Hiroshi Seno
Kyoto University
288 Papers
908 Citations
Hiroshi Seno is an academic researcher from Kyoto University. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 39, co-authored 210 publications. Previous affiliations of Hiroshi Seno include Washington University in St. Louis.
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Papers
Age-related remodelling of oesophageal epithelia by mutated cancer drivers
Akira Yokoyama,Nobuyuki Kakiuchi,Tetsuichi Yoshizato,Yasuhito Nannya,Hiromichi Suzuki,Yasuhide Takeuchi,Yusuke Shiozawa,Yusuke Sato,Kosuke Aoki,Soo Ki Kim,Yoichi Fujii,Kenichi Yoshida,Keisuke Kataoka,Masahiro Nakagawa,Yoshikage Inoue,Tomonori Hirano,Yuichi Shiraishi,Kenichi Chiba,Hiroko Tanaka,Masashi Sanada,Yoshitaka Nishikawa,Yusuke Amanuma,Shinya Ohashi,Ikuo Aoyama,Takahiro Horimatsu,Shin'ichi Miyamoto,Shigeru Tsunoda,Yoshiharu Sakai,Maiko Narahara,J.B. Brown,Yoshitaka Sato,Genta Sawada,Koshi Mimori,Sachiko Minamiguchi,Hironori Haga,Hiroshi Seno,Satoru Miyano,Hideki Makishima,Manabu Muto,Seishi Ogawa,Seishi Ogawa +40 more
TL;DR: In physiologically normal epithelia, age-related expansion of clones that carry mutations in NOTCH1 and other driver genes is accelerated by risk factors for developing oesophageal squamous cell carcinoma, such as alcohol consumption or smoking.
Dclk1 distinguishes between tumor and normal stem cells in the intestine
Yuki Nakanishi,Hiroshi Seno,Ayumi Fukuoka,Taro Ueo,Yuichi Yamaga,Takahisa Maruno,Naoko Nakanishi,Keitaro Kanda,Hideyuki Komekado,Mayumi Kawada,Akihiro Isomura,Kenji Kawada,Yoshiharu Sakai,Motoko Yanagita,Ryoichiro Kageyama,Yoshiya Kawaguchi,Makoto Mark Taketo,Shin Yonehara,Tsutomu Chiba +18 more
TL;DR: It is shown here that Dclk1 does not mark NSCs in the intestine but instead marks TSCs that continuously produce tumor progeny in the polyps of ApcMin/+ mice, suggesting the potential for developing a therapy for colorectal cancer based on targeting D clk1-positive T SCs.
STAT3 is constitutively activated and supports cell survival in association with survivin expression in gastric cancer cells.
Naoki Kanda,Hiroshi Seno,Yoshitaka Konda,Hiroyuki Marusawa,Masashi Kanai,Toshio Nakajima,Tomoko Kawashima,Apichart Nanakin,Tateo Sawabu,Yoshito Uenoyama,Akira Sekikawa,Mayumi Kawada,Katsumasa Suzuki,Takahisa Kayahara,Hirokazu Fukui,Mitsutaka Sawada,Tsutomu Chiba +16 more
TL;DR: It is reported that STAT3 was constitutively activated in various human gastric cancer cells and its inhibition by ectopic dominant-negative STAT3 or Janus kinase inhibitor, tyrphostin AG490, induced apoptosis, and found activated form of STAT3, Tyr-705 phospho-stat3, was found in the nucleus of cancer cells in 11 of 40 human Gastric cancer specimens.
Induced Quiescence of Lgr5+ Stem Cells in Intestinal Organoids Enables Differentiation of Hormone-Producing Enteroendocrine Cells
TL;DR: It is shown that combined inhibition of Wnt, Notch, and MAPK pathways efficiently generates a diversity of EEC hormone-expressing subtypes in vitro and uncouple Wnt-dependent stem cell maintenance from EGF-dependent proliferation.
312
•Journal Article
Cyclooxygenase 2- and prostaglandin E2 receptor EP2-dependent angiogenesis in ApcΔ716 mouse intestinal polyps
Hiroshi Seno,Masanobu Oshima,Tomo-o Ishikawa,Hiroko Oshima,Kazuaki Takaku,Tsutomu Chiba,Shuh Narumiya,Makoto Mark Taketo +7 more
TL;DR: The results suggest that, in both benign and malignant mouse intestinal tumors, stromal expression of COX-2 results in elevated prostaglandin E2 levels that stimulate cell surface receptor EP2, followed by induction of vascular endothelial growth factor that causes tumor angiogenesis.