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Previous Volume 355:1395-1396 September 28, 2006 Number 13 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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To the Editor: The review of melanoma by Miller and Mihm (July 6 issue)¹ clearly characterizes the linear progression of melanocytic lesions, from the morphologic perspective to the molecular perspective.^2,3 However, the genetic alterations would have more relevance if they result in kinetic advantage and progression. My colleagues and I have studied a series of dysplastic nevi (92 low-grade and 31 high-grade lesions) and melanomas in situ (15 lesions) using proliferation (Ki-67 labeling), apoptosis (in situ end labeling), and cell-cycle regulators (RB1, TP53, p21WAF1, and p27Kip1).⁴ Our analysis highlighted a clear topographic heterogeneity at the early stage of melanocytic transformation: . . . [Full Text of this Article]

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