H
Hirokazu Tanaka
Researcher at Kindai University
Publications - 75
Citations - 2439
Hirokazu Tanaka is an academic researcher from Kindai University. The author has contributed to research in topics: Haematopoiesis & Stem cell. The author has an hindex of 17, co-authored 75 publications receiving 2002 citations. Previous affiliations of Hirokazu Tanaka include University of Tokyo & Aichi Medical University.
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Journal ArticleDOI
Landscape of genetic lesions in 944 patients with myelodysplastic syndromes
T Haferlach,Yasunobu Nagata,Vera Grossmann,Yusuke Okuno,Ulrike Bacher,Genta Nagae,Susanne Schnittger,Masashi Sanada,Ayana Kon,Tamara Alpermann,Kenichi Yoshida,Andreas Roller,Niroshan Nadarajah,Yuichi Shiraishi,Yusuke Shiozawa,Kenichi Chiba,Hirokazu Tanaka,H P Koeffler,Hans-Ulrich Klein,Martin Dugas,Hiroyuki Aburatani,Alexander Kohlmann,Satoru Miyano,Claudia Haferlach,Wolfgang Kern,Seishi Ogawa +25 more
TL;DR: Large-scale genetic and molecular profiling of multiple target genes is invaluable for subclassification and prognostication in MDS patients.
Journal ArticleDOI
Comprehensive analysis of genetic alterations and their prognostic impacts in adult acute myeloid leukemia patients.
Rika Kihara,Yasunobu Nagata,Hitoshi Kiyoi,Tomonori Kato,E Yamamoto,Kyogo Suzuki,Fangli Chen,Norio Asou,Shigeki Ohtake,S Miyawaki,Yasuhiko Miyazaki,Toru Sakura,Yukiyasu Ozawa,Noriko Usui,Heiwa Kanamori,Toru Kiguchi,K Imai,Naokuni Uike,Fumihiko Kimura,Kunio Kitamura,Chiaki Nakaseko,M Onizuka,Akihiro Takeshita,Fumihiro Ishida,Hitoshi Suzushima,Y Kato,Hiroshi Miwa,Yuichi Shiraishi,Kenichi Chiba,Hirokazu Tanaka,Satoru Miyano,Seishi Ogawa,Tomoki Naoe +32 more
TL;DR: Results indicate that the prognosis of AML could be stratified by the major mutation status in combination with cytogenetics, and that AML patients could be clearly stratified into five risk groups for overall survival by including the mutation status of DNMT3A, MLL-PTD and TP53 genes in the risk classification system of the European LeukemiaNet.
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PRPF8 defects cause missplicing in myeloid malignancies
Amina Kurtovic-Kozaric,Bartlomiej P Przychodzen,Jarnail Singh,Maria M. Konarska,Michael J. Clemente,Zaher K. Otrock,Megan O. Nakashima,Eric D. Hsi,Kenichi Yoshida,Yuichi Shiraishi,Kenichi Chiba,Hirokazu Tanaka,Satoru Miyano,Seishi Ogawa,Jacqueline Boultwood,Hideki Makishima,Jaroslaw P. Maciejewski,Richard A. Padgett +17 more
TL;DR: The exploration of clinical and functional consequences suggests that PRPF8 is a novel leukemogenic gene in myeloid neoplasms with a distinct phenotype likely manifested through aberrant splicing.
Journal ArticleDOI
The Satb1 Protein Directs Hematopoietic Stem Cell Differentiation toward Lymphoid Lineages
Yusuke Satoh,Takafumi Yokota,Takao Sudo,Motonari Kondo,Anne Y. Lai,Paul W. Kincade,Taku Kouro,Ryuji Iida,Koichi Kokame,Toshiyuki Miyata,Yoko Habuchi,Keiko Matsui,Hirokazu Tanaka,Itaru Matsumura,Kenji Oritani,Terumi Kohwi-Shigematsu,Yuzuru Kanakura +16 more
TL;DR: Comparing gene expression profiles for HSCs and early lymphoid progenitors revealed that Satb1, a global chromatin regulator, was markedly induced with lymphoid lineage specification, and governs the initiating process central to the replenishing of lymphoid lineages.
Journal ArticleDOI
Clinical and biological implications of ancestral and non-ancestral IDH1 and IDH2 mutations in myeloid neoplasms.
Remco J. Molenaar,Remco J. Molenaar,Swapna Thota,Yasunobu Nagata,Bhumika J. Patel,Michael J. Clemente,Bartlomiej P Przychodzen,C. Hirsh,Aaron D. Viny,N. Hosano,Fonnet E. Bleeker,Manja Meggendorfer,Tamara Alpermann,Yuichi Shiraishi,Kenichi Chiba,Hirokazu Tanaka,C. J. F. Van Noorden,Tomas Radivoyevitch,Hetty E. Carraway,Hideki Makishima,Satoru Miyano,Mikkael A. Sekeres,Seishi Ogawa,T Haferlach,Jaroslaw P. Maciejewski +24 more
TL;DR: Cross-sectionally, the frequencies of these mutations increased from lower- to higher risk disease, thus suggesting a role in clinical progression and Variant allelic frequencies indicated that IDH1MT and IDH2MT are ancestral in up to 14/74 (19%) vs 34/99 (34%; P=0.027) of cases, illustrating the pathogenic role of these lesions in myeloid neoplasms.