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( Yusuke Niina ),( Nao Fujimori ),( Taichi Nakamura ),( Hisato Igarashi ),( Takamasa Oono ),( Kazuhiko Nakamura ),( Masaki Kato ),( Robert T. Jensen ),( Tetsuhide Ito ),( Ryoichi Takayanagi ) The Editorial Office of Gut and Liver 2012 Gut and Liver Vol.6 No.3
Multiple endocrine neoplasia type 1 (MEN1) is an inherited autosomal dominant disease presenting with pancreatic neuroendocrine tumors (pNETs), parathyroid tumors, or pitu-itary tumors. Using the PubMed database, we reviewed the literature on information regarding the proper diagnosis and treatment of MEN1-associated pNET. Many cases of MEN1-associated pNET are functioning pNETs. Gastrinomas and insulinomas tend to occur frequently in the duodenum and pancreas, respectively. In addition to diagnostic imaging, the selective arterial secretagogue injection test (SASI test) is useful for localizing functioning pNET. The standard treat-ment is surgical resection. However, in the case of a func-tioning pNET, the tumor should first be accurately located using the SASI test before an appropriate surgical method is selected. In cases of a MEN1-associated non-functioning pNET that exceeds 2 cm in diameter, the incidence of distant metastasis is significantly increased, and surgery is recom-mended. In cases of unresectable pNET, a somatostatin analog has been shown to demonstrate antitumor effects and is considered to be a promising treatment. In addition, molecular-targeted drugs have recently been found to be ef-fective in phase III clinical trials. (Gut Liver 2012;6:287-294)
Masako Tada,Ayaka Hayashi,Yumi Asano,Musashi Kubiura-Ichimaru,Takamasa Ito,Miho Yoshii,Hiroshi Kimura,Yoichi Matsuda,Mitsuo Oshimura 한국유전학회 2021 Genes & Genomics Vol.43 No.3
Background DNA methylation is a signifcant epigenetic modifcation that is evolutionarily conserved in various species and often serves as a repressive mark for transcription. DNA methylation levels and patterns are regulated by a balance of opposing enzyme functions, DNA methyltransferases, DNMT1/3A/3B and methylcytosine dioxygenases, TET1/2/3. In mice, the TET enzyme converts DNA cytosine methylation (5mC) to 5-hydroxymethylcytosine (5hmC) at the beginning of fertilisation and gastrulation and initiates a global loss of 5mC, while the 5mC level is increased on the onset of cell differentiation during early embryonic development. Objective Global loss and gain of DNA methylation may be diferently regulated in diverged species. Methods Chicken B-cell lymphoma DT40 cells were used as an avian model to compare diferences in the overall regulation of DNA modifcation with mammals. Results We found that DNA methylation is maintained at high levels in DT40 cells through compact chromatin formation, which inhibits TET-mediated demethylation. Human and mouse chromosomes introduced into DT40 cells by cell fusion lost the majority of 5mC, except for human subtelomeric repeats. Conclusion Our attempt to elucidate the diferences in the epigenetic regulatory mechanisms between birds and mammals explored the evidence that they share a common chromatin-based regulation of TET–DNA access, while chicken DNMT1 is involved in diferent target sequence recognition systems, suggesting that factors inducing DNMT–DNA association have already diverged.
Kaneko, Takaaki,Shimpo, Kan,Chihara, Takeshi,Beppu, Hidehiko,Tomatsu, Akiko,Shinzato, Masanori,Yanagida, Takamasa,Ieike, Tsutomu,Sonoda, Shigeru,Futamura, Akihiko,Ito, Akihiro,Higashiguchi, Takashi Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.5
High temperature- and pressure-treated garlic (HTPG) has been shown to have enhanced antioxidative activity and polyphenol contents. Previously, we reported that HTPG inhibited 1,2-dimethylhydrazine-induced mucin depleted foci (premalignant lesions) and $O^6$-methylguanine DNA adduct formation in the rat colorectum. In the present study, we investigated the modifying effects of HTPG on N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG)-induced pyloric stomach and small intestinal carcinogenesis in mice. Male C57BL/6 mice were given ENNG (100 mg/l) in drinking water for the first 4 weeks, then a basal diet or diet containing 2% or 5% HTPG for 30 weeks. The incidence and multiplicity of pyloric stomach and small intestinal (duodenal and jejunal) tumors in the 2% HTPG group (but not in the 5% HTPG group) were significantly lower than those in the control group. Cell proliferation of normal-appearing duodenal mucosa was assessed by MIB-5 immunohistochemistry and shown to be significantly lower with 2% HTPG (but again not 5% HTPG) than in controls. These results in dicate that HTPG, at 2% in the diet, inhibited ENNG-induced pyloric stomach and small intestinal (especially duodenal) tumorigenesis in mice, associated with suppression of cell proliferation.