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Departments of Medicine [M. L. D., G. M., A. E. M., W. C., R. B. L., M. A. C.] and Surgery [R. M.], University of Washington, Seattle, Washington 98195; Department of Otolaryngology, Northwestern University, Chicago, Illinois, 60611 [E. C.]; and Friedrich Miescher-Institut [B. G., M. J.] and Ciba-Geigy Limited [N. L., E. M.], Basel, Switzerland
2 A Berlex Oncology Foundation Fellow. To whom requests for reprints should be addressed.
The HER-2/neu protooncogene is amplified and overexpressed in 20–40% of invasive breast cancers. HER-2/neu protein overexpression is associated with aggressive disease and is an independent predictor of poor prognosis in several subsets of patients. The protein may also be related to cancer formation, with overexpression being detectable in 50–60% of ductal carcinomas in situ. It has been suggested that it might be possible to develop specific T-cell therapy directed against proteins involved in malignant transformation. One question is whether normal proteins that are overexpressed are appropriate targets for therapeutic immune attack. This report demonstrates that some patients with HER-2/neu-positive breast cancers have both existent CD4+ helper/inducer T-cell immunity and antibody-mediated immunity to HER-2/neu protein. Initial studies performed on 20 premenopausal breast cancer patients identified antibodies to HER-2/neu in 11 individuals. Similar antibody responses have been found in some normal individuals. The patient with the greatest antibody response was studied in detail. In addition to a humoral immune response this patient had evidence of a significant proliferative T-cell response to the HER-2/neu protein and peptides. Similar T-cell responses have been detected in additional patients. It has been assumed that patients would be immunologically tolerant to HER-2/neu as a self-protein and that immunity might be difficult to generate. If immunity could be generated, the result might be destructive autoimmunity. The current data support the notion that HER-2/neu-specific immunity might be used in therapy without destroying normal tissue but also raises questions as to the role of existent immunity in immune surveillance and cancer progression.
1 This work was supported by Grants T32 CA09515, R01 CA54561, and R37 CA30558, National Cancer Institute, NIH, Department of Health and Human Services.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 9/10/93. Accepted 11/16/93.
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