| Project/Area Number |
17015048
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | The University of Tokyo (2007-2009)
National Cancer Center Research Institute and Research Center for Innovative Oncology, National Cancer Center Hospital East (2005-2006) |
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Principal Investigator |
MURAKAMI Yoshinori The University of Tokyo, 医科学研究所, 教授 (30182108)
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| Co-Investigator(Kenkyū-buntansha) |
MASUDA Mari 国立がんセンター研究所, 研究員 (70435717)
ITO Akihiko 東京大学, 医科学研究所, 准教授 (80273647)
SAKURAI Mika 東京大学, 医科学研究所, 助教 (80508359)
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| Project Period (FY) |
2005 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥59,900,000 (Direct Cost: ¥59,900,000)
Fiscal Year 2009: ¥11,600,000 (Direct Cost: ¥11,600,000)
Fiscal Year 2008: ¥11,700,000 (Direct Cost: ¥11,700,000)
Fiscal Year 2007: ¥11,700,000 (Direct Cost: ¥11,700,000)
Fiscal Year 2006: ¥11,700,000 (Direct Cost: ¥11,700,000)
Fiscal Year 2005: ¥13,200,000 (Direct Cost: ¥13,200,000)
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| Keywords | アレル特異的発現 / RNA difference plot / CADM1 / 非小細胞肺がん / ATL / 細胞接着分子 / RAC / Tiam1 / 細胞運動性 / 上皮様形態形成 / 4.1N / アレル / 遺伝子発現 / がん抑制遺伝子 / 細胞接着 / RDP / 遺伝子欠損マウス / 肺腺癌 / 肺腺腫 / 浸潤 / TSLL2 / CADM4 / DAL-184.1B / メチル化 / 賢明細胞がん / 前立腺がん / DNA修復酵素遺伝子 / TSLL2遺伝子 / DAL-1 / 4.1B遺伝子 / 腎明細胞がん / 予後因子 |
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| Research Abstract |
For the molecular diagnosis of human cancer, novel molecular targets were identified and a useful technique was developed through the genetic analysis of human cancer cells as well as the host individuals. Using RNA difference plot, a highly quantitative method to identify allele-specific gene expression that we have developed previously, we found that the allele-specific expression of the responsible genes for familial cancer were well correlated with the phenotypic variation in the carriers of the relevant gene mutations. Furthermore, we found that a cell adhesion molecule, CADM1, and its binding partner, 4.1B, act as tumor suppressors in human non-small cell lung cancer and renal clear cell carcinoma, whereas CADM1 was ectopically overexpressed in adult T-cell leukemia (ATL). In ATL, CADM1 associated with Tiam1 and enhanced the cell mobility through activation of Rac, providing a possible molecular cascade for suppressing the invasion of ATL.
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