52-year-old male defined a head-ache for a long time
and progressive vision loss for 2 months. He has had urinary
incontinence and weakness at left side recently. At
his physical examination near total vision loss, bilateral
papilla edema markedly at right and papilla atrophy with
pale optic disk at left side were found. He had hemiplegia
at the left side.
Magnetic Resonance Imaging (MRI) and Computed
Tomography (CT) scan showed 4x3x4 cm mass located at
parafalcian region and marked edema at right frontal lobe
with thoracal CT scan 2x2 cm mass at right upper lobe posterior
segment of lung.
Intraoperative pathology assessment of the mass in
the brain was reported as carcinoma metastasis (Figure1).
The excised tumor was in 4x4.5x2.5 cm dimensions
and gray color with irregular borders and solid-necrotic
appearance on sectioning.
The specimen was fixed in 10% formalin. Paraffin
embedded blocks and sections were routinely prepared
and stained with hematoxylin and eosin (H&E;).
Microscopically, the tumor had both solid growth pattern
and necrotic areas. The solid areas were composed of
squamous, intermediate and goblet type cells. The squamous
cells were defined by the presence of eosinophilic
cytoplasm and distinct intercellular bridges. Intermediate
type cells were also seen as similar to normal salivary
gland duct cells. The tumor nests were separated by a fibrous
stroma (Figure 2). Mitotic activity was sparse. Goblet
type tumor cells reacted positively with mucicarmine
(Figure 3), PAS-Alcian blue (pH 2.5).
Fig 1; Abundant vacuolar cytoplasm with eccentrically placed nuclei (MGG, x400)
Fig 2: The solid nest and glandular formations in dens fibrous stroma (H&E;, x40)
Fig 3: Mucicarmine-stained sections of MEC showing strong mucin positivity within cytoplasm of cells and intermediate cells (Mucicarmine stain, x200)
For immunochemistry, the streptoavidine biotin technique
was used with a panel of commercially available
antisera: carcinoembryonic antigen-monoclonal (CEA,
COL-1, monoclonal, Neomarkers, CA, USA), cytokeratin
7 (K72.7, monoclonal, Neomarkers, CA, USA), cytokeratin
8 ( 35BH11, monoclonal, Neomarkers, CA, USA), cytokeratin
18 (K18,7, monoclonal, Neomarkers, CA, USA),
cytokeratin 20 ( N1627, monoclonal, DAKO, CA, USA)
and c-erb-B2 (N1629, Dako, CA, USA). Goblet type tumor
cells reacted with antibodies directed against CEA (Figure 4),
cytokeratin 7 and 18. Squamous type cells reacted only
with cytokeratin 8 (Figure 5). None of the tumor cells was
stained with cytokeratin 20 and c-erb-B2.
Fig 4: Immunohistochemical positivity for CEA-M in mucinous cells (CEA-M, x100)
Fig 5: Positive immunperoxidase reaction for cytokeratin 8 in cytoplasm of intermediate cells (cytokeratin 8, x100)
Our case was defined as MEC with its histomorphology,
histochemical and immunohistochemical features.
Radiological investigations with CT and MRI did not
reveal any primary focus except lung. Unfortunately the
patient died after two months and an autopsy permission
was not available.
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