検索結果 47501 件
| JaLCDOI | 10.18926/AMO/46628 |
|---|---|
| フルテキストURL | 65_3_169.pdf |
| 著者 | Takeda, Masanori| Nagasaka, Takeshi| Dong-Sheng, Sun| Nishie, Hiroyuki| Oka, Tetsuhiro| Yamada, Eiji| Mori, Yoshiko| Shigeyasu, Kunitoshi| Morikawa, Tatsuya| Mizobuchi, Satoshi| Fujiwara, Toshiyoshi| |
| 抄録 | Secreted frizzled-related protein 2, (SFRP2) is a Wnt inhibitor whose promoter CpGs were recently found to be methylated at high frequency in colorectal cancers (CRCs). We hypothesized that the pattern of SFRP2 methylation may differ throughout the promoter during progressive tumorigenesis. Using combined bisulfite restriction analysis (COBRA), two methylation-sensitive regions (Regions A and B) of the SFRP2 promoter were investigated in 569 specimens of colorectal tissue:222 CRCs, 103 adenomatous polyps (APs), 208 normal colonic mucosa from CRC patients (N-Cs), and 36 normal colonic mucosa from subjects with no evidence of colorectal neoplasia at colonoscopy (N-Ns). Extensive (including both Regions A and B) and partial (either Region A or B) SFRP2 methylation levels were found in 61.7% and 24.8% of CRCs, 8.7% and 37.9% of APs, 3.9% and 39.9% of N-Cs, and 0% and 30.6% of N-Ns, respectively. Extensive methylation of the SFRP2 promoter was present primarily in CRCs, while partial methylation was common in APs. Whereas APs with the KRAS mutant showed no correlation to any pattern of SFRP2 methylation, extensive methylation of the SFRP2 promoter was significantly associated with KRAS mutant CRCs (p＜.0001), suggesting that genetic alteration in the RAS-RAF pathway might precede the spread of CpG methylation through the SFRP2 promoter, which is observed in over 60% of advanced colorectal tumors. |
| キーワード | BRAF/KRAS mutations promoter methylation colorectal cancer |
| Amo Type | Original Article |
| 出版物タイトル | Acta Medica Okayama |
| 発行日 | 2011-06 |
| 巻 | 65巻 |
| 号 | 3号 |
| 出版者 | Okayama University Medical School |
| 開始ページ | 169 |
| 終了ページ | 177 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | 英語 |
| 著作権者 | CopyrightⒸ 2011 by Okayama University Medical School |
| 論文のバージョン | publisher |
| 査読 | 有り |
| PubMed ID | 21709714 |
| Web of Science KeyUT | 000292017500003 |
| JaLCDOI | 10.18926/AMO/46627 |
|---|---|
| フルテキストURL | 65_3_163.pdf |
| 著者 | Arai, Minako| Takata, Ken| Takeda, Yoshimasa| Mizobuchi, Satoshi| Morita, Kiyoshi| |
| 抄録 | The mechanism of oxygen toxicity for central nervous system and hyperbaric oxygen (HBO) seizure has not been clarified. Noradrenergic cells in the brain may contribute to HBO seizure. In this study, we defined the activation of noradrenergic cells during HBO exposure by c-fos immunohistochemistry. Electroencephalogram electrodes were pre-implanted in all animals under general anesthesia. In HBO seizure animals, HBO was induced with 5 atm of 100% oxygen until manifestation of general tonic convulsion. HBO non-seizure animals were exposed to 25 min of HBO. Control animals were put in the chamber for 120 min without pressurization. All animals were processed for c-fos immunohistochemical staining. All animals in the HBO seizure group showed electrical discharge on EEG. In the immunohistochemistry, c-fos was increased in the A1, A2 and A6 cells of the HBO seizure group, and in the A2 and A6 cells of the HBO non-seizure group, yet was extremely low in all three cell types in the control group. These results suggest the participation of noradrenaline in HBO seizure, which can be explained by the early excitement of A1 cells due to their higher sensitivity to high blood pressure, hyperoxia, or by the post-seizure activation of all noradrenergic cells. |
| キーワード | hyperbaric oxygen seizure noradrenergic cells immunohistochemistry |
| Amo Type | Original Article |
| 出版物タイトル | Acta Medica Okayama |
| 発行日 | 2011-06 |
| 巻 | 65巻 |
| 号 | 3号 |
| 出版者 | Okayama University Medical School |
| 開始ページ | 163 |
| 終了ページ | 168 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | 英語 |
| 著作権者 | CopyrightⒸ 2011 by Okayama University Medical School |
| 論文のバージョン | publisher |
| 査読 | 有り |
| PubMed ID | 21709713 |
| Web of Science KeyUT | 000292017500002 |
| JaLCDOI | 10.18926/AMO/46626 |
|---|---|
| フルテキストURL | 65_3_151.pdf |
| 著者 | Fujiwara, Toshiyoshi| |
