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Research Article Free access | 10.1172/JCI114315

Blockade of the type I somatomedin receptor inhibits growth of human breast cancer cells in athymic mice.

C L Arteaga, L J Kitten, E B Coronado, S Jacobs, F C Kull Jr, D C Allred, and C K Osborne

Division of Medical Oncology, University of Texas Health Science Center, San Antonio 78284.

Find articles by Arteaga, C. in: PubMed | Google Scholar

Division of Medical Oncology, University of Texas Health Science Center, San Antonio 78284.

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Division of Medical Oncology, University of Texas Health Science Center, San Antonio 78284.

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Division of Medical Oncology, University of Texas Health Science Center, San Antonio 78284.

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Division of Medical Oncology, University of Texas Health Science Center, San Antonio 78284.

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Division of Medical Oncology, University of Texas Health Science Center, San Antonio 78284.

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Division of Medical Oncology, University of Texas Health Science Center, San Antonio 78284.

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Published November 1, 1989 - More info

Published in Volume 84, Issue 5 on November 1, 1989
J Clin Invest. 1989;84(5):1418–1423. https://doi.org/10.1172/JCI114315.
© 1989 The American Society for Clinical Investigation
Published November 1, 1989 - Version history
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Abstract

Insulin and insulin-like growth factors (IGIs) stimulate the growth of human breast cancer cells in vitro. The type I somatomedin receptor (SR) expressed in these cells may mediate the growth effects of these peptides. We have examined the role of this receptor on human breast cancer growth with a monoclonal antibody (alpha-IR-3) that blocks the receptor binding domain and inhibits IGF-I-induced growth. alpha-IR-3 inhibited clonal growth in vitro and blocked the mitogenic effect of exogenous IGF-I in both MCF-7 and MDA-231 breast cancer cell lines. Antibody-induced blockade of the type I SR also inhibited the estrogen-independent MDA-231 cells growing in vivo in nude mice, but growth of the estrogen-dependent MCF-7 cells was unaffected. IGIs are important growth regulators of MDA-231 breast cancer cells. Blockade of this growth stimulatory pathway may provide a new treatment strategy.

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