Sclerosing hemangioma, presenting as a pneumonic pattern with mucinous adenomatous hyperplasia of the lung.

Pulmonary sclerosing hemangioma is generally considered a rare neoplasm presenting as a solitary benign nodule. During routine medical examination multiple abnormal nodular shadows were detected in the right lower lung field on chest X-ray in a 48-year-old asymptomatic woman. The patient underwent wedge resection for the pulmonary lesion. The resected lung had numerous scattered tiny nodules and small nodules congregated together, forming larger nodules. All of these lesions had typical features of sclerosing hemangioma. The authors call this unusual growth pattern of sclerosing hemangioma a 'pneumonic pattern'. Adjacent to the largest lesion, a relatively well-defined small mucinous lesion composed of mucinous tall columnar cells and basaloid squamous cells was detected. Because this lesion did not have expression of thyroid transcription factor-1, it is described as mucinous adenomatous hyperplasia.

A peroxisome proliferator-activated receptor gamma antagonist induces vimentin cleavage and inhibits invasion in high-grade hepatocellular carcinoma.

Increased expression of vimentin in carcinomas correlates with parameters of malignant potential such as tumor grade and tumor metastasis. Peroxisome proliferator-activated receptor gamma (PPARgamma) has been intensively evaluated as a potential target for the inhibition of cell growth and metastasis in cancer cells. In the present study, we examined whether PPARgamma is a possible target molecule for the prevention of cell growth and invasion by treatment with agonists (troglitazone, rosiglitazone) and antagonists (T0070907, GW9662) in four different hepatocellular carcinoma (HCC) cell lines. We also evaluated the effects of the PPARgamma agonists and antagonists on tumor cell migration and invasion. The expression level of PPARgamma protein was higher in the sarcomatoid SH-J1 and poorly differentiated HLE cell lines than that in the well-differentiated HCC cell lines (HepG2 and Huh-7). Expression of vimentin was high in the SH-J1 HCC cell line and minimally detected in the HLE cell line. Treatment with low doses of the PPARgamma antagonists inhibited cell growth and colony formation of all four of the HCC cell lines. Vimentin in the high-grade HCC cells was cleaved by the treatment with the PPARgamma antagonists. Furthermore, treatment with the PPARgamma antagonists also strongly inhibited migration and invasion of the SH-J1 and HLE cells. However, treatment with low doses of the agonists had no effect on vimentin expression, migration, and invasion of the high-grade HCC cells but cell growth was inhibited by treatment with high concentrations of the agonists. Our results indicate that treatment with a PPARgamma antagonist may prevent cell growth and invasion of high-grade HCC cells. Our findings also suggest that PPARgamma antagonists inhibit cell growth and invasion through vimentin disarrangement in high-grade HCC.