PMC3290025_01
FDG-PET/CT scan before (a) and after (b) chemotherapy. a Left level 3 large conglomerate mass (max. SUV of 10.5), left superior mediastinal large conglomerate mass (max. SUV of 7.8), numerous abnormal FDG uptakes involving skeletal structures, and multiple segmental liver abnormal FDG uptakes. b Markedly decreased hypermetabolic involvement of bulky masses involving the left neck, left cervical and left thoracic inlet. Near complete resolution of hypermetabolic liver metastases. Interval complete resolution of hypermetabolic left lower lobe pulmonary nodule and osseous lesions.
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F1
Additionally, there were enhancing lesions compatible with bone metastases in T11, T12, L1 and L3 (fig. 1a). A restaging PET-CT in March 2011 revealed complete resolution of hypermetabolic left lower lobe pulmonary nodules and osseous lesions, and near complete resolution of hypermetabolic liver metastases and neck masses (fig. 1b).
H&E sections from the liver lesion biopsy demonstrated clusters of neoplastic cells in portal areas with a focus of angiolymphatic invasion (arrow; a). The tumor cells are positive for CK7 (b) and OC125 (c), while negative for estrogen receptor (d) and BRST-2 (e).
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F2
A liver lesion biopsy demonstrated small cohesive clusters of atypical epithelial cells, predominately in portal areas, with rare foci of angiolymphatic involvement (fig. 2).
Immunohistochemistry findings of the neck mass biopsy. H&E sections of poorly differentiated adenocarcinoma (a), Topo I (b), Topo II-a (c), thymidylate synthase (d), and androgen receptor (e).
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F3
As demonstrated in fig. 3, an immunohistochemistry study showed high-level expression of the following: topoisomerase I (Topo I; 2+, 10%); androgen receptor (AR; 1+, 20%), and ribonucleoside-diphosphate reductase large subunit (2+, 80%).