Peretinoin, an acyclic retinoid, improves the hepatic gene signature of chronic hepatitis C following curative therapy of hepatocellular carcinoma

BACKGROUND: The acyclic retinoid, peretinoin, has been shown to be effective for suppressing hepatocellular carcinoma (HCC) recurrence after definitive treatment in a small-scale randomized clinical trial. However, little has been documented about the mechanism by which peretinoin exerts its inhibitory effects against recurrent HCC in humans in vivo. METHODS: Twelve hepatitis C virus-positive patients whose HCC had been eradicated through curative resection or ablation underwent liver biopsy at baseline and week 8 of treatment with either a daily dose of 300 or 600 mg peretinoin. RNA isolated from biopsy samples was subjected to gene expression profile analysis. RESULTS: Peretinoin treatment elevated the expression levels of IGFBP6, RBP1, PRB4, CEBPA, G0S2, TGM2, GPRC5A, CYP26B1, and many other retinoid target genes. Elevated expression was also observed for interferon-, Wnt-, and tumor suppressor-related genes. By contrast, decreased expression levels were found for mTOR- and tumor progression-related genes. Interestingly, gene expression profiles for week 8 of peretinoin treatment could be classified into two groups of recurrence and non-recurrence with a prediction accuracy rate of 79.6% (P<0.05). In the liver of patients with non-recurrence, expression of PDGFC and other angiogenesis genes, cancer stem cell marker genes, and genes related to tumor progression was down-regulated, while expression of genes related to hepatocyte differentiation, tumor suppression genes, and other genes related to apoptosis induction was up-regulated. CONCLUSIONS: Gene expression profiling at week 8 of peretinoin treatment could successfully predict HCC recurrence within 2 years. This study is the first to show the effect of peretinoin in suppressing HCC recurrence in vivo based on gene expression profiles and provides a molecular basis for understanding the efficacy of peretinoin

Meta Ring Signature

In this paper, we propose a new concept ``Meta Ring Signature\u27\u27. Suppose that a signature text work as a public key, we may achive a new digital signature ``Meta Signature\u27\u27 such that, the signer of a signature text, in this paper we call basic signature, can sign on to another message by using the basic signature text as the public key of Meta signature scheme. First, we present a concept of Meta Ring Signature such that both basic signature and meta signature are Ring Signature

Surgery for Congenital Duodenal Atresia

Congenital duodenal atresia consists of extrinsic duodenal obstruction of annular pancreas and intrinsic obstruction of intestinal atresia. The aim of this study is to clarify clinical patterns of congenital duodenal atresia on the basis of surgical experiece and discuss major problems with respect to surgical treatment

Inhibition of p600 Expression Suppresses Both Invasiveness and Anoikis Resistance of Gastric Cancer

BACKGROUND: Advanced gastric cancers often metastasize to distant organs and the peritoneum, leading to a poor prognosis. Both invasiveness and resistance to anchorage-independent cell death (anoikis) are important factors in the process of metastasis. p600 (600-kDa protein), recently identified from a cervical cancer cell line, plays a role in both anoikis resistance and cell migration. In this study, we examined whether p600 is involved in the progression of gastric cancer. METHODS: We used both normal gastric mucosal cells and cancer cells laser-microdissected from 42 gastric cancers and their normal counterparts, and compared their p600 mRNA expression levels with quantitative reverse transcriptase–polymerase chain reaction. We inhibited p600 expression in two gastric cancer cell lines with siRNA and examined its effect on the invasiveness and anoikis resistance both in vitro and in vivo. RESULTS: Expression of p600 mRNA was significantly higher in gastric cancer cells than in normal mucosal cells (P = 0.027). The invasion assay revealed that invasiveness was significantly reduced by inhibition of p600 (P < 0.01). In vitro experiments revealed that cell viability and colony-formation capacity under anchorage-independent conditions were significantly reduced by inhibition of p600 (P < 0.05). In vivo experiments also showed that the establishment of intraperitoneal disseminated tumors was significantly suppressed by transient inhibition of p600 (P < 0.001). CONCLUSIONS: Our results strongly suggest that p600 is involved in gastric cancer progression, and has a potential to be a new molecular target for gastric cancer therapy

Virtual Structure Constants as Intersection Numbers of Moduli Space of Polynomial Maps with Two Marked Points

In this paper, we derive the virtual structure constants used in mirror computation of degree k hypersurface in CP^{N-1}, by using localization computation applied to moduli space of polynomial maps from CP^{1} to CP^{N-1} with two marked points. We also apply this technique to non-nef local geometry O(1)+O(-3)->CP^{1} and realize mirror computation without using Birkhoff factorization.Comment: 10 pages, latex, a minor change in Section 4, English is refined, Some typing errors in Section 3 are correcte