Atypical
nevi are the precursors and risk markers of
melanoma. Apart from persistently monitoring these nevocytic lesions and resecting them at the earliest signs of clinical changes, there is as yet no systemic clinical treatment available to interfere with their progression to
melanoma. To explore clinical treatments that might interfere with and possibly prevent atypical
nevus progression, a previous study documented that 3 months systemic low-dose
interferon-alpha (IFN-alpha) treatment of patients with a clinical history of
melanoma and numerous atypical
nevi, led to inactivation of the STAT1 and STAT3
transcription factors in atypical
nevi. Based upon this finding, we initiated a second study to determine whether systemic low-dose IFN-alpha treatment also impairs the expression of upstream regulators and downstream targets of STAT1 and STAT3 in atypical
nevi. Using cyanine
dye-conjugated
antibodies, fluorescence imaging analysis revealed expression of JAK2, JNK1, AKT1,
NF-kappa B, and IFN-alpha/beta receptor in benign and atypical
nevi, and early- and advanced-stage
melanomas. To determine possible changes in the level of expression of these molecules in atypical
nevi, excised before and after 3 months of systemic low-dose IFN-alpha treatment, newly designed optical imaging software was used to quantitate the captured fluorescent hybridization signals on a cell-by-cell basis and across an entire
nevus section. The results of this analysis did not provide evidence that systemic low-dose IFN-alpha treatment alters the level of expression of upstream regulators or downstream targets of STAT1 and STAT3.