1. ¹Department of Bioscience, Royal College, 204 George Street, University of Strathclyde, Glasgow G1 1XW, UK
2. ²Haemato-Oncology Section, Division of Cancer Sciences and Molecular Pathology, University of Glasgow, Level 3 Queen Elizabeth Building, Royal Infirmary, 10 Alexandra Parade, Glasgow G31 2ER, UK

Correspondence: Dr HG Jørgensen, E-mail: hgj1b@clinmed.gla.ac.uk

Received 14 October 2002; Revised 12 December 2002; Accepted 10 January 2003.

Abstract

Imatinib mesylate (Gleevec^® or Glivec^®), a small molecule tyrosine kinase inhibitor for the treatment of chronic myeloid leukaemia, has been said to herald the dawn of a new era of rationally designed, molecularly targeted oncotherapy. Lurking on the same new horizon, however, is the age-old spectre of drug resistance. This review sets the intoxicating clinical perspective against the more sobering laboratory evidence of such divergent mechanisms of imatinib resistance as gene amplification and stem cell quiescence. Polychemotherapy has already been considered to combat resistance, but a more innovative, as yet unformulated, approach may be advocated.