Towards improved melanoma treatment: gene identification, in vivo modeling and drug target discovery
Melanoma is amongst the most aggressive malignancies occurring in man, posing a substantial threat to the patient even when the primary tumor has reached a thickness of only a few millimeters. The presence of distant metastasis is associated with a grim prognosis, since none of the currently used systemic therapies offers a chance of cure. About half of patients succumb to tumor metastasis when the thickness of the primary is 4 mm. As melanoma shows a disconcertingly rapid increase in incidence too, there is an urgent need to improve treatment.
Melanocytic nevus (mole) is a very common, small, benign tumor of cutaneous melanocytes. Most arise in childhood and adolescence. Nevi typically show little proliferative activity and are the benign counterparts of malignant melanoma. Their oncological importance is twofold: melanocytic nevi may give rise to melanoma, and secondly, some nevi are difficult or impossible to distinguish with certainty from melanoma and vice versa. At present, key questions are what genetic factors contribute to development and proliferative standstill of nevi, as well as to melanoma development and progression, and which melanoma factors (or pathways) correspond to druggable targets for therapeutic intervention. We have therefore developed three core objectives:
• Identification, validation, function and molecular mechanism of (epi-) genetic events causing nevogenesis.
• Function-based genome-wide identification of melanoma-susceptibility genes.
• Discovery of specific druggable targets in melanoma.
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