Intra-articular nodular fasciitis of the knee: a rare cause of recurrent hemarthrosis.

A 20-year-old man presented with pain and recurrent hemarthrosis in the right knee. Magnetic resonance imaging of the knee showed a lesion with homogeneous low signal intensity on T1-weighted images and a heterogeneous, low to high signal intensity on T2-weighted images. At arthroscopy, the mass was located between the posterior cruciate ligament and the posterior knee joint capsule. The tumor was excised through a posterior approach and histologically diagnosed as a nodular fasciitis. Intra-articular nodular fasciitis is a very rare clinicopathologic entity. The current case showed the unique clinical feature of recurrent hemarthrosis at initial presentation, which has not been previously reported.

The effect of bevacizumab on tumour growth of malignant fibrous histiocytoma in an animal model.

BACKGROUND: Bevacizumab is a specific inhibitor of angiogenesis and a neutralising antibody against vascular endothelial growth factor (VEGF). The effect of bevacizumab was evaluated on malignant fibrous histiocytoma (MFH) in vivo using an animal model. MATERIALS AND METHODS: MFH cell line, NaraH, was implanted to athymic nude mice which were randomly divided into a treatment and a control group. The change in body weight and tumour volume were evaluated and immunohistochemical analysis was performed of microvessel density (MVD) and VEGF expression in the tumour tissue. RESULTS: Bevacizumab significantly induced inhibition of tumour growth, reducing tumour volume to 48% at the end of experiment. Intratumoural MVD was significantly decreased in the bevacizumab treatment group compared to the control group. A positive correlation was found between tumour volume and MVD. CONCLUSION: Bevacizumab suppressed MFH tumour growth by inhibiting tumoural angiogenesis. The current study suggests that bevacizumab may be a novel therapeutic agent for MFH.

Inhibition of PKCalpha activation in human bone and soft tissue sarcoma cells by the selective PKC inhibitor PKC412.

BACKGROUND: PKC412, formerly CGP41251, N-benzoylstaurosporine, was initially developed as a selective protein kinase C (PKC) inhibitor, and it preferentially inhibits conventional PKC family members. In this study, the expression of PKCa was examined in human osteosarcoma and MFH cell lines, and the inhibitory effect of PKC412 on the proliferation of the cell lines was evaluated. MATERIALS AND METHODS: Three human osteosarcoma cell lines (KTHOS, MG63 and KHOS) and four human MFH cell lines (TNMY1, GBS-1, Nara-F and Nara-H) were used. The expression of PKCalpha and phosphorylated PKCalpha were analyzed using both Western blotting analysis and immunocytochemical analysis. The effect of PKC412 on cell proliferation was evaluated using the MTS assay technique. RESULTS: PKC412 inhibited cell proliferation of all seven cell lines in a dose- and time-dependent manner. Both Western blotting analysis and immunocytochemical analysis revealed that not only PKCalpha but also phosphorylated PKCalpha were expressed in all cell lines incubated with the culture medium without any stimuli. PKC412 suppressed phosphorylation of PKCalpha in all cell lines at a concentration of 1 microM. CONCLUSION: The inhibition of cell proliferation of the human osteosarcoma and MFH cell lines by PKC412 might be due to reduced PKCalpha activity. This suggests PKC412 might be a potent chemotherapeutic agent for human sarcomas.

Magnetic resonance imaging of medullary bone infarction in the early stage.

Medullary bone infarctions, which are believed to arise due to arterial obstructions in the bone, are usually asymptomatic and are noted incidentally in roentgenograms or bone scans performed for other reasons. We present two cases of acute bone infarctions that were found accidentally by magnetic resonance imaging (MRI). In both cases, conventional radiographs could not demonstrate any findings and the cases were clinically asymptomatic. The current two cases suggest that MRI shows various findings in bone infarctions.

Imatinib mesylate inhibits tumorigenicity of malignant fibrous histiocytoma cells in vivo.

BACKGROUND: Malignant fibrous histiocytoma (MFH) is one of the most diffuse and aggressive tumors among soft tissue sarcomas in adults, but still poorly characterized from the molecular viewpoint. MFH cell proliferation is inhibited selectively by imatinib mesylate, a tyrosine kinase inhibitor. The expressions of platelet-derived growth factor receptors (PDGFRs) and c-Kit have been previously examined in MFH cell lines and the inhibitory effect of imatinib mesylate on the MFH cell proliferation was tested. MFH cell lines showed various patterns of PDGFRs and c-Kit expression. Imatinib mesylate inhibited the proliferation of MFH cells that expressed PDGFRs and/or c-Kit. MATERIALS AND METHODS: Four MFH cell lines were used (Nara H, Nara F, GBS-1 and TNMY1). The mRNA expression of PDGFRs and c-Kit was analyzed using RT-PCR; cell proliferation was analyzed using the MTS assay. Immunohistochemistry was used to analyze the inhibitory effect of imatinib mesylate on phosphorylation of PDGFRs and c-Kit in vivo. The Nara H and TNMY1 cell lines were implanted into nude mice and tumor growth was evaluated daily by measuring the two-dimensional diameters of the tumor nodule. RESULTS: PDGFRs and c-Kit were expressed in Nara F, GBS-1 and TNMY1, but not in Nara H cells. Imatinib mesylate inhibited PDGFRs and c-Kit phosphorylation in TNMY1 cells affecting the tumorigenicity, in the control group (139 mm3 SD +/- 1.03) and treatment group (126.2 mm3 SD +/- 1.63) but did not affect the tumorigenicity of Nara H cells. CONCLUSION: Imatinib mesylate reduced in vivo tumor growth of MFH that express PDGFRs and c-Kit associated with phosphorylation suppression.

Expression of VEGF and its receptors and angiogenesis in bone and soft tissue tumors.

BACKGROUND: Tumor angiogenesis and vascularization are essential requirements for the growth and metastasis of tumors. There is evidence that overexpression of the vascular endothelial growth factor (VEGF) is correlated with an adverse prognosis in some tumors. The expression of VEGF, its receptors and microvessel density (MVD) of bone and soft tissue tumors was evaluated. MATERIALS AND METHODS: Tissue specimens of 60 patients including 30 malignant and 30 benign tumors confirmed by biopsy were examined. Expression of VEGF and its receptors (flt-1 and KDR/flk-1) was observed by immunohistochemistry. Tumor angiogenesis was assessed morphologically by measuring intratumoral MVD. RESULTS: Semi-quantitative evaluation of immunoreactivity showed that VEGF was significantly higher in malignant tumors than in benign tumors. A correlation was found between the immunoreactivity of VEGF and KDR. Moreover, correlations were found either between MVD and VEGF or between MVD and KDR/flk-1. CONCLUSION: Signal transduction, in particular by VEGF and KDR, potentially contributes to the angiogenesis of bone and soft tissue tumor.