail: rtalma@post.tau.ac.il

Received 16 December 2008; Revised 28 February 2009; Accepted 2 March 2009; Published online 2 April 2009.

Abstract

After an early report that patients treated with angiotensin-converting enzyme (ACE) inhibitors had a lower than expected incidence of cancers, there was a large number of publications investigating the possible pathophysiological mechanism mediating this effect, as well as population studies comparing the incidence of cancers in patients treated with agents inhibiting the renin–angiotensin system with their incidence in the general population. Several mechanisms are proposed to explain a potential anti-tumour activity of such agents in vitro in experimental animal models. However, the population studies are mostly inconclusive, although they do suggest a possible interaction between ACE genotypes and susceptibility to altered behaviour of certain tumours.