In pathological settings, AHR signaling enhances malignant transformation as well as metastatic progression and impairs the efficacy of T cell-directed immunotherapies. In physiological settings, AHR signaling promotes protective melanocyte responses to UV irradiation. This project is based on the central hypothesis that AHR signaling plays a dual functional role for adaptive responses of melanocytes and melanoma cells to tissue injury and inflammation. This experimental finding supports a role for AHR signaling in melanoma pathogenesis. In our models, we could show that AHR signaling promotes invasive growth and metastatic dissemination upon transplantation into the skin in vivo.

However, AHR signaling has also been shown to promote the development of cancer by promoting cancer cell proliferation and survival as well as by protecting cancer cells from immune attack. This was associated with impaired reactive proliferation and differentiation of AHR knockout melanocytes following sunburning doses of UVB. AHR knockout mice showed decreased tanning responses after UVB-irradiation when compared with wild-type mice. Over the last decade, evidence has accumulated that the aryl hydrocarbon receptor plays a clinically relevant role in melanocyte responses to UVB. The AHR is widely expressed throughout the body. The aryl hydrocarbon receptor (AHR) was originally identified as a sensor for environmental stressors like dioxins. Fair skin and exposure to UVB-light are primary risk factors for the development of melanoma. With an incidence of 20.5 cases per 100,000 inhabitants, Germany is the country with the highest melanoma incidence after Australia, New Zealand and Denmark. The incidence of melanoma accounts for 1.7 % of all cancer cases worldwide with over 300,000 new cases each year.

Thomas Tüting in the Laboratory for Experimental Dermatology at the University Hospital Magdeburg.

We are seeking a motivated PhD student to join the group of Prof.

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