In vivo expression of the insulin-like growth factor-I (IGF-I) receptor in congenital pigmented nevi

E. Hodak, A. B. Gottlieb, S. Colen, M. Anzilotti, J. G. Krueger

Research output: Contribution to journalArticlepeer-review

Abstract

Growth of normal melanocytes, nevus cells and primary melanoma cells is enhanced by insulin/insulin-like growth factor-I (IGF-I) in vitro. It has been shown that a melanoma cell line possesses the IGF-I receptor which plays a role in activation of the chemotactic response. Little is known about the in vivo expression of the IGF-I receptor and its role in melanocytic lesions. In an immunohistochemical study, we investigated the expression of IGF-I receptor in frozen sections of congenital pigmented nevi from 10 patients (ages 8 months to 4 yrs) using the monoclonal antibody αIR 3, which specifically recognizes the extracellular alpha subunit of the IGF-I receptor. The proliferative activity of the nevus cells was examined by staining with Ki67 monoclonal antibody (reactive with all actively cycling cells). IGF-I receptor was found to be widely expressed by the cell surface of the nevus cells. Membrane staining was occasionally stronger in the superficial portion of the congenital pigmented nevi. In contrast, Ki67-positive cells were only sparsely scattered throughout the nevi with some tendency to localization to the superficial portion. This study indicates that in vivo the IGF-I receptor is widely expressed by congenital pigmented nevus cells. As opposed to keratinocytes, in which IGF-I receptor expression defines the proliferation pool of the normal and disordered epidermis, the IGF-I receptor is expressed by all nevus cells, irrespective of their proliferative status. Further studies are needed to assess whether the IGF-I receptor expression can serve as a marker for increased risk for development of malignancy in various types of benign melanocytic lesions.

Original languageEnglish
Pages (from-to)19-24
Number of pages6
JournalJournal of Cutaneous Pathology
Volume23
Issue number1
DOIs
StatePublished - 1996
Externally publishedYes

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