Abstract
A relationship between the pathogenesis of some cancers and growth hormone, insulin-like growth factor-1 and insulin-like growth factors binding protein-3 has been shown. Our aim was to evaluate the expression of growth hormone receptor, insulin-like growth factor-1 receptor and insulin-like growth factors binding protein-3 in actinic keratosis, basal cell carcinoma and squamous cell carcinoma, and to compare the expression patterns of tumoral areas with normal epidermis and skin appendages. The formalin-fixed, paraff in-embedded tissues of 40 patients which were diagnosed as 15 actinic keratosis, 15 basal cell carcinoma and 15 squamous cell carcinoma were analyzed for growth hormone receptor, insulin-like growth factor-1 receptor and insulin-like growth factors binding protein-3 with the immunohistochemical method using the streptavidin-biotin-peroxidase technique. There was no difference between tumoral areas of actinic keratosis, basal cell carcinoma and squamous cell carcinoma in expression of growth hormone receptor and insulin-like growth factors binding protein-3 (P > 0.05). However, a significantly higher expression of insulin-like growth factor-1 receptor was observed in tumoral areas of squamous cell carcinoma (P < 0.01). In basal cell carcinoma, a significantly lower intensity of immunostaining with growth hormone receptor, insulin-like growth factor-1 receptor and insulin-like growth factors binding protein-3 in tumoral areas than skin appendages was seen (P < 0.01). In squamous cell carcinoma, higher expressions of growth hormone receptor, insulin-like growth factor-1 receptor and insulin-like growth factors binding protein-3 in tumoral areas than peritumoral epidermis was found (P =0.06, P < 0.01 and P =0.02, respectively). Our study points out that, growth hormone receptor, insulin-like growth factor-1 receptor and insulin-like growth factors binding protein-3 have a role in the pathogenesis of non-melanoma skin cancers, especially squamous cell carcinoma.
Highlights
The skin is a target organ for growth hormone (GH) that exerts its proliferative and anabolic effects via its receptor
There is no evidence that GH is produced in the skin, insulin-like growth factor-1 (IGF-1) is synthesized in the skin by dermal fibroblasts, melanocytes and possibly by keratinocytes
We aimed to evaluate the differences in expression of Growth hormone receptor (GHR), IGF-1R, and IGFBP-3 between actinic keratoses (AK), basal cell carcinoma (BCC), and squamous cell carcinoma (SCC) tissues and to demonstrate their role in tumorigenesis by comparing the expression patterns of tumoral areas with normal epidermis and skin appendages
Summary
The skin is a target organ for growth hormone (GH) that exerts its proliferative and anabolic effects via its receptor. Growth hormone receptor (GHR) has been shown to be expressed in the epidermis (mainly in stratum basale and spinosum), adnexal structures, dermal fibroblasts, adipocytes, schwann and muscle cells [1,2]. GH stimulates the synthesis of insulin-like growth factor-1 (IGF-1). It is a major mediator of the effect of GH. The action of IGF-1 is predominantly mediated by the IGF-1 receptor (IGF1R) that is overexpressed by many tumor cell lines. The bioavailability of IGF-1 for interaction with its receptor is modulated by insulin-like growth factor binding proteins (IGFBP 1-6), especially by IGFBP-3 [3]. Dermal fibroblasts are sources of IGFBP-3 [5]
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