Tenure-track faculties：Rika Kanezaki
 |
■Name Rika Kanezaki ■Resume [March 1997] Graduated from Department of Biology, Faculty of Science, Hirosaki University [March 1999] Completed Master’s degree at Graduate School of Science, Hirosaki University [April 1999] Laboratory researcher, Department of Pediatrics, Hirosaki University School of Medicine [April 2004] Laboratory assistant, Hirosaki University School of Medicine [April 2007] Laboratory assistant, Hirosaki University Graduate School of Medicine [March 2013] Completed Doctor’s degree at Hirosaki University Graduate School of Medicine [April 2013] Present post |
■Research field
Pediatric hematology
■Research theme
Elucidation of the molecular mechanism of Down syndrome-related acute megakaryocytic leukemia
■Research summary
Down syndrome is the most common chromosome abnormality caused by the presence of an extra copy of chromosome 21. One of its characteristics is an increased risk of childhood leukemia. Transient abnormal myelopoiesis (TAM), a hematologic disease associated with transient and abnormal proliferation of immature megakaryocytes, develops in approximately 10% of neonates with Down syndrome. Generally, TAM remits spontaneously; however, in approximately 20% of them, TAM progresses to acute megakaryocytic leukemia (ML-DS) during a short period, within four years of onset. This leukemia cell originates in the TAM cell. The objective of this research is to identify molecular mechanisms of acquisition of abnormal growth potential and leukemic transformation in TAM. Identification of these mechanisms will help in developing new therapies for treating and preventing ML-DS, while also contributing to the overall advancement of leukemia research.
＜Before assuming the present position＞
◎Original papers
・Yokoyama T, Toki T, Aoki Y, Kanezaki R, Park MJ, Kanno Y, Takahara T, Yamazaki Y, Ito E, Hayashi Y, Nakamura T. TRIB1 R107L gain-of function mutation in human acute megakaryocytic leukemia. Blood. 2012;119;2608-11
・Kanezaki R, Toki T, Terui K, Xu G, Wang R, Shimada A, Hama A, Kanegane H, Kawakami K, Endo M, Hasegawa D, Kogawa K, Adachi S, Ikeda Y, Iwamoto S, Taga T, Kosaka Y, Kojima S, Hayashi Y, Ito E. Down syndrome and GATA1 mutations: mutation classes correlate with progression to myeloid leukemia. Blood. 2010;116;4631-8
・Toki T, Kanezaki R, Adachi S, Fujino H, Xu G, Sato T, Suzuki K, Tauchi H, Endo M, Ito E. The key role of stem cell factor/KIT signaling in the proliferation of blast cells from Down syndrome-related leukemia. Leukemia. 2009;23;95-103
・Sato T, Toki T, Kanezaki R, Xu G, Terui K, Kanegane H, Miura M, Adachi S, Migita M, Morinaga S, Nakano T, Endo M, Kojima S, Kiyoi H, Mano H, Ito E. Functional analysis of JAK3 mutations in transient myeloproliferative disorder and acute megakaryoblastic leukaemia accompanying Down syndrome. Br J Haematol. 2008;141;681-8
・Ogawa J, Kanegane H, Tsuneyama K, Kanezaki R, Futatani T, Nomura K, Ishizawa S, Sasahara M, Ito E, Miyawaki T. Platelet-derived growth factor may be associated with fibrosis in a Down syndrome patient with transient myeloproliferative disorder. Eur J Haematol. 2008;81;58-64
・Kanezaki R, Toki T, Xu G, Narayanan R, Ito E. Cloning and characterization of the novel chimeric gene p53/FXR2 in the acute megakaryoblastic leukemia cell line CMK11-5. Tohoku J Exp Med. 2006;209;169-80
・Xu G, Kanezaki R, Toki T, Watanabe S, Takahashi Y, Terui K, Kitabayashi I, Ito E. Physical association of the patient-specific GATA1 mutants with RUNX1 in acute megakaryoblastic leukemia accompanying Down syndrome. Leukemia. 2006;20;1002-8
・Toki T, Katsuoka F, Kanezaki R, Xu G, Kurotaki H, Sun J, Kamio T, Watanabe S, Tandai S, Terui K, Yagihashi S, Komatsu N, Igarashi K, Yamamoto M, Ito E.
