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Previous Volume 349:1293-1294 September 25, 2003 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 timely review article by DiMauro and Schon (June 26 issue)¹ does not highlight the opportunities for the development of diagnostic, preventive, and therapeutic interventions presented by the study of diseases caused by homoplasmic mutations in mitochondrial DNA (mtDNA). In patients with such diseases, the pathogenic mutation is expressed ubiquitously, yet the diseases tend to be tissue-specific and have highly variable clinical expression.² In most cases, the different phenotypes are attributable to nuclear-encoded modifier genes with complex patterns of inheritance.³ Positional cloning and candidate-gene approaches, as well as the existence of a mouse model,⁴ make it likely . . . [Full Text of this Article]

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