Gadoxetic acid-enhanced MR imaging is the most useful imaging technique for evaluating small HCC, including early HCC.

Purpose: To evaluate the effectiveness of diffusionweighted magnetic resonance imaging (DWI) in estimating the grade of malignancy of hepatocellular carcinoma.Materials and Methods: Dynamic contrast-enhanced computed tomography (CE-CT) and DWI (b value, 1000 s/mm 2 ) were performed on 73 patients. Using DW images, the lesions were classified as ''visible'' or ''invisible.'' The apparent diffusion coefficient (ADC) of the lesions was measured. Furthermore, the lesions were classified as hypervascular or iso-hypovascular using arterial phase CE-CT images. The image findings for each lesion type were compared.Results: The 73 patients had 98 hepatocellular lesions, of which 12 were histologically diagnosed as dysplastic nodules; 39, well-differentiated HCCs; 33, moderately differentiated HCCs; and 14, poorly differentiated HCCs. The mean ADC values of moderately poorly-differentiated HCCs were significantly lower than well-differentiated HCCs and dysplastic nodules (P < 0.01). On DW images, >90% of moderately (30/33) and poorly differentiated HCCs (13/14) were visible, while 51% of well-differentiated HCCs (20/39) and all dysplastic nodules were invisible. Of 22 iso-hypovascular lesions, 4 were visible on DW images and were poorly differentiated HCCs, whereas 18 were invisible and were dysplastic nodules (12/18) or well-differentiated HCCs (6/18). Conclusion:A combination of hypovascularity and visibility on DW images can help distinguish poorly differentiated HCCs from low-grade hepatocellular lesions (dysplastic nodules and well-differentiated HCCs).

Runx2/Cbfa1 is a member of the Runt-related transcription factor family and is an essential regulator of osteoblast/ chondrocyte differentiation. Recently, aberrant expression of Runx2 and its oncogenic functions have been identified in the progression and metastasis of human cancers. In this study, we investigated the expression profile of Runx family genes in normal thyroid tissue, non-neoplastic but abnormal thyroid tissue, various types of thyroid tumors and representative human thyroid carcinoma cell lines. Using reverse transcriptase-PCR and western blotting, we found that Runx2 was consistently upregulated in papillary carcinomas (PCs) and thyroid carcinoma cell lines compared with normal thyroid tissue. With immunohistochemistry, we observed negative or focal immunoreactivity of Runx2 in the nuclei of normal thyroid follicular cells. None of the non-neoplastic thyroid tissues, including Graves' thyroid and adenomatous goiter, had diffuse positivity of Runx2. Expression of Runx2 in benign follicular adenomas varied from negative to diffusely positive. Meanwhile, all malignant thyroid tumors showed some Runx2 immunopositivity. It was diffuse and intense in 83% (19/23) of PCs, 71% (5/7) of follicular carcinomas (FCs) and 40% (4/10) of undifferentiated carcinomas (UCs). In thyroid carcinoma cell lines, the MEK inhibitor U0126 suppressed Runx2, suggesting an association of the MAPK/ERK pathway with Runx2 regulation. Effective silencing of Runx2 by short interfering RNA (siRNA) demonstrated downregulation of EMT-related molecules (SNAI2, SNAI3 and TWIST1), MMP2 and vasculogenic factors (VEGFA and VEGFC) in thyroid carcinoma cells. We also confirmed that Runx2 silencing suppresses thyroid carcinoma cell invasion in transwell assays. In conclusion, this study provides insight into the potential molecular mechanism of thyroid cancer invasion. Our data suggest that enhanced Runx2 is functionally linked to tumor invasion and metastasis of thyroid carcinoma by regulating EMT-related molecules, matrix metalloproteinases and angiogenic/lymphangiogenic factors.

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