The basic and clinical study for the personalized oral cancer therapy
| Project/Area Number |
19390523
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | Meikai University |
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Principal Investigator |
FUKUDA Masakatsu Meikai University, 歯学部, 講師 (10311614)
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| Co-Investigator(Kenkyū-buntansha) |
KUSAMA Kaoru 明海大学, 歯学部, 教授 (20130479)
SAKASHITA Hideaki 明海大学, 歯学部, 教授 (10178551)
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| Project Period (FY) |
2007 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥16,770,000 (Direct Cost: ¥12,900,000、Indirect Cost: ¥3,870,000)
Fiscal Year 2009: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2008: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2007: ¥7,800,000 (Direct Cost: ¥6,000,000、Indirect Cost: ¥1,800,000)
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| Keywords | 頭頸部悪性腫瘍 / 遺伝子変異 / NF-κB / p53 / ING / アポトーシス / NF-кB |
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| Research Abstract |
Human oral squamous cell carcinoma (HOSCC) is the most common malignant tumor in the oral cavity, and that frequent alteration of p53 tumor suppressor gene is associated with the development of HOSCC, especially in 30% to 50% of that. The p33^<ING1b> has a close relationship with p53 and that neither p53 nor p33^<ING1b> alone can cause cell growth inhibition, which prompted us to investigate their potential role in oral carcinogenesis. Furthermore, Nuclear factor-κB (NF-κB) has key roles in inflammation, immune response, tumorigenesis and protection against apoptosis. It has recently been reported that the function of NF-κB is regulated by p53. In this study, to determine whether the p33^<ING1b> isoform plays a role in chemosentivity of HOSCC, we investigated the effect of p33^<ING1b> overexpression on taxol-induced apoptosis and the activation of caspases in HOSCC cells. Previous experimental evidences indicated that p33^<ING1b> functionally cooperates with p53 in controlling cell growth, senescence and apoptosis. The p33^<ING1b> may cooperate with p53 in taxol-induced apoptosis of the HOSCC. To test this hypothesis, the HOSCC cell lines, contained wild-type p53 and mutant p53, were employed to examine the enhancement ofapoptosis by p33^<ING1b> overexpression and its mechanism. We found that overexpression of exogenous p33^<ING1b> in wild-type p53 cell line can dramatically promote taxol-induced apoptosis.
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Report
(4 results)
Research Products
(25 results)
