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Molecular Endocrinology Vol. 3, No. 3 509-517
doi:10.1210/mend-3-3-509
Copyright © 1989 by the Endocrine Society.
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Analysis of Insulin-Like Growth Factor I Gene Expression in Malignancy: Evidence for a Paracrine Role in Human Breast Cancer

Douglas Yee, Soonmyoung Paik, Gail S. Lebovic, Rachel R. Marcus, Roberto E. Favoni, Kevin J. Cullen, Marc E. Lippman and Neal Rosen

Medical Breast Cancer Section, National Cancer Institute Bethesda, Maryland 20892

Address requests for reprints to: Dr. Douglas Yee, Lombardi Cancer Research Center, Georgetown University Medical Center, Washington, D. C. 20007. This is the current address for all authors.

Abstract

Insulin-like growth factor I (IGF-I) activity has been reported to be produced by several human cancers. Identification of RNAs transcribed from the IGF-I gene has been complicated by the detection of multiple hybridizing bands on Northern analysis. To determine if any of these RNAs are transcribed from the IGF-I gene, we have used a sensitive and specific ribonuclease (RNAse) protection assay for IGF-I. We have also studied the breast cancer tissue expression of IGF-I using in situ hybridization histochemistry. We have found no IGF-I mRNA in breast (zero of 11) or colon cancer (zero of 9) cell lines; both of these tumors have been previously reported to express IGF-I mRNA. However, three of three neuroepithelioma and one of two Ewing's sarcoma cell lines express IGF-I mRNA; therefore, in these tumors IGF-I may be an autocrine growth factor. In contrast to breast cancer cell lines, RNA extracted from breast tissues has easily detectable IGF-I mRNA. In situ hybridizations show that IGF-I mRNA is expressed in the stromal cells, and not by normal or malignant epithelial cells. These findings suggest that although IGF-I is not produced by breast epithelial cells it may function as either a paracrine stimulator of epithelial cells or an autocrine stimulator of stromal cells.

Received for publication September 20, 1988. Revision received November 14, 1988. Accepted for publication November 15, 1988.




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