Running Interference on Interferon-gamma

Interferon-gamma, a protein primarily used for intercellular communication by the immune system, acts as a promoter for melanoma, the deadliest form of skin cancer.

Over the past 10 years, scientists have used genetically modeled mice to prove, then to decipher how, UV radiation-exposure is linked to the initiation of melanoma. The latest research is an attempt to identify the molecular mechanisms at play in this cause-and-effect partnership. Results suggest that the suppression of interferon-gamma that occurs immediately after sunburn may inhibit the carcinogenic activation of melanocytes (pigment-producing cells in the skin). Inhibiting interferon-gamma could be a potentially effective preventive measure against melanomas caused by UV radiation.

Scientists looked at dosages of UV radiation equal to what would cause sunburn in human skin and found this amount of radiation increased the amount and movement of melanocytes in the mouse skin. A detailed analysis of gene-expression changes linked to this melanocyte activation revealed abnormal expression of a number of genes that are known to respond to interferon-gamma. This abnormal expression did not occur when interferon-gamma was blocked, however.

The finding, from researchers from the National Cancer Institute (NCI), stemmed from a series of experiments designed to identify how solar ultraviolet (UV) radiation causes melanoma. The results of this study suggest that interferon-gamma might promote melanoma under certain circumstances by enticing tumors. Interestingly, interferon-gamma has been thought to contribute to an innate defense system against cancer.

Approximately 5,550 men and 3,100 women died of melanoma in 2009, according to the American Melanoma Foundation, making the disease the deadliest if least common variant of skin cancer.