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Previous Volume 333:925-927 October 5, 1995 Number 14 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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One of the most startling discoveries in the wake of the cloning of the human -globin gene nearly 20 years ago was that many patients with thalassemia carried mutations outside the gene's coding sequence. In certain cases the change affected just one nucleotide base in a region of DNA upstream of where transcription of the -globin starts. Yet the amount of -globin produced by the red cells of these patients was drastically reduced. It was difficult to imagine how such a subtle change could shut down a whole assembly line. What function could a single nucleotide perform that was so . . . [Full Text of this Article]

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