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Previous Volume 329:958-959 September 23, 1993 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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Acute leukemias result from acquired genetic lesions that activate cellular proto-oncogenes or inactivate tumor-suppressor genes, leading to the loss of growth control in blood-forming cells. In these leukemias, exchanges of genetic information between chromosomes (translocations) are frequently responsible for converting cellular genes to oncogenes by repositioning them at new chromosomal sites. Recent cytogenetic and molecular studies have revealed a remarkable diversity of human genes that, when altered, may contribute to the development of tumors. In this issue of the Journal, Thirman et al.¹ describe more than 20 different rearrangements of a single gene in primary acute leukemias, all of which . . . [Full Text of this Article]

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