Transgenic expression of BACH1 transcription factor results in megakaryocytic impairment. Blood. 2005;105;3100-8
・Uyeda T, Takahashi T, Eto S, Sato T, Xu G, Kanezaki R, Toki T, Sun J, Yonesaka S, Ito E. Three novel mutations of the fibrillin-1 gene and ten single nucleotide polymorphisms of the fibrillin-3 gene in Marfan syndrome patients. J Hum. Genet. 2004;49;404-7
・Ishizaki N, Kanezaki R, Toki T, Ito E. A trial of isolating the novel genes on 21q11-21 to elucidate the gene responsible for transient abnormal myelopoiesis. Hirosaki Med. J. 2004;55;83-94
・Kamio T, Toki T, Kanezaki R, Sasaki S, Tandai S, Terui K, Ikebe D, Igarashi K, Ito E. B-cell-specific transcription factor BACH2 modifies the cytotoxic effects of anticancer drugs. Blood. 2003;102;3317-22
・Xu G, Nagano M, Kanezaki R, Toki T, Hayashi Y, Taketani T, Taki T, Mitui T, Koike K, Kato K, Imaizumi M, Sekine I, Ikeda Y, Hanada R, Sako M, Kudo K, Kojima S, Ohneda O, Yamamoto M, Ito E. Frequent mutations in the GATA-1 gene in the transient myeloproliferative disorder of Down syndrome. Blood. 2003;102;2960-8
・Tandai(Yamada) S, Sato H, Kanezaki R, Toki T, Igarashi K, Ito E. B cell specific transcription factor BACH2 negatively regulates expression of BCL-2 related A1 gene. Hirosaki Med. J. 2002;54;8-20
・Kanezaki R, Toki T, Yokoyama M, Yomogida K, Sugiyama K, Yamamoto M, Igarashi K, Ito E. Transcription factor BACH1 is recruited to the nucleus by its novel alternative spliced isoform. J Biol Chem. 2001;276;7278-84
・Sato H, Sasaki S, Kanezaki R, Toki T, Ito E. Identification of the target genes for B cell specific transcription factor BACH2. Hirosaki Med. J. 2001;53;73-81
・Sasaki S, Ito E. Toki T, Maekawa T, Kanezaki R, Umenai T, Muto A, Nagai H, Kinoshita T, Yamamoto M, Inazawa J, Taketo MM, Nakahata T, Igarashi K, Yokoyama M. Cloning and expression of human B cell-specific transcription factor BACH2 mapped to chromosome 6q15. Oncogene. 2000;19;3739-49
＜2013＞
◎Original papers
・Yoshida K, Toki T, Okuno Y, Kanezaki R, Shiraishi Y, Sato-Otsubo A, Sanada M, Park MJ, Terui K, Suzuki H, Kon A, Nagata Y, Sato Y, Wang R, Shiba N, Chiba K, Tanaka H, Hama A, Muramatsu H, Hasegawa D, Nakamura K, Kanegane H, Tsukamoto K, Adachi S, Kawakami K, Kato K, Nishimura R, Izraeli S, Hayashi Y, Miyano S, Kojima S, Ito E, Ogawa S. The Landscape of gene mutations in Down syndrome-related myeloid disorders. Nat Genet. 2013;45;1293-9.
・Toki T, Kanezaki R, Kobayashi E, Kaneko H, Suzuki M, Wang R, Terui K, Kanegane H, Maeda M, Endo M, Mizuochi T, Adashi S, Hayashi Y, Yamamoto M, Shimizu R, Ito E. Naturally occurring oncogenic GATA1 mutants with internal deletions in transient abnormal myelopoiesis in Down syndrome. Blood. 2013;121;3181-4