| 抄録 | Replication-selective tumor-specific viruses constitute a novel approach for treatment of neoplastic disease. These vectors are designed to induce virus-mediated lysis of tumor cells after selective viral propagation within the tumor. Human telomerase is highly active in more than 85ｵ of primary cancers, regardless of their tissue origins, and its activity correlates closely with human telomerase reverse transcriptase (hTERT) expression. We constructed an attenuated adenovirus 5 vector (Telomelysin, OBP-301), in which the hTERT promoter element drives expression of E1 genes. Since only tumor cells that express telomerase activity would activate this promoter, the hTERT proximal promoter would allow for preferential expression of viral genes in tumor cells, leading to selective viral replication and oncolytic cell death. Lymphatic invasion is a major route for cancer cell dissemination, and adequate treatment of locoregional lymph nodes is required for curative treatment in patients with gastrointestinal tumors. We demonstrated that intratumoral injection of Telomelysin mediates effective in vivo purging of metastatic tumor cells from regional lymph nodes. Moreover, using noninvasive whole-body imaging, we found that intratumoral injection of Telomelysin followed by regional irradiation induces a substantial antitumor effect, resulting from tumor cell-specific radiosensitization, in an orthotopic human esophageal cancer xenograft model. These results illustrate the potential of oncolytic virotherapy as a promising strategy in the management of human gastrointestinal cancer. |
| キーワード | telomerase adenovirus metastasis lymph node colorectal cancer |
| Amo Type | Review |
| 出版物タイトル | Acta Medica Okayama |
| 発行日 | 2011-06 |
| 巻 | 65巻 |
| 号 | 3号 |
| 出版者 | Okayama University Medical School |
| 開始ページ | 151 |
| 終了ページ | 162 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | 英語 |
| 著作権者 | CopyrightⒸ 2011 by Okayama University Medical School |
| 論文のバージョン | publisher |
| 査読 | 有り |
| PubMed ID | 21709712 |
| Web of Science KeyUT | 000292017500001 |
| 著者 | 岡山医学会| |
|---|---|
| 発行日 | 1929-07-31 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 41巻 |
| 号 | 7号 |
| 資料タイプ | その他 |
| 著者 | 大道 直一| |
|---|---|
| 発行日 | 1929-07-31 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 41巻 |
| 号 | 7号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | 得能 倫二| |
|---|---|
| 発行日 | 1929-07-31 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 41巻 |
| 号 | 7号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | 滋野井 至孝| |
|---|---|
| 発行日 | 1929-07-31 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 41巻 |
| 号 | 7号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | 勝呂 學| |
|---|---|
| 発行日 | 1929-07-31 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 41巻 |
| 号 | 7号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | 須之内 權三| |
|---|---|
| 発行日 | 1929-07-31 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 41巻 |
| 号 | 7号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | 藤野 源三| |
|---|---|
| 発行日 | 1929-07-31 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 41巻 |
| 号 | 7号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | 高橋 昌造| |
|---|---|
| 発行日 | 1929-07-31 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 41巻 |
| 号 | 7号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | 大森 三彦| |
|---|---|
| 発行日 | 1929-07-31 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 41巻 |
| 号 | 7号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | 藤原 晧| |
|---|---|
| 発行日 | 1929-07-31 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 41巻 |
| 号 | 7号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | 大畑 豐| |
|---|---|
| 発行日 | 1929-07-31 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 41巻 |
| 号 | 7号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | 小橋 政香| |
|---|---|
| 発行日 | 1929-07-31 |
| 出版物タイトル | 岡山医学会雑誌 |
| 巻 | 41巻 |
| 号 | 7号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | 石田 展久| |
|---|---|
| 発行日 | 2011-03-25 |
| 出版物タイトル | |
| 資料タイプ | 学位論文 |
| 著者 | 柳 文修| |
|---|---|
| 発行日 | 2011-03-25 |
| 出版物タイトル | |
| 資料タイプ | 学位論文 |
| 著者 | 神野 透人| |
|---|---|
| 発行日 | 2011-03-25 |
| 出版物タイトル | |
| 資料タイプ | 学位論文 |
| 著者 | 譚 東| |
|---|---|
| 発行日 | 2011-03-25 |
| 出版物タイトル | |
| 資料タイプ | 学位論文 |
| 著者 | 酒見 由美| |
|---|---|
| 発行日 | 2011-03-25 |
| 出版物タイトル | |
| 資料タイプ | 学位論文 |