© 2000 by Oxford University Press
Journal of the National Cancer Institute, Vol. 92, No. 23, 1866-1868,
December 6, 2000
© 2000 Oxford University Press
EDITORIAL |
HER2 in Prostate Cancer—a Viable Target or Innocent Bystander?
Affiliations of author: Genitourinary Oncology Service, Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY, and Department of Medicine, Weill Medical College of Cornell University, New York.
Correspondence to: Howard I. Scher, M.D., Genitourinary Oncology Service, Department of Medicine, Memorial Sloan-Kettering Cancer Center, 1275 York Ave., New York, NY 10021 (e-mail: scherh@mskcc.org).
The promise of molecular medicine is that clinical outcomes will be improved by directing therapy toward the mechanisms and targets associated with the growth of an individual patient's tumor. In practice, the targets are not static and change as the disease progresses (1–3). For prostate cancer, the framework to address this dynamic is provided by a model that considers the disease as a series of states from diagnosis to death (Fig. 1
). Therapeutic aims and trial hypotheses are defined by determining the clinical and biologic factors associated with tumor growth at the state a given patient resides. Factors determined to be present on the majority of cancers within a state can be targeted without profiling an individual patient's tumor. Those present at a lower frequency, or that change over time, would require individual profiling so that those patients most likely to benefit from a specific
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