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Tissue Iodine Content and Serum-Mediated ¹²⁵I Uptake-Blocking Activity in Breast Cancer¹

University College Dublin, St. Vincent’s University Hospital, Dublin 4, Ireland; and University of Sheffield, Sheffield S57AV, United Kingdom

Address all correspondence and requests for reprints to: Dr. P. P. A. Smyth, Endocrine Laboratory, Department of Medicine and Therapeutics, Woodview, University College Dublin, Dublin 4, Ireland. E-mail: PPA.SMYTH{at}UCD.IE

In the thyroid, active transport of iodide is under control of the TSH-dependent Na⁺/I^- symporter (NIS), whereas in the breast such control is less well understood. In this study, NIS expression was demonstrated by RT-PCR in 2 of 2 fibroadenomata and 6 of 7 breast carcinoma messenger ribonucleic acid isolates. In addition, mean total tissue iodine levels of 80.9 ± 9.5 ng I/mg protein in 23 benign tumors (fibroadenomata) were significantly higher than those in 19 breast cancers taken from either the tumor (18.2 ± 4.6 ng I/mg) or morphologically normal tissue taken from within the tumor-bearing breast (31.8 ± 4.9 ng I/mg; P < 0.05 in each case). Inhibition of ¹²⁵I uptake into NIS-transfected CHO cells was observed in serum from 20 of 105 (19.0%) breast carcinoma, 8 of 49 (16.3%) benign breast disease, and 27 of 86 (31.4%) Graves’ patients, but in only 1 of 33 (3.0%) age-matched female controls. IgG purified from serum of patients showing positive ¹²⁵I uptake inhibition also inhibited iodide uptake, suggesting that such inhibition was antibody mediated. ¹²⁵I uptake inhibition was significantly associated with thyroid peroxidase antibody positivity (P < 0.05) in sera from breast cancer patients, but not in those with benign breast disease, once again suggesting an association between thyroid autoimmunity and breast carcinoma.

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