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Expression of cyclo‐oxygenase‐2 in ependymal tumors
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Up‐regulation of cyclo‐oxygenase‐2 (COX‐2), a cytokine‐induced enzyme that metabolizes arachidonic acid into prostaglandins, has been described in some brain tumors, including astrocytomas. Little is known about its expression in ependymal neoplasms. The objective of the present study was to assess COX‐2 immunostaining of ependymal tumors. Retrospective COX‐2 immunohistochemical analysis was conducted on 117 ependymal tumors. Statistical analysis was performed using Student t‐test. The study group (56 men and 44 women, mean age, 30.8 years) was comprised of 48 low‐grade ependymomas (WHO grade II), 12 anaplastic ependymomas (WHO grade III), 27 myxopapillary ependymomas (WHO grade I) and 13 subependymomas (WHO grade I). At last known follow‐up (range, 12–226 months; mean, 74 months), 52 patients were alive with no evidence of tumor, 16 patients were alive with residual tumor, nine patients died with tumor, one patient died with no tumor and three died with tumor status unknown. Nineteen patients had less than 12 months of follow‐up. Thirty‐six (36%) patients had tumors, which demonstrated positive COX‐2 staining, including 16/27 (59%) myxopapillary ependymomas, 3/13 (23%) subependymomas, 14/48 (29%) ependymomas and 3/12 (25%) anaplastic ependymomas. Statistically significant COX‐2 positive immunostaining was observed in myxopapillary ependymomas versus WHO grade II (P = 0.03) and grade III (P = 0.02) tumors. Increased COX‐2 expression in myxopapillary ependymoma as compared to the WHO grade II and II ependymoma was observed. The reason for this apparent increased immunoexpression in these low‐grade tumors is uncertain. COX‐2 inhibitors may play a role in treatment of the subset of ependymal tumors that demonstrate increased expression. COX‐2 staining did not reliably predict tumor behavior.
Title: Expression of cyclo‐oxygenase‐2 in ependymal tumors
Description:
Up‐regulation of cyclo‐oxygenase‐2 (COX‐2), a cytokine‐induced enzyme that metabolizes arachidonic acid into prostaglandins, has been described in some brain tumors, including astrocytomas.
Little is known about its expression in ependymal neoplasms.
The objective of the present study was to assess COX‐2 immunostaining of ependymal tumors.
Retrospective COX‐2 immunohistochemical analysis was conducted on 117 ependymal tumors.
Statistical analysis was performed using Student t‐test.
The study group (56 men and 44 women, mean age, 30.
8 years) was comprised of 48 low‐grade ependymomas (WHO grade II), 12 anaplastic ependymomas (WHO grade III), 27 myxopapillary ependymomas (WHO grade I) and 13 subependymomas (WHO grade I).
At last known follow‐up (range, 12–226 months; mean, 74 months), 52 patients were alive with no evidence of tumor, 16 patients were alive with residual tumor, nine patients died with tumor, one patient died with no tumor and three died with tumor status unknown.
Nineteen patients had less than 12 months of follow‐up.
Thirty‐six (36%) patients had tumors, which demonstrated positive COX‐2 staining, including 16/27 (59%) myxopapillary ependymomas, 3/13 (23%) subependymomas, 14/48 (29%) ependymomas and 3/12 (25%) anaplastic ependymomas.
Statistically significant COX‐2 positive immunostaining was observed in myxopapillary ependymomas versus WHO grade II (P = 0.
03) and grade III (P = 0.
02) tumors.
Increased COX‐2 expression in myxopapillary ependymoma as compared to the WHO grade II and II ependymoma was observed.
The reason for this apparent increased immunoexpression in these low‐grade tumors is uncertain.
COX‐2 inhibitors may play a role in treatment of the subset of ependymal tumors that demonstrate increased expression.
COX‐2 staining did not reliably predict tumor behavior.
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