1. ¹Medical Oncology, Department of Medicine, Princess Margaret Hospital, University of Toronto, 610 University Avenue, Toronto, Ontario, Canada M5G 2M9
2. ²Department of Environmental Health, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA
3. ³ Department of Medicine, Massachusetts General Hospital Cancer Center, Harvard Medical School, 665 Huntington Avenue, Boston, MA 02115, USA
4. ⁴Department of Surgery, Massachusetts General Hospital, 10 Blossom Street, Boston, MA 02114, USA
5. ⁵ Endoscopy Unit, Department of Medicine, Massachusetts General Hospital, 10 Blossom Street, Boston, MA 02114, USA
6. ⁶Pulmonary Unit, Department of Medicine, Massachusetts General Hospital, 10 Blossom Street, Boston, MA 02114, USA
7. ⁷Applied Molecular Oncology, Ontario Cancer Institute, 610 University Avenue, Toronto, Ontario, Canada M5G 2M9

Correspondence: Dr G Liu, Ontario Cancer Institute/Princess Margaret Hospital, Suite 7-124, 610 University Avenue, Toronto, Ontario, Canada M5G 2M9; E-mail: Geoffrey.Liu@uhn.on.ca

Received 16 August 2007; Revised 4 January 2008; Accepted 9 January 2008; Published online 5 February 2008.

Abstract

Helicobacter pylori (HP) infection appears protective against oesophageal adenocarcinoma (EA) risk. Matrix metalloproteinases (MMPs) are released in the presence of HP infection. In MMP2 wild-type individuals, HP was significantly protective of EA risk (adjusted odds ratio: 0.29; 95% confidence interval=0.1–0.7). Matrix metalloproteinases may modulate the EA–HP relationship.