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Histological examination of a biopsy specimen revealed atypical spindle cell proliferation with active mitosis, partial tumor necrosis and occasional osteoclast-like giant cells (arrows). (A) Hematoxylin and eosin staining; magnification, x400. Immunohistochemical staining was positive for (B) alpha-smooth muscle actin (SMA), (C) anti-actin monoclonal antibody (HHF-35), (D) h-caldesmon and (E) vimentin; magnification, x100.
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Osteoclast-like giant cells were occasionally observed (Fig. 1). Immunohistochemical analyses revealed expression of alpha-smooth muscle actin (smooth muscle-specific actin), h-caldesmon and vimentin (Fig. 1).
Thoracic vertebra (A) prior to treatment and (B) 2 months after treatment with denosumab and radiation therapy.
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Osteosclerotic changes were observed in multiple osteolytic lesions following denosumab and radiation combination therapy and denosumab therapy alone (Figs. 2 and 3).
Costal lesion (A) prior to treatment and (B) 2 months after treatment with denosumab alone.
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Osteosclerotic changes were observed in multiple osteolytic lesions following denosumab and radiation combination therapy and denosumab therapy alone (Figs. 2 and 3).
Quantitative polymerase chain reaction analysis of receptor-activator of nuclear kappaB ligand (RANKL) expression in bone leiomyosarcoma (LMS), giant cell tumor of bone (GCTB), aneurysmal bone cyst (ABC), fibrous dysplasia (FD) and bone metastasis from breast cancer (BC). Relative gene expression is calculated as copy number of the target gene (RANKL)/copy number of the reference gene (GAPDH)/copy number of the target gene (RANKL) in the RPMI-8226 myeloma cell line.
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Table I. The median fold changes for RANKL relative expression levels were 994-, 1,030-, 616- and 69-fold for GCTB, ABC, FD and bone metastasis from BC, respectively (Fig. 4).