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Lady Davis Research Institute, McGill University, 3755 Cote St. Catherine Road, Montreal, Quebec, Canada H3T 1E2 [M. P., H. H., X-F. Y.] and The Jackson Laboratory, Bar Harbour, Maine [W. B.]
Insulin-like growth factor I (IGF-I) is a potent breast cancer mitogen. Growth hormone (GH) up-regulates hepatic IGF-I gene expression and circulating IGF-I level. Tissue IGF bioactivity is influenced not only by circulating IGF-I and IGF-II levels but also by autocrine and paracrine production of these growth factors and by IGF binding proteins. There is considerable person-to-person variability in GH-IGF-I physiology. Both laboratory and epidemiological data are consistent with the hypothesis that the host GH-IGF-I axis influences breast cancer behavior, but such an effect has not been directly demonstrated. To determine whether breast cancer growth in an in vivo model is influenced by the host GH-IGF-I axis, we compared the growth of human MCF-7 breast cancer cells in control mice to that in mice homozygous for lit, a missense mutation resulting in loss of function of the pituitary GH-releasing hormone receptor and secondary suppression of GH and IGF-I. Breast cancer growth was significantly reduced in lit/lit animals compared to control hosts [tumor size (mean ± SD) on day 39, 444 ± 82 versus 845 ± 444 mm3, respectively; P < 0.001, Mann-Whitney U test]. These data demonstrate that in our model, host GH-IGF-I axis physiology plays a role in determining breast cancer behavior. The results a) suggest that patient-to-patient variability in GH-IGF-I physiology may contribute to the large variability between patients regarding breast cancer behavior, and b) motivate clinical trials of novel hormonal treatment strategies that target the GH-IGF-I axis.
1 Supported by grants from MRC (Canada) and the Canadian Breast Cancer Initiative (to M. P.) and by American Cancer Society Grant BE-170 and National Cancer Institute grants CA-34196 and CA-62434 (to W. B.).
2 To whom requests for reprints should be addressed. Phone: (514) 340-8222, Extension 5527; Fax: (514) 340-8302.
Received 1/22/96. Accepted 2/21/96.
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