Epidermal Growth Factor Receptors in Different Skin Tumors

Abstract

Specific binding of ¹²⁵I-labeled epidermal growth factor (EGF) was measured in 62 skin tumors of different severity. Within a group of 28 benign tumors, 11 of 15 condylomata acuminata were receptor positive, whereas the investigated mesenchymal tumors and normal skin as a control were receptor negative. 6 of 18 basal cell epitheliomas bound EGF specifically. In the group of precancerous and malignant skin tumors, 7 of 8 squamous cell carcinomas had the highest number of EGF binding sites and a high affinity state, whereas 5 malignant melanomas were receptor negative. The clinical relevance of these findings is not yet clear due to the short follow-up of the patients.

Dual Inhibition of Both the Epidermal Growth Factor Receptor and erbB2 Effectively Inhibits the Promotion of Skin Tumors during Two-Stage Carcinogenesis

“…EGFR expression was also found in sebocytes, outer root sheath cells of hair follicles, smooth muscle cells of arrector pili, and dermal arteries (38, 39). Overexpression of EGFR protein has been reported in approximately 50 to 100% of basal cell carcinomas (BCCs) (40) and 90 to 100% of SCCs (40, 41), as determined by immunohistochemical analysis. Highly elevated mRNA levels of EGFR were reported in 38, 57, and 80% in normal epidermis, BCCs, and SCCs, respectively (42).…”

Somatic Mutation of Epidermal Growth Factor Receptor in a Small Subset of Cutaneous Squamous Cell Carcinoma

“…To determine whether RTKs are mutated in SCC, we searched the literature to identify RTKs that play a role in epidermal homeostasis and thus could be candidate oncogenes in squamous lesions. We chose to analyze epidermal growth factor receptor (EGFR) that is highly expressed in a small subset of metastatic cutaneous SCCs (Bauknecht et al, 1985; Shimizu et al, 2001; Maubec et al, 2005); FGFR3 that is mutated in familial acanthosis nigricans and Crouzon’s syndrome, a type of craniosynostosis (Berk et al, 2007) and induces acanthosis and benign tumors in transgenic mice (Logie et al, 2005); FGFR2, that is also mutated in Crouzon’s syndrome and in this disease is associated with acanthosis nigricans (Meyers et al, 1995). We included the insulin like growth factor receptor 1(IGF1R); mice lacking this receptor have hypoplastic skin (Liu et al, 1993; De Moerlooze et al, 2000), and MET the receptor for the ligand HGF.…”

13. Growth Factors and Growth Factor Receptors

“…Once its amino acid sequence had been ascer tained, the intracellular and membrane por tions of the receptor were found to exhibit homology with the v erb-B oncogene protein [HiBinding data, using labeled EGF, and immunocytochemical studies, using a mono clonal antibody to EGFR, have shown its presence in a variety of human tumors as well as in normal keratinocytes [11][12][13][14][15][16], In creased expression has been found in squa mous carcinomas of the lung, but not in other types of bronchial carcinomas. Cell line analysis has shown that in most, but not all instances, enhanced EGFR expression is due to gene amplification.…”