Brain Pathology Case of the Month - September 2005

Contributed by 1Miletic H, 2Scheid C, 1Stenzel W, 3Lee JY, 1Deckert M
    1Department of Neuropathology, University of Cologne, Germany
    2Clinic I for Internal Medicine, Universitiy of Cologne, Germany
    3Clinic for Neurosurgery, University of Cologne, Germany
Published on line in September 2005


A 43-year-old woman was admitted with headache over a 3 week period. The clinical examination was completely unremarkable. The past medical history included breast cancer three years before presentation with a contralateral relapse another two years later. Treatment consisted of surgical resection, radiotherapy and post-operative chemotherapy with 4 cycles of epirubicine and cyclophosphamide. The relapse was treated by resection, radiotherapy and anti-estrogen therapy. Two years before current admission, acute myeloid leukemia FAB M4 Eo was diagnosed and treated with induction and consolidation chemotherapy according to the German AMLCG protocol with TAD/HAM double-induction and TAD consolidation chemotherapy followed by 4 weekly alternating maintenance chemotherapy.

T-1 weighted MRI scans showed a hypointense mass in the left temporal lobe with little surrounding edema and compression of the left cerebral peduncle (Figure 1). After intravenous Gadolinium application, the tumor exhibited homogenous contrast enhancement (Figure 2). Metastasis and meningeoma were considered as differential diagnoses.


Histology showed a highly cellular tumor consisting of monotonous tumor cells with large nuclei, prominent nucleoli and a scanty, eosinophil cytoplasm (Figure 3). Mitotic figures were abundant. Tumor cells were embedded in a rich reticulin-fibre network. Moreover areas of tumor necrosis were evident (Figure 4). Blood vessel walls were thickened and sometimes showed proliferation of the endothelium. Brain parenchyma was diffusely infiltrated by tumor cells with prominent perivascular cuffing (Figure 5). Staining with chloroacetate esterase was positive in many tumor cells (Figure 6).

Immunohistochemistry for LCA (Figure 7), CD34, CD68 and HLA-DR revealed a strong positive staining in the majority of tumor cells. Additionally most tumor cells were positive for the tyrosine kinase receptor c-kit. A fraction of tumor cells were immunoreactive for lysozyme (Figure 8), CD15 and CD56. Expression of B- and T-cell markers (CD20 and CD3) was detectable only in single tumor cells. Proliferation activity was evidenced by MIB-1 labeling in 70% of the tumor cell nuclei. Some foamy macrophages diffusely distributed in the tumor were identified by CD68 (Figure 9).


International Society of Neuropathology