© 2001 by Oxford University Press
Journal of the National Cancer Institute, Vol. 93, No. 24, 1830-1832,
December 19, 2001
© 2001 Oxford University Press
EDITORIAL |
Unraveling Resistance to Trastuzumab (Herceptin): Insulin-Like Growth Factor-I Receptor, a New Suspect
Affiliations of authors: J. Albanell, Medical Oncology Service, Vall d'Hebron University Hospital, Barcelona, Spain; J. Baselga, Medical Oncology Service, Vall d'Hebron University Hospital, and Universitat Autonoma de Barcelona.
Correspondence to: Jose Baselga, M.D., Medical Oncology Service, Vall d'Hebron University Hospital, Paseo Vall d'Hebron 119–129, 08035 Barcelona, Spain (e-mail: baselga@hg.vhebron.es).
Trastuzumab (Herceptin) is a humanized antibody directed against the extracellular domain of the tyrosine kinase receptor HER2 that has shown clinical activity against HER2-overexpressing breast tumors (1–4). HER2, the targeted receptor, is a member of the epidermal growth factor (EGF) receptor family of receptors, also known as the type I receptor tyrosine kinase family [for review, see (5)]. HER2 is overexpressed in 25%–30% of breast cancers, and its overexpression is associated with a high risk of relapse and death (6). In this group of tumors with unfavorable prognosis, trastuzumab has been a valuable addition to standard therapy, with the pivotal studies demonstrating a clear survival benefit (2,3). However, even in the selected group of patients with very high levels of HER2 overexpression who derive the greatest
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