Project/Area Number |
21390180
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Laboratory medicine
|
Research Institution | Hamamatsu University School of Medicine |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
TAKESHITA Akihiro 浜松医科大学, 医学部, 准教授 (00242769)
IINO Kazumi 浜松医科大学, 医学部附属病院, 助教 (90402263)
WATANABE Watanabe 浜松医科大学, 医学部, 助教 (00362187)
HASHIMOTO Dai 浜松医科大学, 医学部, 講師 (20467236)
FUJISAWA Tomouki 浜松医科大学, 医学部附属病院, 助教 (20402357)
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥19,240,000 (Direct Cost: ¥14,800,000、Indirect Cost: ¥4,440,000)
Fiscal Year 2011: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2010: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2009: ¥7,280,000 (Direct Cost: ¥5,600,000、Indirect Cost: ¥1,680,000)
|
Keywords | エピジェネティクス / マイクロRNA / ゲノム / 臨床検査値 / miRNA / ゲノム不安定性 / 染色体バンド境界 / DNA複製タイミング / 染色体工学 / CA19-9 / ルイス酵素 / 遺伝子多型 / 複製タイミング / ゲノム不安定 / 乳酸デヒドロゲナーゼ / ワールブルグ効果 / DNAメチル化 / K-ras / HIF1α |
Research Abstract |
Even genuinely Le-negative patients, who genetically lack the Le enzyme and theoretically never produce CA19-9, occasionally show a slight increase in serum CA19-9 level. We analyzed this mechanism and found the phenomena are occurred when the patients are homozygous for Se-negative genotypes and suffer from advanced cancer with overproduction of glycans as precursors of CA19-9. The human genome is composed of large-scale compartmentalized structures, including replication-timing zones and long-range GC% mosaic structures, which are related to chromosome bands. We found that the early/late-switch regions of replication timing, which generally correspond with transitions in GC content, are correlated with R/G-chromosome band boundaries, and such specific regions in the human genome correspond to "unstable" regions of the genome in which increased DNA damage occurs. Information acquired through genome-wide studies of replication timing will contribute substantially to our understanding of the molecular mechanisms in the pathogenesis of diseases.
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