Previous studies using comparative genomic hybridization have identified copy number changes in specific chromosomal segments characteristic of melanomas but not of nevi.1 Copy number changes in DNA can also be detected by interphase fluorescent in situ hybridization (FISH). Over the last year, we have been using an interphase FISH assay with probes targeting specific chromosomal segments gained or lost in melanoma but not in nevi, including a probe for 11q13. Gains or amplifications of the cyclin D1 gene (OMIM 168461) located at 11q13 are commonly identified in melanomas, particularly those on chronically sun-damaged skin.2 These gains and amplifications are typically identified in the form of double-minute chromatin bodies (dmins), acentric and atelomeric structures that appear by FISH as distinct units of increased copy number of the targeted DNA chromosomal segment.3 Occasionally, DNA amplification as identified by FISH can be seen in the form of a homogeneous staining region (HSR), which results from the integration of multimerized dmins into the chromosome.4
Gerami P, Guitart J, Martini M, Wayne JD, Kuzel T. Cyclin D1 Homogeneous Staining Regions by Fluorescent In Situ Hybridization: A Possible Indicator of Aggressive Behavior in Melanomas. Arch Dermatol. 2008;144(9):1235–1236. doi:10.1001/archderm.144.9.1235-b
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