Mitogen-activated protein kinase in gliosis and pilocytic astrocytoma.

Pilocytic astrocytoma (PA), featuring activation of the mitogen-activated protein kinase (MAPK) pathway, is the most common tumor of the pediatric central nervous system. However, it remains unknown whether MAPK activation is present in the reactive gliosis of non-neoplastic lesions. Therefore, we investigated the expression of MAPK in reactive gliosis associated with cavernous angiomas. Immunohistochemical expression and the extent of BRAF, ERK, p38, and JNK were investigated in 10 patients with gliosis surrounding cavernous angiomas (GS group) and 10 patients with PA (PA group). Evaluation of these parameters was scored as 0, none; 1, scarce; 2, moderate; 3, global. In the GS group, histopathologic features of PA (piloid cells, Rosenthal fibers, microcysts with eosinophilic granular bodies) were identified. Expression of ERK, and p38 was shown in all patients in the GS and PA group. Expression of BRAF was identified in 5 patients (50%) in the GS group and in 8 (80%) in the PA group. The mean score of BRAF expression in the PA group was significantly higher than that in the GS group (p = 0.019). Reactive gliosis may resemble PA in histological findings and MAPK activation. Therefore, PA could be indistinguishable from reactive gliosis with classic histopathologic and/or immunohistochemical methods.
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Clinicopathological features in the recurrence of oligodendroglioma and diffuse astrocytoma.

To investigate whether grade II oligodendroglioma was transformed to glioblastoma or not, histopathological evaluation of recurrent oligodendrogliomal tumors (OG) and diffuse astrocytomas (DA) was performed. The OG group was composed of ten patients with OG, including seven oligodendrogliomas and three oligoastrocytomas. The DA group was composed of ten patients with DA, including eight fibrillary astrocytomas and two gemistocytic astrocytomas. The histopathological parameters of glioblastoma including nuclear atypia, multinucleated giant cells, glomeruloid tufts (GT) as a marker of microvascular proliferation, necrosis, and the Ki-67 staining index were investigated. Evaluation of these parameters was scored as follows: 0, none; 1, sporadic; 2, partial; 3, extensive. There were no cases of transformation to glioblastoma in the OG group. There were five cases of transformation to secondary glioblastoma in the DA group. In recurrent tumors, scores of GT and necrosis in the OG group were significantly lower than those in the DA group (p < 0.005). Nuclear atypia and high proliferative activity (Ki-67 index) were identified in recurrent tumors of the OG group. Our study suggested that the extent of GT and necrosis in recurrent OG was less than that in recurrent DA, and transformation to glioblastoma from oligodendroglial tumor was exceptional.

Glioblastoma with oligodendroglial components: glioblastoma or anaplastic oligodendroglial tumors.

There have been some recent reports about glioblastoma with oligodendroglial (OG) components and malignant glioma with primitive neuroectodermal tumor (PNET)-like components. We investigated whether the presence and extent of OG components and PNET-like components influenced the prognosis in patients with glioblastoma. Eighty-six patients with glioblastoma were divided into an OG group (28 %), which revealed areas with a honeycomb appearance, and a non-OG group (72 %) without a honeycomb appearance. Patients with glioblastoma were also divided into a PNET group (27 %), which revealed areas with PNET-like features defined as neoplastic cells with high N/C ratios and hyperchromatic oval-carrot-shaped nuclei, and lacked the typical honeycomb appearance, and a non-PNET group (73 %) without PNET features. There were no significant differences in overall survival among the OG, the non-OG, the PNET, and the non-PNET groups. Two patients who survived longer than 36 months had both OG and PNET components with 1p or 19q loss of heterozygosity. Perinuclear halo, which is a characteristic feature of oligodendrogliomas, is an artifact of tissue fixation. Therefore, we should not readily use the term glioblastoma with OG components. PNET-like components, which are considered rare in malignant gliomas, may be frequently identified in glioblastomas.