BACKGROUND: The endothelial cell marker PAL-E is not reactive to vessels in the normal brain. The present study concerns the PAL-E reactivity in brain tumors in contrast to normal brain and nonneoplastic brain disease. METHODS: A total of 122 specimens were examined: brain tumors (n = 94), nonneoplastic brain disease (n = 19), normal brain (n = 8), and fetal brain (n = 1). Standard immunohistochemical procedures using a panel of endothelial cell markers were applied to detect vessels reactive to PAL-E. RESULTS: PAL-E reactivity to endothelial cells was found in all cases of glioblastoma multiforme, in 75% of the cases of anaplastic astrocytoma, and in 46% of the cases of astrocytoma. Furthermore, PAL-E reactivity was present in diseases with a developmental etiology, such as primitive tumors and congenital vascular malformations. The developing human brain (6-weeks' gestation age) and special sites of the mature brain, sites without blood-brain barrier, showed a strong reactivity, which indicates a relation with the status of blood-brain barrier development. CONCLUSIONS: PAL-E is the only marker out of a panel of endothelial cell markers that shows no reactivity to endothelial cells in the normal brain with an intact blood-brain barrier. In primary and metastatic brain tumors, PAL-E is reactive to endothelial cells, except for 25% of anaplastic astrocytoma and 54% of astrocytoma. PAL-E reactivity in brain tumors most likely is related to angiogenesis and to blood-tumor barrier properties not present in the normal blood-brain barrier.
BACKGROUND: The endothelial cell marker PAL-E is not reactive to vessels in the normal brain. The present study concerns the PAL-E reactivity in brain tumors in contrast to normal brain and nonneoplastic brain disease. METHODS: A total of 122 specimens were examined: brain tumors (n = 94), nonneoplastic brain disease (n = 19), normal brain (n = 8), and fetal brain (n = 1). Standard immunohistochemical procedures using a panel of endothelial cell markers were applied to detect vessels reactive to PAL-E. RESULTS: PAL-E reactivity to endothelial cells was found in all cases of glioblastoma multiforme, in 75% of the cases of anaplastic astrocytoma, and in 46% of the cases of astrocytoma. Furthermore, PAL-E reactivity was present in diseases with a developmental etiology, such as primitive tumors and congenital vascular malformations. The developing human brain (6-weeks' gestation age) and special sites of the mature brain, sites without blood-brain barrier, showed a strong reactivity, which indicates a relation with the status of blood-brain barrier development. CONCLUSIONS: PAL-E is the only marker out of a panel of endothelial cell markers that shows no reactivity to endothelial cells in the normal brain with an intact blood-brain barrier. In primary and metastatic brain tumors, PAL-E is reactive to endothelial cells, except for 25% of anaplastic astrocytoma and 54% of astrocytoma. PAL-E reactivity in brain tumors most likely is related to angiogenesis and to blood-tumor barrier properties not present in the normal blood-brain barrier.
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