We treated a 56-year-old woman who had a right temporal lobe
tumor found by chance after a traffic accident. MRI confirmed a heterogeneously enhanced
tumor in the temporal lobe with large peritumoral
edema extending to the superior parietal lobe. The patient underwent
tumor resection. The
tumor consisted largely of distinct cells with discrete borders and granular cytoplasm. In granular cells, the accumulation of PAS-positive granules was observed. Immunohistochemical analysis demonstrated positive staining for GFAP, S-100, and
oligodendrocyte transcription factor 2 and negative staining for
synaptophysin. CD68 was negative in granular cells, but positive in stromal cells. Ki-67 labeling index was quite low. The
tumor was diagnosed as a granular cell
astrocytoma (GCA). Postoperative
radiotherapy combined with
temozolomide was administered. One month after
chemoradiotherapy, the
tumor occurred in the parietal lobe, and a tumorectomy was performed. The
tumor was composed of poorly differentiated astrocytic
tumor cells with prominent microvascular proliferation and
necrosis. A small number of granular cells were locally observed and the
tumor was diagnosed as a
glioblastoma. O6-methylguanine-DNA
methyltransferase promoter methylation was detected in the GCA but not in the
glioblastoma.
Isocitrate dehydrogenase mutations were not detected in either
tumor. Comparative genomic hybridization analysis demonstrated that no
chromosomal abnormality was found in the GCA; however, a gain of chromosomes 7 and 19 and a loss of chromosomes 10 and 9p21 (CDKN2A) were found in the
glioblastoma. p53 was strongly expressed in both the GCA and
glioblastoma. The
tumor progressed despite extensive
chemotherapy, and the patient died 1 year after the initial treatment. Our immunohistochemical, genetic and chromosomal analyses indicate that the
glioblastoma was transformed from the GCA.