THE GLUCOSE TRANSPORTER AND BLOOD-BRAIN-BARRIER OF HUMAN BRAIN-TUMORS

被引:60
作者
GUERIN, C
LATERRA, J
HRUBAN, RH
BREM, H
DREWES, LR
GOLDSTEIN, GW
机构
[1] JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSURG,BALTIMORE,MD 21205
[2] JOHNS HOPKINS UNIV,SCH MED,DEPT ONCOL,BALTIMORE,MD 21205
[3] JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205
[4] JOHNS HOPKINS UNIV,SCH MED,DEPT PATHOL,BALTIMORE,MD 21205
[5] JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205
[6] KENNEDY INST,BALTIMORE,MD
[7] UNIV MINNESOTA,SCH MED,DEPT BIOCHEM,DULUTH,MN 55812
关键词
D O I
10.1002/ana.410280606
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The glucose transporter of the human brain has been localized to endothelial cells expressing the blood‐brain barrier, but little is known regarding its mechanism of induction or whether its expression is exclusively linked with restricted vascular permeability. We investigated glucose transporter expression by vessels in human astrocytic tumors and pulmonary metastases to the brain using immunohistochemical techniques. Vessels in 9 of 10 low‐grade astrocytomas and 8 of 10 anaplastic astrocytomas were positive for glucose transporter. Glioblastoma vessels were transporter‐positive in only 2 of 10 specimens. Vessels in all three metastatic tumors were negative for the glucose transporter. The decrease in transporter expression observed in higher‐grade tumors occurred independently of increases in vascular permeability. In low‐grade astrocytomas and glioblastomas transporter expression and contrast enhancement were inversely related, but vessels in 6 of 9 anaplastic astrocytomas were transporter‐positive despite contrast enhancement. These findings suggest that separate mechanisms induce the glucose transporter and the permeability restrictions of the human blood‐brain barrier. They also have potential implications for the therapy and prognosis of astroglial neoplasms. Copyright © 1990 American Neurological Association
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页码:758 / 765
页数:8
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