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Jack M. Rozental, MD, PhD; Ross L. Levine, MD
University of Wisconsin Medical School and William S. Middleton Veterans Hospital 2500 Overlook Terr Madison, WI 53705

Arch Neurol. 1991;48(6):569-570.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

In Reply.

—In his letter to the editor, Maker raises an interesting issue regarding our article "Glucose Uptake by Gliomas After Treatment."¹ Maker states that tumor cells in a well-oxygenated environment (closer to blood vessels) tend to be more vulnerable to chemotherapy. Thus, tumor cells in a relatively hypoxic environment would be more likely to survive treatment. Furthermore, the rate of glucose uptake by tumor cells increases and becomes deregulated with increasing hypoxia (increasing distance from blood vessels). Therefore, if hypoxic cell populations predominate following exposure to chemotherapy, glucose uptake would appear to increase relative to the baseline state.

This alternative explanation for the increase in glucose uptake observed after chemotherapy was only briefly considered in our discussion for several reasons. We stated that the phenomenon "... might have originated from the chemoresistant (ie, also hypoxic) subpopulation of cells, it could represent a mechanism for synchronization, release from growth arrest, . . . [Full Text PDF of this Article]

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