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Research Article Free access | 10.1172/JCI114315
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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Division of Medical Oncology, University of Texas Health Science Center, San Antonio 78284.
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Published November 1, 1989 - More info
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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