| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Research Abstract |
Hepatitis C virus (HCV) infection leads to the development of hepatic diseases, as well as extra hepatic disorders such as B-cell non-Hodikin's lymphoma (B-NHL). To reveal the molecular signaling pathways responsible for HCV-associated B-NHL development, we utilized transgenic (Tg) mice that express the full-length HCV genome specifically in B cells and develop non-Hodgkin type B-cell lymphomas (BCLs). The gene expression profiles in B cells from BCL-developing HCV-Tg mice, from BCL-non-deceloping HCV-Tg mice, and from BCL-non-developing HCV-negative mice were analyzed by genome-wide microarray.
Markedly modified genes such as Fos, C3, LTbR, A20, NF-kB and miR-26b in BCLs were further characterized using specific assays. We propose that activation of both canonical and alternative NF-kB signaling pathways and down-regulation of miR-26b contribute to the development of HCV-associated B-NHL.
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