Dan F. Spandau, PhD

The primary environmental factor that influences the development of skin cancer is exposure to the spectrum of ultraviolet wavelengths (particularly UVB) found in sunlight. In vitro evidence and epidemiological data from Dr. Dan Spandau’s lab have indicated that one mechanism responsible for UVB-induced skin cancer involves the suppression of the IGF-1R signaling network in epidermal keratinocytes. Furthermore, there is a strong correlation between developing skin cancer and increasing age, as 80 percent of all non-melanoma skin cancers (NMSCs) are found in people over the age of 60. Dr. Spandau’s lab has identified that aging-associated squamous cell carcinoma is due in part to the accumulation of aging, senescent fibroblasts in the skin of geriatric patients. These senescent fibroblasts silence the expression of IGF-1 in the skin which in turn leads to a deficient activation of the IGF-1R on keratinocytes, increasing their sensitivity to photocarcinogenesis.

Fortunately, this newly identified mechanism has also generated potential new therapies to aid individuals that are highly susceptible to skin cancer by targeting senescent dermal fibroblasts. Treatment modalities which remove senescent fibroblasts and recruit new fibroblasts thereby normalizing the secretion of IGF-1 could potentially prevent the initiation of UVB-induced carcinogenesis caused by ongoing sun exposure. Taking advantage of routinely used cosmetic therapies, the research demonstrated that these wounding therapies could increase IGF-1 expression and restore the appropriate UVB response in geriatric individuals. This team of investigators is currently actively exploring the mechanism for IGF-1 silencing in geriatric fibroblasts and refining the wounding therapies so that they can be widely used as treatment to prevent squamous cell carcinoma in geriatric individuals.