Endocrine Abstracts

The demonstration in extrathyroidal tissues of the sodium iodide symporter (NIS) has raised the possibility that 131I, commonly used as a therapeutic ablative agent in hyperthyroidism and thyroid cancer, might be applied in the treatment of tumours in other NIS expressing tissues such as human breast cancer. As thyroidal uptake of 131I is known to be inversely proportional to circulating stable I- concentration, the aim of this study was to determine how I- would effect such uptake in human breast cancer cell lines MCF-7, MDA-MB-231, and in NIS- transfected HeLa cells. Cells were incubated with KI (O-100mM) for 72 hours after which 125I was added. Incubation continued for 4 hours and uptake of 125I by cells was counted. Timed efflux of 125I was measured every five minutes. KI in the incubation medium blocked 125I uptake in a dose dependent manner in the E receptor positive MCF-7 cell line giving maximum effect at 10mM which plateaued thereafter. The effect was less marked in the E receptor negative MDA-MB-231cells with significant uptake being maintained even at an I- concentration of 50mM. A similar blockade was seen in the HeLa cell line with maximum blockade at 25mM I-. The rate of efflux of 125I was similar in both MCF-7 and MDA-MB-231 cell lines with t 1/2 of 35 and 40 minutes respectively. In contrast, efflux from the NIS transfected HeLa cells was faster (t 1/2 = 15 mins). In common with the thyroid, radioactive iodine uptake by breast cell lines is inversely proportional to stable iodine concentration. However, I- concentration does not appear to influence 125I efflux in breast cells. As the human breast has a much lower avidity for I- than the thyroid, control of dietary intake would assume even greater importance in radioactive iodine treatment of breast tumours or their metastases.