Transarterial chemoembolization (TACE) is the current standard of treatment for unresectable intermediate-stage hepatocellular carcinoma (HCC). Brivanib, a selective dual inhibitor of vascular endothelial growth factor and fibroblast growth factor signaling, may improve the effectiveness of TACE when given as an adjuvant to TACE. In this multinational, randomized, double-blind, placebo-controlled, phase III study, 870 patients with TACE-eligible HCC were planned to be randomly assigned (1:1) after the first TACE to receive either brivanib 800 mg or placebo orally once-daily. The primary endpoint was overall survival (OS). Secondary endpoints included time to disease progression (TTDP; a composite endpoint based on development of extrahepatic spread or vascular invasion, deterioration of liver function or performance status, or death), time to extrahepatic spread or vascular invasion (TTES/VI), rate of TACE, and safety. Time to radiographic progression (TTP) and objective response rate were exploratory endpoints. The trial was terminated after randomization of 502 patients (brivanib, 249; placebo, 253) when two other phase III studies of brivanib in advanced HCC patients failed to meet OS objectives. (brivanib, 18% vs. placebo, 5%) and hypertension (13% vs. 3%). Conclusions: In this study, brivanib as adjuvant therapy to TACE did not improve OS. (HEPATOLOGY 2014;60:1697-1707

The aim of the study was to investigate the value of intravoxel incoherent motion diffusion-weighted magnetic resonance imaging (IVIM-DWI) and dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) in predicting the early and short-term responses to chemoradiotherapy (CRT) in patients with nasopharyngeal carcinoma (NPC).Forty-three NPC patients underwent IVIM-DWI and DCE-MRI at baseline (pretreatment) and after the first cycle of induction chemotherapy (posttreatment). Based on whether locoregional lesions were identified, patients were divided into the residual and nonresidual groups at the end of CRT and into the good-responder and poor-responder groups 6 months after the end of CRT. The pretreatment and posttreatment IVIM-DWI parameters (ADC, D, D∗, and f) and DCE-MRI parameters (Ktrans, Kep, and Ve) values and their percentage changes (Δ%) were compared between the residual and nonresidual groups and between the good-responder and poor-responder groups.None of perfusion-related parametric values derived from either DCE-MRI or IVIM-DWI showed significant differences either between the residual and nonresidual groups or between the good-responder and poor-responder groups. The nonresidual group exhibited lower pre-ADC, lower pre-D, and higher Δ%D values than did the residual group (all P <0.05). The good-responder group had lower pre-D and pre-ADC values than did the poor-responder group (both P <0.05). Based on receiver operating characteristic (ROC) curve analysis, pre-D had the highest area under the curve in predicting both the early and short-term responses to CRT for NPC patients (0.817 and 0.854, respectively).IVIM-DWI is more valuable than DCE-MRI in predicting the early and short-term response to CRT for NPC, and furthermore diffusion-related IVIM-DWI parameters (pre-ADC, pre-D, and Δ%D) are more powerful than perfusion-related parameters derived from both IVIM-DWI and DCE-MRI.

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Abstract. microRNAs (miRNAs/miRs) are crucial regulators of gene expression at the post-translational level through promoting mRNA degradation or the repression of translation of target genes. miRs have been confirmed to serve a dominant role in tumor biology. miR-486-5p has been ascertained to be involved in non-small-cell lung cancer, breast cancer and hepatocellular carcinoma; however, the expression and function of miR-486-5p in esophageal squamous cell carcinoma (ESCC) has yet to be elucidated. The present study aimed to analyze the expression levels of miR-486-5p in ESCC tissues and paired normal adjacent tissues, and determine the effects of miR-486-5p on esophageal cancer cells using MTT, wound scratch and apoptosis assays. The current results showed that miR-486-5p was significantly downregulated in ESCC specimens. Ectopic expression of miR-486-5p by synthetic mimics reduced cell proliferation and migration and induced increased cell apoptosis. The results indicated miR-486-5p may function as a tumor suppressor in ESCC. The present study demonstrated that miR-486-5p was downregulated in ESCC and served a anti-oncogene role in ESCC via affecting cellular migration.