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Research Article Free access | 10.1172/JCI114910

Insulin-like growth factor I expression by tumors of neuroectodermal origin with the t(11;22) chromosomal translocation. A potential autocrine growth factor.

D Yee, R E Favoni, G S Lebovic, F Lombana, D R Powell, C P Reynolds, and N Rosen

Lombardi Cancer Research Center, Georgetown University Medical Center, Washington, D.C. 20007.

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Lombardi Cancer Research Center, Georgetown University Medical Center, Washington, D.C. 20007.

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Lombardi Cancer Research Center, Georgetown University Medical Center, Washington, D.C. 20007.

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Lombardi Cancer Research Center, Georgetown University Medical Center, Washington, D.C. 20007.

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Lombardi Cancer Research Center, Georgetown University Medical Center, Washington, D.C. 20007.

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Lombardi Cancer Research Center, Georgetown University Medical Center, Washington, D.C. 20007.

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Lombardi Cancer Research Center, Georgetown University Medical Center, Washington, D.C. 20007.

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Published December 1, 1990 - More info

Published in Volume 86, Issue 6 on December 1, 1990
J Clin Invest. 1990;86(6):1806–1814. https://doi.org/10.1172/JCI114910.
© 1990 The American Society for Clinical Investigation
Published December 1, 1990 - Version history
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Abstract

Expression of insulin-like growth factor I (IGF-I) mRNA by some tumor cell lines of neuroectodermal origin has been described. To further explore the significance of IGF-I mRNA expression in these tumors, a more extensive analysis was performed. Most (9 of 10) neuroectodermal tumor cell lines with a t(11;22) translocation (primitive neuroectodermal tumor [PNET], Ewing's sarcoma, esthesioneuroblastoma) expressed IGF-I mRNA, whereas 0 of 15 cell lines without the translocation (PNET, neuroblastoma) expressed IGF-I. Furthermore, inasmuch as all neuroblastoma (12 of 12) cell lines examined expressed IGF-II RNA, the pattern of IGF expression could distinguish between these closely related tumors. CHP-100, a PNET cell line with the t(11;22) translocation, was shown to secrete both IGF-I protein and an IGF binding protein, IGFBP-2. This cell line also expressed the type I IGF receptor mRNA, and blockade of this receptor by a monoclonal antibody (alpha IR3) inhibited serum-free growth. These data demonstrate that IGF-I expression is a property of neuroectodermal tumors with a t(11;22) translocation and that interruption of an IGF-I autocrine loop inhibits the growth of these tumor cells.

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