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Previous Volume 347:67-68 July 4, 2002 Number 1 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: Savage and Antman (Feb. 28 issue)¹ summarize the pathogenesis of BCR-ABL–positive chronic-phase leukemias that are responsive to imatinib mesylate therapy. The authors point out that the mechanism of the antiproliferative action of imatinib lies in its effective control of BCR-ABL tyrosine kinase activity, thus interfering with the promotion of the phosphorylation of multiple substrates of mitogenic signaling pathways. The precise oncogenic mechanism of BCR-ABL is still unknown.

There are important changes in the metabolic profile of BCR-ABL–positive cells after their reversion as a result of imatinib mesylate treatment. Hematopoietic cells transfected with BCR-ABL express the high-affinity GLUT-1 . . . [Full Text of this Article]

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