Integrated analysis of genetic and epigenetic alterations in hepatocellular carcinoma.
| Project/Area Number |
26293172
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Kyoto University |
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Principal Investigator |
Marusawa Hiroyuki 京都大学, 医学(系)研究科(研究院), 准教授 (80324630)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥15,340,000 (Direct Cost: ¥11,800,000、Indirect Cost: ¥3,540,000)
Fiscal Year 2016: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2015: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2014: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
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| Keywords | 肝癌 / 遺伝子変異 / AID |
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| Outline of Final Research Achievements |
Liver cancers, including hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma, generally arise in liver chronically inflamed due to various diseases such as hepatitis virus infection and steatohepatitis. Chronic inflammation triggers the aberrant expression of a DNA mutator enzyme, activation-induced cytidine deaminase (AID), and contributes to tumorigenesis through the accumulation of genetic aberrations. To gain further insight into the inflammation-mediated genotoxic events required for carcinogenesis, we examined the role of chronic inflammation in the emergence of genetic aberrations in the liver with constitutive AID expression. We found that inflammation-mediated transcriptional upregulation of target genes, including putative tumor suppressor genes, enhances the opportunity for inflamed cells to acquire somatic mutations and contributes to the acceleration of tumorigenesis in the inflamed liver tissues.
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Report
(4 results)
Research Products
(19 results)
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[Journal Article] TERT promoter mutations and chromosome 8p loss are characteristic of nonalcoholic fatty liver disease-related hepatocellular carcinoma.2016
Author(s)
Ki Kim S, Ueda Y, Hatano E, Kakiuchi N, Takeda H, Goto T, Shimizu T, Yoshida K, Ikura Y, Shiraishi Y, Chiba K, Tanaka H, Miyano S, Uemoto S, Chiba T, Ogawa S, Marusawa H.
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Journal Title
Int J Cancer
Volume: 139
Pages: 2512-2518
DOI
Related Report
Peer Reviewed / Int'l Joint Research / Acknowledgement Compliant
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[Journal Article] Activation-induced cytidine deaminase contributes to pancreatic tumorigenesis by inducing tumor-related gene mutations.2015
Author(s)
Sawai Y, Kodama Y, Shimizu T, Ota Y, Maruno T, Eso Y, Kurita A, Shiokawa M, Tsuji Y, Uza N, Matsumoto Y, Masui T, Uemoto S, Marusawa H, Chiba T.
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Journal Title
Cancer Res
Volume: 15
Pages: 32923301-32923301
DOI
Related Report
Peer Reviewed
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[Journal Article] Accumulation of somaticn T mutations TP53 in gastric epithelium with Helicobacter pylori infection.2014
Author(s)
Shimizu T, Marusawa H, Matsumoto Y, Inuzuka T, Ikeda A, Fujii Y, Minamiguchi S, Miyamoto S, Kou T, Sakai Y, Crabtree JE, Chiba T.
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Journal Title
Gastroenterrology
Volume: 147
Pages: 407-417
DOI
NAID
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] Leptin Receptor Somatic Mutations are frequent in HCV-infected Cirrhotic Liver and associated with Hepatocellular Carcinoma.2014
Author(s)
Ikeda A, Shimizu T, Matsumoto Y, Fujii Y, Eso Y, Inuzuka T, Mizuguchi A, Shimizu K, Hatano E, Uemoto S, Chiba T, Marusawa H
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Journal Title
Gastroenterology
Volume: 146
Pages: 222-232
DOI
NAID
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] A model of liver carcinogenesis originating from hepatic progenitor cells with accumulation of genetic alterations2014
Author(s)
Soo Ki Kim, Akihiro Nasu, Junji Komori, Takahiro Shimizu, Yuko Matsumoto, Yasuko Minaki, Kenji Kohno, Kazuharu Shimizu, Shinji Uemoto, Tsutomu Chiba, Hiroyuki Marusawa.
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Journal Title
Int. J. Cancer
Volume: 134
Pages: 1067-1076
DOI
NAID
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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