The current study suggests that PR in the astrocytic tumors correlates with histologic grade and PR may participate in the growth of these tumors and tumor angiogenesis. The measurement of PR in these tumors may indirectly represent tumor growth potential.
1. Cellular expression and distribution of the stress response small heat shock protein 27 (hsp27) in 39 high-grade astrocytomas (27 glioblastoma multiformes, 12 anaplastic astrocytomas) and in 27 low-grade astrocytomas (grade I-II) were analyzed immunohistochemically. 2. The correlation between hsp27 expression and tumor growth fractions of the astrocytomas was examined following Ki-67 immunostaining. 3. The hsp27 staining was cell cytoplasmic. The hsp27 immunopositive rate was significantly higher in high-grade astrocytomas; the rates was 74% for glioblastomas, 58% for anaplastic astrocytomas, and 37% for low-grade astrocytomas. The small and large tumor cells, especially in glioblastomas, multinucleated tumor giant cells, tumor cells in the pseudopalisading and necrotic areas, cells of the microvascular endothelial proliferations, and tumor vascular smooth muscles were usually hsp27 positive. The mean percentage of hsp27-positive cells was significantly higher in the glioblastomas alone and in the combined high-grade astrocytomas, compared to the low-grade, and in recurrent rather than in primary high-grade astrocytomas. 4. The high-grade astrocytomas had a highly statistical significant Ki-67 labeling index. The Ki-67 labeling indices were significantly higher in the hsp27-positive than the hsp27-negative astrocytomas, irrespective of the histological grade. In the high-grade astrocytomas with a Ki-67 labeling index of five and above, 81% of those tumors were hsp27 positive. 5. Thus, a large number of human astrocytomas express hsp27, and hsp27 expression correlates with histological grades of astrocytoma and with tumor growth fractions. This being the case, hsp27 is likely to have a role in the growth of human astrocytomas.
Background. Expression of the estrogen receptor‐related antigen (ER‐D5) has been reported in some normal and neoplastic tissues. The authors evaluated the expression of ER‐D5 in 143 intracranial tumors of different histologic types.
Methods. Formalin fixed, paraffin embedded tumor sections were stained with the monoclonal D5 antibody by avidin‐biotin complex immunohistochemistry.
Results. Eighty‐eight (62%) of the 143 brain tumors showed positive ER‐D5 immunoreactivity. ER‐D5 expression was observed in 9/30 low grade astrocytomas, in 6/13 anaplastic astrocytomas, in 16/27 glioblastomas, in 2/5 ependymomas, in 5/8 medulloblastomas, in 10/15 meningiomas, in 20/23 schwannomas, in 11/11 hemangioblastomas, in 9/9 germ cell tumors, in 0/2 oligodendrogliomas, and in 17/28 pediatric and childhood brain tumors. The mean percentage of ER‐D5‐positive cells varied in different tumor types, was lowest in the meningotheliomatous meningiomas, and was highest in the hemangioblastomas. ER‐D5 immunoreactivity was also observed in the microvascular endothelial proliferations and in tumor blood vessels. ER‐D5 expression in tumors was not related to the overall tumor grades, but a statistically significant higher percentage of ER‐D5‐positive cells was noted in the glioblastomas compared with the low grade astrocytomas (P < 0.05) and in the combined high grade tumors compared with the low grade tumors (P < 0.005) if vascular‐origin tumor hemangioblastomas are considered a separate entity from other brain tumors.
Conclusion. The current study suggests that the ER‐D5 antigen may participate in the growth of the intracranial tumors and tumor angiogenesis. ER‐D5 in embryonal and germ cell brain tumors suggests that ER‐D5 may be a developmentally regulated protein. Cancer 1995;75:2571‐8.
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