H
Hitoshi Kiyoi
Researcher at Nagoya University
Publications - 334
Citations - 14347
Hitoshi Kiyoi is an academic researcher from Nagoya University. The author has contributed to research in topics: Leukemia & Myeloid leukemia. The author has an hindex of 56, co-authored 311 publications receiving 12756 citations. Previous affiliations of Hitoshi Kiyoi include University of California, San Diego.
Papers
More filters
Journal ArticleDOI
Activating mutation of D835 within the activation loop of FLT3 in human hematologic malignancies.
Yukiya Yamamoto,Hitoshi Kiyoi,Yasuyuki Nakano,Ritsuro Suzuki,Yoshihisa Kodera,Shuichi Miyawaki,Norio Asou,Kazutaka Kuriyama,Fumiharu Yagasaki,Chihiro Shimazaki,Hideki Akiyama,Kenji Saito,Miki Nishimura,Toshiko Motoji,Katsuji Shinagawa,Akihiro Takeshita,Hidehiko Saito,Ryuzo Ueda,Ryuzo Ohno,Tomoki Naoe +19 more
TL;DR: Analysis of the mutation of D835 of FLT3, which corresponds to D816 of c-KIT, in a large series of human hematologic malignancies demonstrates that the FLT 3 gene is the target most frequently mutated to become constitutively active in AML.
Journal ArticleDOI
Prognostic Implication of FLT3 and N- RAS Gene Mutations in Acute Myeloid Leukemia
Hitoshi Kiyoi,Tomoki Naoe,Yasuyuki Nakano,Shohei Yokota,Saburo Minami,Shuichi Miyawaki,Norio Asou,Kazutaka Kuriyama,Itsuro Jinnai,Chihiro Shimazaki,Hideki Akiyama,Kenji Saito,Hakumei Oh,Toshiko Motoji,Eijiro Omoto,Hidehiko Saito,Ryuzo Ohno,Ryuzo Ueda +17 more
TL;DR: The FLT3 gene mutation, whose presence is detectable only by genomic polymerase chain reaction amplification and gel electrophoresis, might serve as an important molecular marker to predict the prognosis of patients with AML.
Journal ArticleDOI
Tandem-duplicated Flt3 constitutively activates STAT5 and MAP kinase and introduces autonomous cell growth in IL-3-dependent cell lines.
Fumihiko Hayakawa,Masayuki Towatari,Hitoshi Kiyoi,Mitsune Tanimoto,Toshio Kitamura,H Saito,Tomoki Naoe +6 more
TL;DR: In this paper, the internal tandem duplication of the human Flt3 gene in approximately 20% of acute myeloid leukemia (AML) cases was identified, and the wild-type and the mutant FLt3 genes were transfected into two IL-3-dependent cell lines, 32D and BA/F3 cells.
Journal ArticleDOI
Internal tandem duplication of the FLT3 gene is a novel modality of elongation mutation which causes constitutive activation of the product.
Hitoshi Kiyoi,Masayuki Towatari,Shohei Yokota,Michinari Hamaguchi,Ryuzo Ohno,Hidehiko Saito,Tomoki Naoe +6 more
TL;DR: Findings suggest that the elongation of the JM domain rather than increase of tyrosine residues causes gain-of-function of FLT3, and ITD is a novel modality of somatic mutation which activates its product.
Journal ArticleDOI
Internal tandem duplication of the FLT3 gene is preferentially seen in acute myeloid leukemia and myelodysplastic syndrome among various hematological malignancies. A study on a large series of patients and cell lines
Shouhei Yokota,Hitoshi Kiyoi,Mitsushige Nakao,Toshiki Iwai,Shinichi Misawa,Tsukasa Okuda,Yoshiaki Sonoda,Tatsuo Abe,K Kahsima,Y Matsuo,Tomoki Naoe +10 more
TL;DR: In the various cell lines examined, this abnormality was determined in only one derived from AML and never found in other hematological malignancies, emphasizing that the length mutation of FLT3 at JM/TK-I domains were restricted to AMl and MDS.