Endothelial cell marker PAL‐E reactivity in brain tumor, developing brain, and brain disease

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.