Insulin-like growth factors in human breast cancer

Neal Rosen, Douglas Yee, Marc E. Lippman, Soonmyoung Paik, Kevin J. Cullen

Research output: Contribution to journalArticlepeer-review

65 Scopus citations


Several protooncogenes and suppressor genes and a variety of growth factors and their receptors have been shown to be mutated, deleted, or activated in human breast cancer. These changes may account for the unregulated growth of breast carcinoma cells. Insulin-like growth factors I and II (IGF-I, IGF-II) belong to a family of polypeptides with growth promoting properties and structural homology to insulin. They exert their mitogenic effects by binding to the IGF-I receptor and activating its tyrosine protein kinase. Other proteins that specifically bind the IGFs include the plasma membrane IGF-II receptor, which also binds lysosomal hydrolases, and several IGF-binding proteins which may serve to modulate IGF interactions with receptors. Breast cancer cell lines express IGF-I and IGF-II receptors and different patterns of binding proteins. IGF-I and IGF-II are each mitogenic for subsets of breast cancer cell lines. This effect is inhibited by antibodies directed against the IGF-I receptor. In breast tumors, IGF-I is expressed by stromal cells, but not carcinoma cells; it is not expressed by breast cancer cell lines. IGF-I is therefore a potential paracrine regulator of breast cancer cell growth. Similarly, IGF-II is expressed in breast tumors, predominantly in stromal cells, but sometimes also in carcinoma cells and in a subset of cell lines. Thus, IGF-II is also a potential paracrine regulator of breast cancer cell growth; in addition, it can be an autocrine regulator in some breast cancer cells.

Original languageEnglish (US)
Pages (from-to)S55-S62
JournalBreast Cancer Research and Treatment
Issue number1 Supplement
StatePublished - May 1 1991


  • breast cancer
  • growth factors
  • insulin-like growth factors


Dive into the research topics of 'Insulin-like growth factors in human breast cancer'. Together they form a unique fingerprint.

Cite this