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Division of Surgical Oncology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115 [I. Y., P. S. G., G. E. P., A. S. P., T. J. E.]; Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710 [J. M. D., H. K. L.]; and Department of Pathology, Harold C. Simmons Comprehensive Cancer Center, Dallas, Texas 75235 [A. F. G.]
Previously, we have reported a correlation between the expression of HER2/neu and sensitivity to HLA-A2-restricted cytotoxic T-cells (CTL) in ovarian cancer. To investigate the role of HER2/neu in human non-small cell lung cancer (NSCLC), we established autologous tumor-specific CTL from tumor-infiltrating lymphocytes of HLA-A2+ HER2/neu+ NSCLC patients. These CTL lines specifically recognized HLA-A2+ HER2/neu+ autologous and allogeneic NSCLC cell lines as well as HLA-A2+ HER2/neu+ heterologous ovarian cancer cell lines. Furthermore, these CTL recognized an overexpressed, HER2/neu-derived peptide. From these results, we conclude that HLA-A2 serves as a restriction element in NSCLC. More importantly, at least one HER2/neu-derived peptide is a tumor-associated antigen in NSCLC and ovarian cancer.
1 This work was supported by National Institute of Health Grants ROI CA45484 and CA09535, and Grant FRA-407 from the American Cancer Society.
2 To whom requests for reprints should be addressed, at Division of Surgical Oncology, Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115.
Received 4/ 8/94. Accepted 5/17/94.
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