| Project/Area Number |
21790970
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pediatrics
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| Research Institution | The University of Tokyo |
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Principal Investigator |
MOTOMURA Ai The University of Tokyo, 医学部附属病院, 助教 (40511465)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 先天性奇形症候群 / Noonan症候群 / 結節性硬化症 / SNP array / 卵巣がん / Sotos症候群 / 肝芽腫 / 神経膠腫 / 有馬症候群 / 網膜芽腫 |
|---|
| Research Abstract |
Although congenital anomaly syndromes (CAS) often complicate malignant tumors, pathogenesis of CAS and these tumors are not fully understood. Thus, to investigate molecular pathogenesis of CAS and complicated tumors, we performed genome-wide copy number analysis of hepatoblastoma in Sotos syndrome, retinoblastoma in Arima syndrome and ovarian cancer in Noonan syndrome using SNP-genotype microarrays. Several unknown copy number changes including high-grade amplification of 2q24, gain of chromosome 2 and uniparental disomy of 18p were identified in these tumors. Our results suggest that candidate target genes involved in the pathogenesis of complicated tumors would be exist within the regions showing copy number abnormalities.
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