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A survivor of breast cancer with immunity to MUC-1 mucin, and lactational mastitis
Authors:Keith R. Jerome  Allan D. Kirk  Gabriele Pecher  Wayne W. Ferguson  O. J. Finn
Affiliation:Department of Laboratory Medicine, Box 357110, University of Washington Medical Center, Seattle, WA 98195, USA, US
Department of Surgery, University of Wisconsin, Madison, WI 53792, USA, US
Robert-R?ssle-Clinic at the Max-Delbrück-Center for Molecular Medicine, Department of Medical Oncology and Tumor Immunology, 13125 Berlin, Germany, DE
Department of Surgery, Virginia Beach General Hospital, Virginia Beach, VA 23451, and Department of Surgery, University of North Carolina, Chapel Hill, NC 27514, USA, US
Department of Molecular Genetics and Biochemistry, W1143 BST, University of Pittsburgh, Pittsburgh, PA 15261, USA Fax: (412) 383-8859, US
Abstract: The human mucin, MUC-1, is a transmembrane glycoprotein that is produced by both normal an malignant epithelium. The MUC-1 produced by malignant epithelium is underglycosylated, which leads to the expression by tumors of novel T and B cell epitopes on the mucin polypeptide core. Similar underglycosylation occurs in the lactating breast. In this report, we describe a long-term survivor of breast cancer whose tumor strongly expressed the T- and B-cell-stimulatory epitopes. Five years after presenting with the tumor, the patient had her first pregnancy, at which time she developed fulminant lymphocytic mastitis. We demonstrate that the lactating breast produced mucin expressing the same “tumor-specific” epitopes as the original cancer. The patient had circulating anti-mucin antibodies of both the IgM and IgG isotypes (these are not found in normal controls), and mucin-specific cytotoxic T lymphocytes in the peripheral blood. Limiting  –  dilution analysis for mucin  –  specific cytotoxic T lymphocytes in three different experiments yielded frequencies of 1 in 3086, 1 in 673, and 1 in 583, compared to approximately 1 in 106 in normal controls. The patient remains clinically free of carcinoma after 5 additional years of follow-up. We propose that the original tumor primed the patient’s immune response against the mucin epitopes, and that the re-expression of these epitopes on the lactating breast evoked a secondary immune response. It is tempting to speculate that the vigor of her anti-mucin immunity may have helped protect this patient against recurrent tumor. Received: 12 February 1996 / Accepted: 5 November 1996
Keywords:  Immunization  Carcinoma  Lymphocyte  Glycosylation  Tumor antigen
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