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Your search keyword '"Tanaka, Seiji"' showing total 16 results
Start Over Author "Tanaka, Seiji" Publisher springer japan
16 results on '"Tanaka, Seiji"'

6. Ground-surface application of pheromones through a mini-dispenser for mating disruption of the white grub beetle Dasylepida ishigakiensis (Coleoptera: Scarabaeidae)

Author

Arakaki, Norio, Nagayama, Atsushi, Kijima, Keisuke, Yasui, Hiroe, Tsujii, Nao, Tanaka, Seiji, Ueda, Miyuki, Kanayama, Shoko, Kawaguchi, Kosei, Jitsuno, Sakiko, Oike, Masahiro, Watanabe, Kisaki, Wakamura, Sadao, Mochizuki, Fumiaki, Saguchi, Ryuichi, Fujii, Tatsuya, and Naito, Takayuki

Published
2017
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16. The Nup98::Nsd1 fusion gene induces CD123 expression in 32D cells.

Author

Okamoto K, Imamura T, Tanaka S, Urata T, Yoshida H, Shiba N, and Iehara T

Subjects
Animals, Mice, Interleukin-3 Receptor alpha Subunit genetics, Nuclear Pore Complex Proteins genetics, Histone-Lysine N-Methyltransferase, Interleukin-3 genetics, Interleukin-3 metabolism, Leukemia, Myeloid, Acute therapy
Abstract

The NUP98::NSD1 fusion gene is associated with extremely poor prognosis in patients with acute myeloid leukemia (AML). NUP98::NSD1 induces self-renewal and blocks differentiation of hematopoietic stem cells, leading to development of leukemia. Despite its association with poor prognosis, targeted therapy for NUP98::NSD1-positive AML is lacking, as the details of NUP98::NSD1 function are unknown. Here, we generated 32D cells (a murine interleukin-3 (IL-3)-dependent myeloid progenitor cell line) expressing mouse Nup98::Nsd1 to explore the function of NUP98::NSD1 in AML, including comprehensive gene expression analysis. We identified two properties of Nup98::Nsd1 + 32D cells in vitro. First, Nup98::Nsd1 promoted blocking of AML cell differentiation, consistent with a previous report. Second, Nup98::Nsd1 increased dependence on IL-3 for cell proliferation, due to overexpression of the alpha subunit of the IL-3 receptor (IL3-RA, also known as CD123). Consistent with our in vitro data, IL3-RA was also upregulated in samples from patients with NUP98::NSD1-positive AML. These results highlight CD123 as a potential new therapeutic target in NUP98::NSD1-positive AML., (© 2023. Japanese Society of Hematology.)

Published
2023
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