| First Author | van Schanke A | Year | 2003 |
| Journal | Pigment Cell Res | Volume | 16 |
| Issue | 5 | Pages | 579-80 (Abstr.) |
| Mgi Jnum | J:85678 | Mgi Id | MGI:2675937 |
| Citation | van Schanke A, et al. (2003) IL-18 UV-induced melanocyte proliferation and nevi in mice. Pigment Cell Res 16(5):579-80 (Abstr.) |
| abstractText | To establish experimentally whether and how short-wave ultraviolet (UVB) radiation can effectively induce and/or stimulate the growth of nevi in mice, and perhaps cause melanomagenesis, we subjected transgenic hairless mice to repeated erythemal/edemal UVB exposures in the neonatal and adult stages of their lives. Based on epidemiological data, we sought to optimize the sensitivity by using mice with defective Xpa (lacking DNA excision repair) and/or Ink4a (lacking in tumor - melanoma - suppression) genes. Neonatal treatments consisted of exposures to 4 times the minimal erythemal dose (MED) UVB at the ages of 3,4 and 5 days. Adult treatments entailed daily, weekly or bi-weekly exposure to 1, 4 or 6 MED, resp., from day 28 onward. The latter adult regimen proved most effective of the three, which accords with a most effective induction of melanocyte proliferation. The highest increase in number and size of nevi occurred in mice exposed both neonatally and in adulthood, followed by mice only exposed in adulthood. Occurrence of nevi in unexposed control mice was very rare. Neonatal treatment with DMBA proved to be more effective than UV exposures, but chemical promotion by TPA (2 times a week) was less effective than intermitted UV overexposure. These data identify sunburn as a powerful stimulus for the induction and growth of nevi, which is consistent with the epidemiological finding that the number of severe sunburns rather than cumulative exposure to sunlight is an important determinant of melanoma risk. However, the Ink4a defect did not appear to enhance nevi development, nor did it facilitate progression of nevi into melanomas in the present mouse model. |
