| Title | Expression of insulin-like growth factor-binding protein 2 in melanocytic lesions. | | Author(s) | Wang H, Shen SS, Wang H, Diwan AH, Zhang W, Fuller GN, Prieto VG | | Institution | Department of Pathology and Laboratory Medicine, The University of Texas Medical School at Houston, USA. | | Source | J Cutan Pathol 2003 Nov; 30(10):599-605. | | MeSH | Dysplastic Nevus Syndrome
Humans
Immunohistochemistry
Insulin-Like Growth Factor Binding Protein 2
Melanocytes
Melanoma
Nevus, Pigmented
Skin Neoplasms
Staining and Labeling
| | Abstract | BACKGROUND: Insulin-like growth factor-1 (IGF-1) is one of the most critical proteins required for the survival, migration, and growth of melanoma cells. IGF-binding protein 2 (IGFBP2), which binds and regulates the function of IGF-1, is upregulated in a dose-dependent manner in melanoma cells treated with IGF-1, suggesting a possible role of IGFBP2 in the pathogenesis of melanoma.
METHODS: Tissue microarrays were constructed using formalin-fixed, paraffin-embedded archival tissue blocks from 94 melanocytic lesions: 20 benign nevi, 20 dysplastic nevi, 23 primary melanomas, and 31 metastatic melanomas. IGFBP2 expression was evaluated immunohistochemically using a polyclonal antibody against the C-terminus of IGFBP2. The number of cells and labeling intensity were assessed semiquantitatively.
RESULTS: Positive IGFBP2 labeling was observed in 5.0% of benign nevi, which was significantly lower than in dysplastic nevi (35.0%), primary melanomas (52.2%), or metastatic melanomas (54.8%) (p < 0.05). Among the IGFBP2-positive cases, moderate-to-strong immunostaining was observed in 64.7% of metastatic melanomas and 33.3% of primary melanomas. But none of the dysplastic nevi had moderate-to-strong immunostaining (p < 0.05).
CONCLUSIONS: Our study shows that IGFBP2 expression increases from benign and dysplastic nevi to primary and metastatic melanomas and suggests that it may play a role in melanoma progression. | | Language | eng | | Pub Type(s) | Journal Article
| | PubMed ID | 14744083 |
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