Purpose To evaluate the potential role of diffusion kurtosis imaging and conventional magnetic resonance (MR) imaging findings including standard monoexponential model of diffusion-weighted imaging and morphologic features for preoperative prediction of microvascular invasion (MVI) of hepatocellular carcinoma (HCC). Materials and Methods Institutional review board approval and written informed consent were obtained. Between September 2015 and November 2016, 84 patients (median age, 54 years; range, 29-79 years) with 92 histopathologically confirmed HCCs (40 MVI-positive lesions and 52 MVI-negative lesions) were analyzed. Preoperative MR imaging examinations including diffusion kurtosis imaging (b values: 0, 200, 500, 1000, 1500, and 2000 sec/mm) were performed and kurtosis, diffusivity, and apparent diffusion coefficient maps were calculated. Morphologic features of conventional MR images were also evaluated. Univariate and multivariate logistic regression analyses were used to evaluate the relative value of these parameters as potential predictors of MVI. Results Features significantly related to MVI of HCC at univariate analysis were increased mean kurtosis value (P < .001), decreased mean diffusivity value (P = .033) and apparent diffusion coefficient value (P = .011), and presence of infiltrative border with irregular shape (P = .005) and irregular circumferential enhancement (P = .026). At multivariate analysis, mean kurtosis value (odds ratio, 6.25; P = .001), as well as irregular circumferential enhancement (odds ratio, 6.92; P = .046), were independent risk factors for MVI of HCC. The mean kurtosis value for MVI of HCC showed an area under the receiver operating characteristic curve of 0.784 (optimal cutoff value was 0.917). Conclusion Higher mean kurtosis values in combination with irregular circumferential enhancement are potential predictive biomarkers for MVI of HCC. RSNA, 2017.
Valuable MR features and clinical factors varied for differential diagnosis of IMCCs and HCCs according to tumor size. Advances in knowledge: MR features for differential diagnosis of large IMCC and HCC (>3 cm) are in keeping with that recommended by LI-RADS. However, for small IMCCs and HCCs (≤3 cm), only rim enhancement on arterial phase and target appearance at DWI are reliable predictors.
Objective. The purpose of the study was to elucidate the molecular mechanism of tenacissoside H (TDH) inhibiting esophageal carcinoma infiltration and proliferation. Methods. In vitro, EC9706 cells were treated with TDH. Cells proliferation and cell cycle were assayed. PI3K and NF-κB mRNAs expression were determined by real time PCR. In vivo, model of nude mice with tumor was established. Mice were treated with TDH. Inhibition ratio of tumor volume was calculated. PCNA expression was examined. Protein expression in PI3K/Akt-NF-κB signaling pathway was determined. Results. In vitro, TDH significantly inhibited cells proliferation in a time-and-dose-dependent manner. TDH arrested the cell cycle in S phase and significantly inhibited PI3K and NF-κB mRNA expression, compared with blank controlled group (P < 0.05). In vivo, TDH strongly inhibits tumor growth and volume. PCNA expression was significantly decreased after treatment of TDH. TDH downregulated proteins expression in PI3K/Akt-NF-κB transduction cascade (P < 0.05). Conclusion. TDH inhibited esophageal carcinoma infiltration and proliferation both in vitro and in vivo. The anticancer activity has relation to arresting the cell cycle at the S phase, inhibited the PCNA expression of transplanted tumors in nude mice, and regulated the protein expression in the PI3K/Akt-NF-κB transduction cascade.
TLD inhibited Eca109 cell proliferation by arresting cells in S phase. The possible mechanism might be related to inhibiting the NF-κB transduction cascade. The combination of the herbs found in the three separate formulae, H, Q and Z, work synergistically in TLD to produce the inhibitory effects of TLD treatment on Eca109 proliferation.
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