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Experimental Therapy of Human Breast Tumors with ¹³¹I-labeled Monoclonal Antibodies Prepared against the Human Milk Fat Globule¹

John Muir Cancer and Aging Research Institute, Walnut Creek, California 94596

Breast tumors are susceptible to attack by unconjugated anti-human milk fat globule monoclonal antibodies (MoAbs) and most particularly by their mixture (cocktail) (Cancer Res., 47: 532–540, 1987). In the present study the same MoAbs (Mc1, Mc3, Mc5, and Mc8) labeled with ¹³¹I, either singly or in cocktails, were used for a similar purpose. Biodistribution studies showed that a transplantable human breast tumor line (MX-1) implanted in BALB/c nude mice (nu/nu) had the maximum incorporation of injected ¹³¹I-MoAbs at day 4 while levels in circulation and in normal tissue declined steadily from day 1. Also, these studies showed that the amount of radiolabeled Mc3 MoAb incorporated by MX-1 tumors was greater than that for cocktail of MoAbs and MoAb Mc5.

Tumor destruction by injected ¹³¹I-MoAb cocktail was shown in therapy experiments to be dose dependent. A single injection (500 µCi/mouse) of ¹³¹I-MoAb Mc3, or of cocktail, produced large breast tumor volume diminution and inhibition of growth for up to 30 days while a similar dose of ¹³¹I-labeled control IgG had no effect. A second dose of 500 µCi ¹³¹I-MoAb of Mc3 or of cocktail, injected at an appropriate interval, again diminished tumor mass significantly and inhibited its growth for another 20 days. In control experiments, non-breast tumors (colon) were marginally affected by the ¹³¹I-MoAbs. These results show that the systemic injection of radioiodinated MoAbs against human milk fat globule destroy the epithelial cells of human breast tumors and control their growth for an appreciable length of time. Radioiodoconjugated MoAbs proved to be more effective than unconjugated MoAbs in reducing breast tumor mass and also in inhibiting growth for longer periods of time at immunoglobulin doses 100 to 200 times lower. Further exploration of their role in breast cancer treatment seems warranted by these results.

¹ This investigation was supported by Grants RO1-CA39932 and RO1-CA39933 from the National Cancer Institute, NIH, and BRSG Grant S07-RR05929.

² To whom requests for reprints should be addressed.

Received 4/13/87. Revised 2/ 1/88. Revised 5/16/88. Accepted 5/20/88.

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